Heart Attack Blues 42t6w

Copyright © 2013 by Luminosity Records All rights reserved.

ISBN: 978-0-615-80311-1

Project editor: Sheila Buff Cover design: Savva Teteriatnikov

The information in this book and the associated Web site http://heart-attackblues.com is intended to help you make informed decisions about your health. It is not intended as a substitute for medical treatment. This information should be used in conjunction with the guidance and care of your physician. If you think you have a medical problem, seek competent professional help. If you think you are having a heart attack, call 911 at once.

To my wife with all my love, without you I could not be where I am.

Contents About the Author Introduction Prologue: Are You at Risk of a Heart Attack? 1. The Epidemic of Heart Disease 2. Heart Attack!! 3. Naming the Enemy 4. Treating Heart Attacks 5. Know Your Risk Factors 6. The Gold Standard 7. Women and Heart Attacks 8. How to Save Your Own Life 9. Other Causes of Chest Pain that Can Kill You 10. How to Prevent a Heart Attack Epilogue

About the Author

Terrence Baruch, MD, FACC has been practicing interventional cardiology since 1992 in the Pasadena-Arcadia area of Los Angeles County, California. He has performed more than 10,000 cardiac procedures in that time; well over 500 have been emergency angioplasties for treatment of acute myocardial infarction. He is the director of the Cardiac Catheterization Laboratory and the founder and director of the Heart Attack Program at the Methodist Hospital of Southern California. Dr. Baruch played an active role in the development of one of the first regional heart attack programs in southern California. He helped develop a program that trained emergency medical services (EMS) personnel to recognize a suspected heart attack, stabilize the patient, and then transport him or her to a cardiac center of excellence. Because of his expertise and vast experience, Dr. Baruch has been a national speaker on the state-of-the-art treatment of myocardial infarction, sponsored by companies such as Schering-Plough, Lilly, and Aventis. He has lectured at multiple hospitals in more than 20 different states, including Alaska and Hawaii. He has provided educational materials, guidelines, pathways, and sample hospital orders to these institutions so that they could organize their own STEMI programs.

Introduction

When I was a young cardiologist-in-training back in the mid-1980s, we were taught how to use clot-busting drugs to treat heart attacks. The drugs dissolved the clot in a coronary artery that was causing the heart attack. Although these drugs were a big step forward in treating heart attacks, they had some drawbacks. The biggest was that they worked well only about half the time. Then, when I was halfway through my training, my world was rocked by the introduction of angioplasty. By snaking a catheter into the clogged coronary artery of someone having a heart attack, we could open the artery and restore normal blood flow to the heart. I was fortunate to be able to learn this technique from many of the doctors who pioneered it. I was fortunate again to be able to develop the first heart attack program at Methodist Hospital of Southern California in Los Angeles. We were among the first in southern California to use catheterization as the preferred treatment for a heart attack. Percutaneous coronary intervention (PCI), as this catheterization technique is called, works best when it is performed quickly. The gold standard is 90 minutes from arrival in the emergency room to the cath lab. At Methodist Hospital, we were soon able to achieve the goal of 90 minutes or less (sometimes much less) for almost every patient. Even so, our outcomes weren’t always as good as possible. Why? Because when it comes to heart attacks, time is muscle. We could get a heart attack victim’s artery unclogged soon after he or she arrived at the hospital. What we couldn’t do was fix the damage that happened before that. Too many patients were waiting too long to call 911. When they did, they were taken directly to the nearest hospital—even if that hospital didn’t have a cath lab—and then transferred on to us at Methodist. That meant further delay and further permanent damage to the heart muscle. While we could quickly unclog a blocked heart artery when the patient finally got to us, we couldn’t repair the damage that had occurred before then. I wasn’t the only cardiologist who was frustrated by this problem. In the early 2000s, hospitals around the country began setting up receiving programs for heart attack patients. The idea was to designate a central hospital in the area as a

cardiac care center of excellence. The hospital needed to have a fully equipped cath lab with a full-time staff on round-the-clock call. Patients with suspected heart attacks would be sent directly to this hospital, even if it was further away than the nearest emergency room. The idea wasn’t that different from tiered trauma centers, a life-saving concept that was already in place. In 2007, I worked closely with the Emergency Medical Services in Los Angeles County to create a county-wide heart attack network of STEMI receiving centers, or SRCs (STEMI is doctor-speak for a heart attack). The end result was an outstanding SRC network, one that has saved many lives since then. In 2008, we developed the pilot program for the Call 911 protocol. In 2009 the program became official policy and was accepted by all 33 of the STEMI receiving centers in Los Angeles County. I am still the chair of the Los Angeles County Emergency Medical Services SRC Advisory Committee. There’s no doubt that SRCs save lives—but only if patients use them. Too often, we find that people with heart attack symptoms don’t realize what is happening to them. They ignore or endure the symptoms, often for hours, and then finally take themselves to the nearest emergency room. I’ve treated many, many patients who waited too long to get treatment for their heart attack. When I talk with them about why they waited, they usually tell me that they didn’t know their symptoms meant heart trouble. They thought they were having bad indigestion or a stomach bug, or that they had strained a chest or arm muscle, or that their gall bladder was acting up again, or that they were just overtired. Some were pretty sure they were having a heart attack but decided not to call 911. Instead, they waited until someone could drive them to the hospital. I can unclog your heart in 20 minutes—but you have to get to me first! That means knowing your risk of having a heart attack, knowing what the symptoms are, and knowing to call 911 at once. In places that don’t have SRC networks, it also means knowing which hospital in your area is a cardiac center of excellence and going directly to it. My goal with this book and the accompanying video is to help you save your own life. I hope it will help you understand what a heart attack, how it should be treated, and most importantly, why time is muscle.

Prologue: Are You at Risk of a Heart Attack?

Death first became a reality to me on Friday, November 22, 1963. I took the day off from the fifth grade, claiming not to be feeling well. My real intention was getting started on a three-day weekend. At 10:30 a.m. PST, I was just about to watch a rerun of the situation comedy, Pete and Gladys. When you’re 10 years old, just about anything is funny. Suddenly, a news flash broke and interrupted the show. A teary-eyed Walter Cronkite announced that John F. Kennedy, the thirty-fifth president of the United States, had been shot in Dallas, Texas. He had been rushed to the nearest hospital for treatment. I stuck like glue to the TV. Both my parents were working, so I had no one to tell what was happening. After about an hour, the announcement was made that JFK was dead. All of us who are old enough the precise details of where we were at that moment. Although the president was a distant figure to a 10-year-old, his death still felt very personal to me. Prior to this, I had never known anyone who had died. My only experience with death was when people died on TV, but I knew that wasn’t real. The next week they would be alive again on some different show. A couple of days later, I clearly watching the funeral with my Grandpa Joe. I couldn’t believe JFK was really dead and that we would never see him again. Grandpa Joe said that everyone who lives will eventually have to die. You just hope that you get to live a long, healthy, and happy life. This, of course, was not very comforting. The funeral brought the reality of death home to me. It was quite scary.

Only a few months later, I was on the playground at my school, just blocks away from where I lived. I heard a siren and then saw an ambulance speed by toward the local hospital. My first thought was that I hoped the poor soul in the ambulance did not have to die. When I got home later that day, I could tell that something was seriously wrong. I saw that my mom had been crying. She took me aside and told me that Grandpa Joe, her father, had gotten sick and had to go to the hospital. She said that he had been on top of his house, putting on a new roof. While smoking a Lucky Strike and carrying a large pile of shingles on his shoulder, he suddenly developed severe chest pain, became short of breath, and broke out in a cold sweat. I immediately realized that it was him in the ambulance I had seen ing the school. The first thing I said was, “Is he dead?” My mother said no, thank God, he was actually doing fairly well. His pain had gone away and he was breathing much easier. The doctors said that he had only suffered “a mild heart attack” and he looked like he would do well. They would observe him in the hospital for a few days and he would be coming home soon. Of course, I was relieved by this. I was very close to my grandfather and the thought of him not being around was devastating. I asked what a heart attack was and was told that a blood clot can form in the heart causing it to be damaged. I’d never heard of that before. All was well the next day. I wanted to go to the hospital to visit my grandfather. I was told I was too little and I would be seeing him tomorrow when he came home anyway. About 3:00 a.m., the phone rang. I couldn’t ever getting a call that early in the morning. My mother picked up the phone and cried, “Oh, no.” My parents immediately went to the hospital. My sister and I waited for hours before my parents finally came home. By the look on their faces, I knew right away that Grandpa Joe had died. I asked how he could be dead if he only had a mild heart attack. My mom said that he sleeping,

then he suddenly awoke and complained of the same chest pain, but this time more severe. He then lost consciousness and died suddenly. He was only 59 years old. We are all afraid to die. The mere thought of death provokes fear and anxiety. Death is the unknown. It is mysterious. It is the arrival of the Grim Reaper, the Angel of Death. It threatens to instantly take away everything we love and care about in this world. The concept of our lives ending creates uneasy thoughts and fears about what may happen. I think we are most troubled by the fact that we may die prematurely. We all know that life’s a bitch and then you die. Even so, when all is said and done, it’s actually quite nice to be here on earth. And not knowing what the other options are, we would all like to get as much mileage out of this current lifetime as we possibly can.

Death by Heart Attack There are said to be about six thousand common ways to die. Some ways are quite unusual. Attila the Hun bled to death from a nosebleed on his wedding night in 453 A.D. Alexander I of Greece, king of the Hellenes starting in 1917, died October 25, 1920, from blood poisoning after being bitten by his gardener’s pet monkey. The most likely way you will die, however, is by having a heart attack. Someone has a heart attack every 20 seconds in the United States. About half of all deaths each year are from heart attacks. There are approximately 300,000,000 people in the U.S. today. About 2,000,000 of those people die every year. Approximately 1,000,000 of these deaths—about half—are due to cardiovascular disease. Some 60 to 70 percent of people who have heart attacks get no warning. About 30 percent of people having heart attacks die before they can even reach the hospital. Another 15 to 20 percent can die in the hospital if optimal care is not provided. A heart attack is damage to the heart muscle as a result of a sudden interruption of its blood supply. This is almost always due to the formation of a blood clot

(thrombosis) somewhere within the arteries that supply the heart with blood. The medical term for this condition is acute myocardial infarction. Acute means all of a sudden. Myocardium is the muscular tissue of the heart. Infarction means death of body tissue caused by lack of blood supply. Even though many thousands of people die each year from heart attack, most people are incredibly unaware of the magnitude of the problem. They are also unaware that dying from this killer can almost completely be avoided if the appropriate measures are taken in a timely fashion.

What To Do if You Have a Heart Attack Knowing what to do if you are having a heart attack will save your life. You must take two important steps immediately. First, call 911 for help. Don’t delay. Paramedics will come quickly to your location, stabilize you, and then get you to the hospital as soon as possible. This will significantly reduce your chances of dying. Second, make sure you get taken to the right hospital. Your odds of survival increase greatly if you are taken quickly to a hospital that is prepared to treat your heart attack promptly with life-saving procedures. Unfortunately, today only a small percentage of hospitals can do this. Know which hospital in your area is best for treating a heart attack and be sure you are taken to it. If you delay your 911 call or go to the wrong hospital ,your chances of dying are much, much higher. The rest of this book will tell you why what happens in the critical 90 minutes after a heart attack is the difference between life and death.

1. The Epidemic of Heart Disease

An epidemic is an outbreak of a disease that develops and spreads rapidly. Over the centuries, many infamous epidemics have affected the human race profoundly. The Black Death, caused by bubonic plague, is probably the most well known. Three major bubonic plague epidemics, in the sixth, fourteenth, and nineteenth centuries, rapidly killed many millions worldwide. The death rate from this disease was about 90 percent. The time from infection to death was usually less than one week. The Black Death outbreak that lasted from 1348 to 1350 reduced the total population of Europe from about 450 million to between 350 and 375 million—at least 100 million people died in just two years. Today, even though bubonic plague is rare and easily treated with antibiotics, just the mention of the Black Death evokes a sense of fear. Despite these ominous numbers, the Black Death wasn’t the worst epidemic the world has seen. The influenza pandemic (an epidemic that spreads worldwide) of 1918–1919 was even more deadly. The death toll from that disaster was at least 50 million people all around the world in one year! The flu pandemic killed more people than World War I did.

Our Silent Epidemic Today, we are facing an epidemic that is every bit as severe as the epidemics of the past. It is a silent epidemic of atherosclerosis, the culprit behind the million heart attacks, many of them fatal, that occur every year in the United States. Worldwide, atherosclerosis is the most common cause of death—by far. This Public Enemy No. 1 is the underlying cause of most heart attacks, strokes, and other serious health problems such as kidney disease. Your doctor has probably warned you about this extremely dangerous disease. He or she may even have told you that you have it. Yet despite how common atherosclerosis is, very few people really understand what it is, what causes it, and why it has a good chance of killing you. Let’s look closer.

Atherosclerosis comes from two Greek words: athero, meaning gruel or paste, and sclerosis, meaning scarring or hardening. In fact, atherosclerosis is sometimes called, somewhat inaccurately, hardening of the arteries. The process commonly leads to the clogging and hardening of the blood vessels by a mixture of cholesterol and calcium. This very often compromises blood flow to the body’s organs, including the heart, brain, and kidneys. Reduced or blocked blood flow to an organ is called ischemia (pronounced iss-KEE-mee-ah), another word from the Greek, meaning “restrained blood.” Anatomy of an Artery What causes an artery carrying blood to your heart or brain to clog up so much that the blood flow is partially or even fully blocked? To answer that question, let’s first take a quick look at the anatomy of an artery (I’ll go into this in more detail in the next chapter). Blood vessels that carry blood from the heart to the body are called arteries. If you were to look at a cross-section of a normal human artery, you would see that it is divided into three distinct layers. The innermost layer, the part that is in with the blood flowing through the artery, is called the intima. It is a sheet of endothelial cells that forms a barrier that protects the vessel from the development of atherosclerosis. The middle layer is the media. It consists of smooth muscle fibers that regulate the amount of blood flowing through the artery by contracting and relaxing. The outer layer is the adventitia. This is a network of tiny blood vessels that actually provide the artery itself with blood. The open central part of the artery—the part the blood flows through—is called the lumen. The intima is lined with a very thin layer of cells that do a superb job of protecting the artery from clogging. The lining usually holds up well for many decades. After years of exposure to factors that promote development of atherosclerosis, however, the lining starts to break down. What are those clogpromoting factors? Conditions that are all too common in today’s world, including high blood pressure, diabetes, high cholesterol, and smoking (those factors will be discussed in greater detail later in this book). When the intima barrier in an artery breaks down, the atherosclerosis process begins. The area becomes inflamed—it swells as white blood cells move into the

area to counteract the damage. At the same time, cholesterol and calcium build up in the inflamed area. The cholesterol/calcium mixture is called plaque, and the buildup of this material is called plaque formation. Your body tries to cope with plaque in an artery by forming a sort of fibrous cap to hold in the material and keep the artery open. The danger is that the fibrous cap on a plaque deposit is very likely to spontaneously rupture. When the plaque deposit breaks open, the material inside spills out into the lumen. When that happens, a blood clot, or thrombosis, forms on top of the ruptured material and abruptly and completely terminates blood flow to the organ. That causes the part of the organ that relies on that artery for blood flow to die—you have an infarction. When you have thrombosis in one of the arteries that nourishes your heart, you have a heart attack. When thrombosis happens in one of the arteries that nourishes your brain, you have a brain attack, or a stroke.

How Common Is Atherosclerosis? The plaque that builds up in the artery starts out as a soft streak of fatty material. Fatty streaks in the arteries that feed the heart and brain are common. In fact, 43 percent of infants aged 1 to 12 months have been found to have this lesion. After the age of 1 year, fatty streaks are present in everyone to various degrees. Among young men in their late teens and early twenties killed in the Vietnam war, a high percentage of them had extensive fatty streaks. Autopsy studies show that the majority of people (almost 90 percent) have evidence of significant disease by the age of 40. Thickened and calcified coronary arteries have been found in the mummy of a 50-year-old Egyptian man who died around 1,000 BC. The frozen and mummified body of Oetzi the Ice Man, who probably lived around five thousand years ago, has evidence of hardened arteries. Today, about half of the people with evidence of coronary artery plaque will go on to develop heart disease or have a heart attack. In the past century, the most common causes of death have dramatically changed. Prior to the twentieth century, very few people actually died of atherosclerotic vascular disease. In the early 1900s, many people died relatively young, usually as a result of fatal infectious diseases: pneumonia, influenza, tuberculosis, diarrhea, and enteritis combined to cause 30 percent of all deaths at

that time. Advances in the treatment of infectious diseases since the mid-1900s means that life expectancy in the United States has increased greatly. The causes of death have shifted to chronic diseases, including heart disease and diabetes. Industrialization has made the life of most people today much less physically demanding. Physical labor is less common—machines do the work previously done by people. People drive cars instead of walking or riding bicycles. As technology continues to progress, the need for physical activity becomes less and less. As people moved from working on farms to working in factories and offices, their diets changed as well. Instead of low-fat foods such as complex grains and fresh vegetables, people have shifted to foods that are fast and easy to get. Processed foods, foods high in saturated fat, and foods loaded with sugar have become the foundation of the American diet. The combination of a sedentary lifestyle and the consumption of rich foods has sparked the atherosclerosis epidemic. The widespread use of tobacco throughout the twentieth century also accelerated the development of the disease. Smoking increases the risk of atherosclerosis exponentially. Today, nearly 62 million Americans have atherosclerotic vascular disease—in other words, they have clogged arteries that will almost certainly lead to heart disease, a heart attack, a stroke, kidney disease, and other serious and often fatal health problems. At least 50 million Americans—and probably many more— have high blood pressure, which contributes to causing atherosclerotic vascular disease and makes it advance more rapidly. Of those, perhaps as many as 30 percent have no idea they have high blood pressure. Among the people who are diagnosed, as many as one-third are probably not adequately treated. Nearly 13 million Americans already have coronary artery disease—7.5 million have already had a heart attack, and 6.5 million have angina, or chest pain caused by exertion. About 4.6 million people have had strokes. The prevalence of peripheral vascular disease (poor circulation to the legs) and kidney disease from clogged arteries is not accurately known, but it is almost certainly high. We don’t know for sure because health care professionals are not doing an adequate job of making these diagnoses. These numbers are serious. Of the million people who die every year in the

United States, half will die of atherosclerotic vascular disease. Sadly, many of those deaths—about 150,000—will be in people younger than age 65. All the other causes of death combined still don’t compare to the death rate from atherosclerosis. Cancer kills about 500,000 people a year. Almost 120,000 people die every year from chronic obstructive lung disease (COPD). About 100,000 people die as a result of accidents; 15,000 people die each year from HIV/AIDS. Atherosclerosis is a worldwide epidemic that is occurring right now and is getting worse at a fast rate. By 2020, cardiovascular disease will cause one of every three deaths worldwide.

2. Heart Attack!!

To understand all the bad things that happen when you have a heart attack, it helps to understand how your heart works—and what can go terribly wrong when you have coronary artery disease. Your Heart and Circulatory System The circulatory system consists of the heart and its vast network of blood vessels. This system moves blood steadily—circulates it—throughout your body. Your heart is at the center of your circulatory system. Your heart is a hollow organ made of muscle. It’s about the size of your fist and sits under and just to the left of your breastbone (sternum). Your heart’s function is to pump blood throughout the body. It does this by contracting (systole) and relaxing (diastole). (See chapter 5 for a discussion of “systolic” and “diastolic” blood pressure measurements.) The heart is divided into four chambers. The two smaller chambers on the top of the heart are called atria (the singular is atrium). The two chambers on the bottom of the heart are called ventricles. The right atrium and right ventricle work together to pump oxygen-poor blood arriving from the body to the lungs, where it is enriched with this vital nutrient. The blood, now full of oxygen, then returns from the lungs to the left atrium and left ventricle. The left side of the heart pumps oxygen-containing blood into the large artery called the aorta, also known as the great vessel, which then carries it to the various organs by way of its many branches. Your heart beats—contracts and relaxes—about 80 times a minute, 4,800 times an hour, 115,200 times a day, 8,064,400 times a week, 32,256,600 times a month, and 387,079,200 times a year. If you are lucky enough to get to be 80 years old, your heart has beaten 3,096,575,000 times. Three billion times! Its durability is unparalleled. I wish I could find a cellular phone with only a fraction of this reliability. During diastole, when the heart is relaxed, it ively fills with blood until the ventricles are about 70 percent filled. At that point, the atria contract and pump their contents into the ventricles, filling them to their most efficient volume. You

can think of this as priming the pump for the big push of blood to come. The ventricles contract during systole and eject about 80 milliliters (2.4 ounces or about a third of a cup) of blood with each heart beat. This is called the stroke volume. The total amount of blood pumped per minute is called the cardiac output. The heart pumps about 5.5 liters, or nearly 6 quarts, every minute. That works out to over 2,000 gallons a day, or about forty-five large water-cooler bottles. Blood vessels that carry blood to the body are called arteries. The blood vessels that return oxygen-depleted blood to the heart are called veins. Blood must be pumped in one direction. To keep the blood flowing in the right direction, the heart has four valves, two on the right side and two on the left. The tricuspid valve lies between the right atrium and the right ventricle. The pulmonic valve lies between the right ventricle and the pulmonary artery. The mitral valve lies between the left atrium and the left ventricle. The aortic valve lies between the left ventricle and the aorta. The heart pumps blood to the rest of the body, including itself. The heart is supplied with blood by the very first blood vessels that branch from the aorta. These are the coronary arteries. (The word coronary comes from the Latin word corona, meaning crown. The arteries surrounding the heart do look a bit like crown.) Two arteries supply the heart with blood. The left coronary artery has an initial short segment (approximately 20 to 30 mm) called the left main coronary artery. This artery quickly divides into two large branches. The left anterior descending artery (LAD) supplies the front part of the heart. The circumflex artery (Cx) supplies the back part of the heart. The right coronary artery (RCA) supplies the bottom of the heart.

Coronary Artery Disease (CAD) Coronary artery disease (CAD) is atherosclerosis affecting the coronary arteries, which supply blood to the heart. CAD is the single leading cause of death in the United States today. A dramatic increase in the prevalence of this problem is anticipated because of the aging population. The baby boomers (anyone born between 1946 and 1964) total about 78 million people. They are at extremely high risk for heart attacks and will have plenty of them over the coming years.

The estimated cost per year of CAD is between $50 billion and $100 billion. The progress of coronary artery disease can be divided in two distinct phases. The chronic phase begins early in life and takes many years to develop. The process involves inflammation of the lining of the blood vessel and deposition of fat (lipid) into its walls, causing plaque, or atherosclerosis. The acute phase can develop in a matter of seconds. It involves spontaneous rupture of a blockage (lipid plaque) and the development of blood clot (thrombus) that compromises blood flow and can quickly result in heart damage. Frequently, it first manifests itself as sudden death.

The Chronic Phase of CAD The term chronic means of long duration. In the field of medicine, it denotes a disease that lasts a long time, a disease that lingers. When you think of someone having a chronic disease, you assume that a person will have significant signs and symptoms and, possibly, quite a bit of suffering. Paradoxically, individuals with CAD may have no idea they have a problem—until it is too late. CAD can be chronic but stable for many years. Many people have no symptoms at all, but others will develop angina pectoris, usually called angina for short. The classic definition of angina pectoris is severe, constricting pain in the chest, often radiating to the left shoulder and down the arm. The term derives from the Greek ankhon (strangling) and the Latin pectus (chest), and can therefore be translated as “a strangling feeling in the chest.” That’s exactly how patients often describe the sensation. Angina is caused by lack of blood flow to the heart muscle—ischemia—usually as a result of a clogged artery. Angina often doesn’t have the classic symptoms of chest and arm pain. Some people will describe it as a feeling of pressure into the throat. Others will say they don’t have chest pain but describe shortness of breath. Some have palpitations (skipping or racing of the heart). One of my patients had jaw pain that could not be explained by his dentist or his doctors. It turned out that he had severe blockages in all three of his coronary arteries and ultimately needed coronary artery by surgery. Women often don’t have the classic signs of angina; they may have an unusual presentation. Women with angina often describe it as back pain. One of my patients is a 49-year-old female kindergarten teacher who had intermittent back

pain and treated herself with over-the-counter painkillers. When the pain persisted, her doctor sent her to an orthopedic surgeon, who prescribed physical therapy. When this failed, she went to see her chiropractor, who also couldn’t help her. Finally, her astute internist sent her to me for a treill stress test. This is a commonly used test to see if the heart is getting enough blood. The patient walks on a treill while the heart is monitored by a continuously recording EKG. If the heart is not getting enough blood, the EKG can change in a specific way that lets us know there is a clogged artery. This patient’s treill was extremely positive for a blocked artery. This lead to an angiogram (X-ray picture of the blood vessels), which showed a 99 percent blockage of the right coronary artery leading to the bottom of her heart. Thus, her pain was really an atypical form of angina. Angina can be either stable or unstable. Chronic stable angina means that there is a low risk of developing a heart attack. Unstable angina signifies an extremely high risk of proceeding to a heart attack and commonly death in a very short period of time. Its development is a medical emergency. An example of chronic stable angina is when for years a person has chest discomfort with exertion after walking six blocks, but the pain goes away promptly with rest. People can live for many years without developing a heart attack if they have stable angina. That’s because the blocked artery is already nearly or totally closed—it can’t be blocked any further by a clot. People with stable angina have usually developed collateral circulation, or smaller blood vessels that carry enough blood to the heart muscle to keep it going, though not enough for any real exertion. Unstable angina means that chronic stable angina has stopped being stable— there’s a change in its pattern. This could be as subtle as when a person who previously walked six blocks a day can now only walk four. It could be as dramatic as chest pain at rest or even possibly more dangerous, the onset of new chest pain. Unstable angina means that there has been a change in the lesion (blockage) responsible for limiting blood flow to the heart. This blockage now has the potential for developing a thrombus (blood clot), which can cut off the blood flow abruptly, and frequently completely, leading to a heart attack!

The Acute Phase

The chronic phase of coronary artery disease can start early in life and can exist for many years. Most people don’t even know they have clogged arteries until they actually have a heart attack. Why is this? You would expect that as the artery narrows, it would gradually reduce blood flow to the point when symptoms occur. These blockages, however, grow in a way that many times does not compromise the open part (lumen) of the blood vessel. They grow in an outward fashion, maintaining the diameter of the vessel fairly constant so that blood flows through it evenly. This process is known as remodeling and explains why a clogged artery often has no symptoms. Most heart attacks do not commonly occur in the arteries with the highest degree of blockage. In reality, it’s the plaque in moderately blocked arteries that is more likely to spontaneously rupture and cause a heart attack. However, at any unpredictable moment, you may enter into the acute phase of coronary artery disease. The acute phase can develop in a matter of seconds. A spontaneous rupture of a lipid plaque (blockage) inside the artery causes a thrombus (blood clot), which restricts or completely shuts off blood flow and can quickly result in heart damage. Frequently, it can first manifest itself as sudden death. Why is it that these dangerous blockages can rupture so unpredictably? A plaque is a blockage along the wall of an artery. The plaque is made up of a pool of fat (lipid core) contained within a protective structure made of smooth muscle cells and others cells. These cells produce connecting fibers that create a layer of tissue known as a fibrous cap. The fibrous cap walls off the fatty deposit—and only this thin layer of tissue separates the fatty pool of atheromatous gruel from the lumen of the blood vessel. The resilience of the fibrous cap determines whether the plaque is stable (as it is in the chronic phase of CAD) or if it becomes unstable. The plaque is vulnerable to becoming unstable when the fibrous cap is weakened to the point of rupture. A plaque probably becomes unstable due to erosion and fissuring caused by destructive enzymes produced by inflammatory cells circulating in the blood. This leads to thinning and disruption of the fibrous cap, with ultimate rupturing. Whether the rupturing of plaque is a random event or related to a specific stimulus has long been a subject of debate. We know that heart attacks are more common in the morning hours. This may be due to increased levels of body hormones (thyroid, cortisol, and epinephrine), which are released in the early morning to get us ready to wake up and get out of bed. Monday mornings are a

common time for heart attacks, possibly related to the stress of going to work after a nice weekend off. One study from Sweden showed that employees who worked under an intense deadline were six times more likely to suffer a heart attack. Recently, the New England Journal of Medicine published a study showing that people with recent, intense emotional traumas were at much higher risk of having a heart attack. This is known as broken heart syndrome or takotsubo syndrome. (Because this happens primarily to women, I will talk more about it in chapter 7.) Once the plaque ruptures for whatever reason, the between the blood and the fatty material that spills out leads to a clot. Our blood clots (coagulates) fairly easily. In prehistoric times, the clotting of blood was a good thing. If a saber tooth tiger bit a caveman, the clotting of blood in the wounds prevented him from bleeding to death. But this same lifesaving mechanism can be deadly to modern humans. When plaque ruptures, it releases potent natural chemicals into the blood that cause it to clot by stimulating its coagulation system. This begins with the platelets. A platelet is an irregular, disc-shaped particle in the blood that assists in blood clotting. You have trillions of them—a single drop of blood contains anywhere from 150 million to 450 million platelets. Although platelets are often classified as blood cells, they are actually fragments of large bone marrow cells called megakaryocytes. A platelet interacts with the ruptured plaque and its components by adhering to the site of the injury. Once the platelet attaches to the injured area, it becomes activated. The activated platelet releases a variety of chemical substances that attract other platelets and cause them to aggregate at the site of the injury. This leads to the formation of a platelet plug. This plug then interacts with a complex system of coagulation factors to form a mesh that traps red blood cells and stabilizes them into a clot. Once the plaque ruptures, the whole coagulation process can happen very quickly, in just seconds. The blood clot and its effect on blood flow causes a heart attack. Thus, almost all heart attacks are due to rupturing of plaque in a clogged artery to the heart with subsequent formation of blood clots, which interrupts the heart’s blood supply and leads to the death of heart muscle cells. This is the most common way people die.

Acute Coronary Syndromes The interruption of blood flow from a clot can be either complete or partial. This is mainly a function of the extent of the blood clot formation. If the interruption of blood flow is complete, then the clinical presentation is that of a full-blown heart attack: The Big One. The person has prolonged, unremitting symptoms, progressive heart damage, and, frequently, death—often sudden death. Half of all deaths from a heart attack occur within the first hour. About 30 percent of the people who die from a heart attack never reach a hospital. If the formation of thrombus is not complete and some blood is still getting through the artery, the person may experience a mini-heart attack or The Little One. The symptoms may be intermittent and the damage may be small, at least at first. The third possibility is frequent chest pain even while resting, but without measurable heart damage—unstable angina. If untreated, mini-heart attacks and unstable angina progress on to death in about 5 to 10 percent of patients. They progress to a full-blown heart attack in about 10 to 20 percent of patients. A heart attack or death is extremely likely within a few days to a few weeks of the start of the first symptoms. The Big One, The Little One, and unstable angina are all classified as acute coronary syndromes. While The Big One is the one most likely to kill you suddenly, all three types of acute coronary syndrome are life-threatening.

The Big One The culprit lesion of a full-blown heart attack, The Big One, is a totally blocked coronary artery with complete termination of blood flow. From the time the clot forms, it takes only between eight to twelve hours for permanent damage to the heart to occur. The chance of dying without state-of-the-art treatment can be as high as 40 percent, depending on what you do and where you go. The culprit lesion could be located in any one of the arteries feeding the heart. The usual locations for clots are the left main coronary artery, the left anterior descending artery (LAD), the right inferior coronary artery, and the circumflex artery at the back of the heart. The left anterior descending artery is such

common spot for a fatal clot that this vessel is often called “the widow maker.”

Congestive Heart Failure Of the people who survive a heart attack, many do not make a full recovery. Residual damage to the heart muscle can be profound and can leave people with varying degrees of heart weakness. This is a condition called ischemic cardiomyopathy (a weak heart as a result of damage caused by a lack of blood supply). A weak heart can often result in congestive heart failure. Because the damaged heart can no longer beat strongly, it doesn’t circulate the blood well, which means it can’t meet the body’s needs for blood and oxygen. This leads to retention of fluid in the body. When the fluid is retained in the lungs it makes them swell, a condition called pulmonary edema. (Pulmonary means lungs; edema means swelling.) This leads to shortness of breath, inability to exercise very much or at all, and inability to breathe comfortably. The fluid can also be retained in the legs, causing them to swell, a condition called pedal edema. Today, nearly 5 million Americans have heart failure; nearly half a million new cases are diagnosed every year. Congestive heart failure is the number one itting diagnosis at hospitals in the United States today. Although we’re getting better at treating heart failure, it is still a very dangerous condition to have. Nearly half of all people with congestive heart failure are dead within five years of their diagnosis. The culprit lesions in unstable angina and mini-heart attacks are basically the same. They are usually high-grade blockages in the coronary artery with some residual blood flow. The difference in these two syndromes depends on the presence of measurable damage to the heart muscle. When heart muscle is damaged, it releases a substance called troponin. This can be quickly and easily measured by a simple blood test. If the troponins are positive, then you have had damage to your heart, a heart attack. If they are negative, then you have unstable angina. The small amounts of damage are a result of tiny blood clots and other particles, which are thrown from the site of injury into the very small vessels supplying the heart muscle cells (embolizaton). The lack of oxygen-containing blood causes death of these cells. As discussed previously, a full-blown heart attack is quite common. A heart

attack occurs every twenty seconds in the United States. A full-blown heart attack is also extremely dangerous. Some 30 percent of people with heart attacks die before they can even get to a hospital. Another 10 to 20 percent may die in the hospital if they are not adequately treated. What is not well recognized is that mini-heart attacks and unstable angina are almost as dangerous as full-blown heart attacks. If only treated with bed rest and nitroglycerin, these disorders can progress to a heart attack in only a few months about 40 percent of the time. The chance of dying of that heart attack is about 15 to 20 percent. People with heart attacks successfully treated with thrombolytic therapy (a potent clot-dissolving medication that will be thoroughly be discussed later) have a better prognosis than others with some forms of mini-heart attacks. A big problem with mini-heart attacks and unstable angina is that they can be easy to miss. Of the approximately 3 million people with chest pain who are sent home from emergency rooms across the country, 40,000 go on to have heart attacks. Too many of these people will die.

3. Naming the Enemy

In order to effectively fight the tremendous public health care problem of heart attacks, we must identify and understand the enemy. Heart attacks go by many names. They’re also known as coronary thrombosis, coronary occlusion, myocardial infarction (and its variants, myocardial infarct or MI), myocardial necrosis syndrome, and The Big One. For the sake of simplicity, in this book I’m going to use heart attack whenever I can. In general, a heart attack means a blockage in one of the coronary arteries that nourishes the heart. There are different kinds of heart attacks, however, depending on where the blockage is and what effect it has on the heart. To reduce confusion, cardiologists (heart doctors) use a system that standardizes the different types of heart attacks. Each type has its own name (or nomenclature if you’re a doctor). Because the treatment and outlook are different for the different heart attack types, it’s important to understand the differences. Otherwise, you might not get the best information and care available. Also, standardizing the different types of heart attacks helps prevent medical mistakes and saves lives.

What an EKG Tells Us The naming system for heart attacks is based on the electrocardiogram, or EKG (also sometimes abbreviated as ECG). Every time your heart beats, a pattern of electrical activity is generated. By attaching wires called leads to the chest area, we can record the activity and see how well your heart is beating. If everything is normal, that’s usually a good sign, although you’re not necessarily out of the woods. In a surprising number of cases, people who are having symptoms of an acute coronary syndrome have normal EKGs. Usually, however, specific changes in the wave pattern recorded by the EKG tells us not only that you’re having a heart attack but also what kind of heart

attack you’re having. If the EKG is done after the heart attack, it can still tell us what type of heart attack you had. At that point, unfortunately, it’s also likely to tell us how much irreversible damage was done to your heart muscle. Let’s look more closely at how an EKG works and what it tells us. Each time your heart beats, the chambers have to contract in a coordinated fashion. If each chamber contracted independently, this would lead to chaos and the system could never function properly. Your heart has its own electrical system that makes the contractions occur in a synchronous fashion. Even if all the nerves to the heart from the body’s nervous system are cut, the heart will continue to beat. Even more fantastic, if the heart is cut into pieces, each individual piece will continue to beat. This is because of the specialized conductive tissue that makes up the electrical control system of the heart. At the beginning of each heart beat, an electrical impulse is generated in the heart’s own natural pacemaker, the sinus node (a node is a localized mass of tissue). The sinus node is located in the upper part of the heart, near the left atrium. That electrical impulse is then transmitted throughout both atria and pauses at another node located just at the point on the heart where the atria and the ventricles . This is called, not surprisingly, the atrioventricular node, abbreviated as the AV node. During this pause, both atria simultaneously contract, forcing out the blood they hold and filling the ventricles with the optimum amount of blood. The electrical impulse then moves on to activate both ventricles via the left and right bundle branches of the electrical system. Ventricular contraction then occurs, pushing the blood out to the lungs and to the rest of the body. This whole process takes only about three-quarters of a second. Electrocardiograms have been around for quite some time. In 1887, a British physiologist, Augustus D. Waller of St. Mary’s Medical School in London, published the first human electrocardiogram. However, it wasn’t until the early 1900s that the EKG became a useful clinical tool, mainly as a result of the phenomenal work of Willem Einthoven, a Dutch physician and physiologist. In 1924, Einthoven won the Nobel Prize for inventing the first practical electrocardiogram. During the first twenty years of its existence, the EKG was mainly used to

evaluate arrhythmias (irregularities) of the heartbeat, In 1920, Harold Pardee in New York published the first EKG of a human having a heart attack. We learned from his work that the EKG quickly changes in a specific way if the blood flow to the heart is suddenly interrupted. Since that that time, the EKG has been a cornerstone in diagnosing heart attacks. It is easy to perform. It is widely available. It is safe and inexpensive to do. These are all very good qualities of a diagnostic test.

Doing the EKG To get an EKG, twelve electrical leads are attached to various parts of the body, using ten wires. Six are placed on various parts of the chest; the rest go on each arm and each leg. The leads are attached to the body using a self-adhesive pad and at the other end are attached to an EKG recorder that captures the pattern of electrical activity from each lead on a moving piece of graph paper. Since all we’re doing is recording the heart’s own electrical activity, an EKG doesn’t send any electricity through the body. An EKG takes less than five minutes to obtain. It is virtually painless, unless you suffer from hirsutism—that is, if you have a very hairy chest, pulling the leads off afterward can sting. The twelve-lead EKG allows us to visualize the electrical activity of the heart in multiple views, thus maximizing the amount of useful information. To break the wave pattern of a single heartbeat out into its various segments, we use an alphabetical system that starts with the letter P and ends with T. Why these letters? Because those are the letters the great Einthoven himself chose. He thought that using letters from the middle of the alphabet would leave room to add more letters on either end if additional aspects of the wave pattern were discovered in the future. The P wave represents the contraction of the atria at the start of the beat. The QRS complex represents the next part of the beat, the contraction of the ventricles. The ST segment represents the relaxation of the ventricles. An EKG is usually recorded on a moving sheet of graph paper so that we can look at it and see at a glance how long each part of the heartbeat lasts and the

shape of the wave. We generally record about five or six heartbeats at a time, which usually takes only three to four seconds.

Acute Coronary Syndromes on the EKG While there is some variation from person to person, the wave of a normal heartbeat is always pretty much the same—with a big spike at the QRS interval and a smaller upward spike for the ST segment. In an acute coronary syndrome, the alteration in blood flow to the heart can cause a characteristic change in the EKG. More specifically, we can often see a very specific change in the ST segment. If blood flow is cut off completely, as it is in a full-blown heart attack, the ST segments will elevate. As a result, this kind of heart attack has been named a STEMI, short for ST Elevation Myocardial Infarction. This is the characteristic sign of The Big One. If the interruption of blood flow is partial, as it is in a mini-heart attack or unstable angina, then the opposite happens: the ST segments become depressed. The T wave portion becomes inverted—instead of going up, it curves downward. This type of acute coronary syndrome is called a Non-STEMI or Non-ST Elevation Myocardial Infarction. When the T wave is inverted, it may mean you’re having an ischemic episode, usually from a mini-heart attack or unstable angina. Your chances of going on to have The Big One and die suddenly are very high at this point. It could be a matter of just a few hours or maybe as long as a few days, but unless you are treated immediately to clear the blockage, it will almost certainly happen. An EKG tells us a lot about what’s going on with your heart. If you’re having a heart attack, we can get a good idea of exactly where the blockage is by looking at the waves recorded by each of the different leads. Later on, we’ll confirm that by doing an angiogram (I’ll discuss angiograms in detail in chapter 4).

The Value of the EKG The EKG has been and continues to be a valuable tool in the diagnosis of heart attacks. It is the gold standard, but we must always be aware of its limitations.

An EKG can, at times, be falsely positive, suggesting a person is having a heart attack when in reality he or she is fine. More often, the EKG may be falsely negative. This means that the EKG may read as normal even while a person is actually in the process of having a heart attack. A 1999 article in the American Heart Journal reported that 40 percent of people with mini-MIs and unstable angina had EKGs that were considered normal! When a high-risk individual with symptoms has a normal EKG, this can create a false sense of security. The person could still very well be in serious trouble. Further testing must be done quickly to be completely sure acute coronary syndrome isn’t the cause of the symptoms. An excellent example of a false negative is what happened to one of my patients a few years ago. This 73-year-old woman had no history of heart disease when she came into the ER at the hospital where I usually work, complaining of severe back pain. She said it had been happening on and off for three months. It sometimes occurred with exertion, but frequently came on at rest. That day’s episode was the most severe she had yet experienced, which is why she finally came to the ER. The patient had a family history of heart disease—her grandmother died at age 84 from congestive heart failure. Her doctor had told her she had “borderline” high blood pressure and advised her to restrict her salt intake and get more exercise. He also told her she had mildly elevated cholesterol levels in her blood and advised her to eat a low-fat diet. Her blood sugar was normal. Her only “vice” was that she smoked between fifteen and twenty-five cigarettes a day and had been doing so since college. She had tried to quit in the past but doing so caused her to gain weight. Because of her long-term smoking, she had mild emphysema and needed to use an inhaler a couple times a day. In the ER, she looked quite comfortable. She was pain-free and wasn’t short of breath. Her blood pressure was slightly elevated, 130/90. Her pulse was about 88 beats per minute. Because the ER doctor suspected a heart attack, an EKG was done. It showed no evidence of a heart problem. In fact, it seemed normal. Compared to an EKG done at her doctor’s office a year earlier, no changes could be seen. To be on the safe side, the ER doctor ordered a blood test for troponin, a protein that is usually elevated in the blood after a heart attack. The test was negative.

I was consulted to see if the patient could be sent home from the emergency room and get a heart evaluation later on as an outpatient. The ER physician requesting the consultation felt there was no objective evidence of a blocked artery and believed the patient’s symptoms were atypical of angina but not dangerous. I feel that if a patient is so concerned about her symptoms that she comes to the hospital, she needs to be thoroughly evaluated to rule out disease to as high a degree as possible. Because of her high-risk factor profile, I itted her to the hospital for close observation. If she was stable the next morning, I would have her do a stress test to investigate her heart further. At 2:45 in the morning, she had the most severe episode of back pain that she had ever had. This time, though, she was also profoundly short of breath and was drenched in sweat. Another EKG was done immediately. This time, it showed an acute MI with ST elevation in the electrical leads monitoring the bottom of the heart. This represented complete closure of the right coronary artery supplying the bottom of her heart. Because she was already in the hospital, she was able to undergo a prompt emergency angiogram and then an angioplasty, which restored the blood flow to this area and minimized the amount of damage. If she had been sent home, her chances of survival would have been far less. A high index of suspicion is necessary to adequately evaluate people who are at high risk of developing a heart attack. If the person is at risk and the EKG is negative, other diagnostic methods must still be used to make sure a heart problem isn’t happening. This is especially true if the person is having ongoing symptoms, because this could mean the heart muscle is continuing to be damaged. Today, my patient is doing quite well, although I still can’t get her to stop smoking. She figures if she has another heart attack, she’ll just come back to the hospital and get roto-rootered again. Some people are just stubborn.

4. Treating Heart Attacks

There are basically two ways to die from a heart attack. The first is from electrical complications. Because of the sudden injury to its muscle and its electrical system, the heart becomes irritable. It commonly starts to beat at dangerously fast rates, to the point where it can’t efficiently pump blood. This is called ventricular tachycardia, meaning a rapid or accelerated heart rate that goes beyond the normal range for a resting heart rate. In general, you’re having tachycardia if your resting heart rate is faster than about 100 beats a minute (normal is about 80 beats a minute). If the heart beasts fast enough, ventricular tachycardia can further degenerate into an even more dangerous and uncoordinated rhythm where the heart is essentially not pumping blood at all, a situation known a ventricular fibrillation. Death from this complication is sudden. The second way to die is from mechanical complications or pump failure. So much damage is sustained that the heart can’t beat hard enough to effectively supply the needs of the body. The lungs fill with fluid, and respiratory failure and death ensue. This can take anywhere from seconds to minutes to hours to days to weeks to months to years. Pump failure, also known as heart failure, is truly this variable and unpredictable.

Improved Treatments Means Fewer Complications The risk of dying of either of these complications has been reduced significantly over the past few decades. Dramatic developments over the last thirty years have led to a tremendous amount of progress in rapidly diagnosing and aggressively treating heart attacks. This has saved the lives of many, many heart attack victims. In fact, in these last thirty years, the chance of dying of a heart attack has been reduced by about 30 percent. This is a huge improvement. It is such an improvement that in 2005, heart disease, for the first time in a hundred years, fell to the No. 2 ranking as the most common cause of death for Americans, behind cancer. Because there is still considerable room for improving the number of

lives that can be saved after a heart attack, there are good reasons to be optimistic going forward. To understand why the future of heart care is looking very positive, let’s take a look backward.

The Pre-CCU Era: 1912 to the Late 1950s Before the twentieth century, doctors felt that anyone who developed a totally occluded coronary artery would just die suddenly—there was little that could be done. In 1912, James B. Herrick, a cardiologist from Chicago, published an innovative paper in the Journal of the American Medical Association that was the first to suggest that a clot in a coronary artery was the cause of a myocardial infarction. The title of the article says it all: Clinical Features of Sudden Obstruction of the Coronary Arteries. In that paper, based on his fifty years of practice, Dr. Herrick beautifully described the treatment for heart attacks at that time. The management of the disorder was ive and ive. A heart attack was simply accepted, and the only measures taken were directed at preventing a second one. Here are some of the fascinating treatment recommendations from Dr. Herrick’s article: “Complete physical and mental rest is the immediate indication.” “Pain is treated with the liberal use of morphine hypodermically. Doses of ½ grain are not too large, and may be repeated within a half hour if the pain continues.” “If respiration is shallow and labored, caffeine sodiobenzoate should be given intra muscularly in doses of 0.5 gram (7½ grains), repeated as often as necessary, even if it is every few minutes.” I have an uncle who was a general practitioner in Santa Monica, California, from the 1940s until the late 1970s. In those days, a GP could not only treat coughs and colds and give vaccinations, but he could also take out your appendix, gallbladder, or tonsils, deliver your baby, or ister general anesthesia if he

needed to. In those days, someone having a heart attack wouldn’t go to the hospital. Someone would call Uncle Harry, and he would come to the house to take care of the patient. (The practice of house calls has since that time become entirely extinct.) He would put the patient to bed and ister as much morphine as needed to help with the pain. If the morphine suppressed the patient’s breathing, as it can commonly do at those high doses, he would give shots of caffeine directly into the buttocks to stimulate the breathing. Starbucks, do not get any wise ideas, please! The next day, Uncle Harry would call on the phone to see how the patient was doing. If the patient survived the night, he would go back out to the house to check on the him or her. If the patient didn’t make it, he would convey his condolences to the family. Heart attack patients at that time would die about half the time with the conventional treatment. Uncle Harry, by the way, is still alive and doing fine at age 96, except he can’t hear worth a damn (a lot of that, I think, is by choice). And he still plays bridge at his club three or four times a week.

The CCU Era: The Early 1960s to the Late 1970s In 1960, the treatment for a heart attack had not advanced much beyond the treatment described by Dr. Herrick in 1912. Treatment was largely still bed rest and morphine, and many hospitalized patients still died suddenly from electrical complications. The vast majority of deaths due to ventricular fibrillation occur within the first twenty-four hours of the onset of symptoms; over half of these deaths occur in the first hour. Death from ventricular defibrillation usually happens in just seconds or a few minutes at most. In the late 1950s, however, we began to be able to treat electrical complications using a machine called a defibrillator. By delivering an electrical shock to the heart, the defibrillator restored a normal rhythm. Although the concept had been around since the turn of the century, the first case of a human life being saved by

defibrillation was reported in 1947. Claude Beck successfully revived a patient in an operating room using an open-chest electric defibrillation device. This worked because the patient’s chest was already open for a heart operation. The first closed-chest defibrillators didn’t come into use until 1959. These defibrillators are the forebears of the kind you see now in the movies and on TV, where a central unit (the black box) is dramatically rushed in on a crash cart. Paddles are placed against the patient’s chest, the doctor (or whoever) shouts “Clear!” and applies the electric current. If all goes well, the chaotic rhythm of ventricular fibrillation is converted into a normal heartbeat. Once defibrillators became widely available, hospitals set up coronary care units (CCU). A CCU is a specialized area within the hospital where patients can be closely monitored for the complications of heart attacks. A CCU nurse is usually responsible for a maximum of only two patients. Here, dangerous cardiac arrhythmias can be quickly diagnosed and promptly treated. In the CCU, patients are connected to a continuous EKG monitor so that each heartbeat can be observed. If the patient develops a life-threatening arrhythmia, it can be quickly detected and promptly treated. Code Blue! The development of the monitored unit has significantly contributed to the reduction in mortality associated with heart attacks. In 1966, Frank Pantridge, an Irish cardiologist, developed the first mobile defibrillator. He installed these devices in ambulances in Belfast, Northern Ireland. For the first time, people could be diagnosed and treated for these malignant arrhythmias at the site where they developed their attack. The widespread use of mobile defibrillators in ambulances has greatly contributed to the reduction of mortality from a myocardial infarction. In the 1980s, advancing technology led to smaller, more portable defibrillators, making their use even more widespread. Another crucial development that started in the 1960s was the start of coronary angiography. This is a way of seeing blood vessels by injecting a dye into them and then recording the images using X-rays. To image the arteries of the heart, a catheter is snaked into the heart. The dye is released and X-rays are taken. Blockages show up very clearly—we can easily see how many coronary arteries are blocked, where the blockages are, and how much of each artery is clogged by the blockages. We can also see other heart problems, such as damaged valves. The ability to safely visualize the heart and its arteries led directly to major innovations in treating heart attacks.

The Reperfusion Era: The Late 1970s to Now The next therapeutic modality to reduce mortality associated with heart attacks is treatment, which limits the amount of heart muscle damage. The goal is to prevent mechanical complications, or pump failure, and keep the heart as strong as possible. Your life expectancy is directly related to how strong your heart is. The weaker your heart, the higher the risk you will die. From 1912 to 1978, the management of heart attacks was ive and ive. A heart attack was simply accepted. Even through the late 1970s, the treatment for heart attacks remained unchanged from that given by Dr. Herrick. The bible for doctors studying to be internists is Harrison’s Principles of Internal Medicine. In my training during the early 1980s, I used the ninth edition of this textbook. Under the section for treatment of heart attacks, the authors recommend the following measures: Analgesia (pain relief) Oxygen Bed rest Bowels Sedation Even though we now know that heart attacks were caused by blood clots blocking the coronary arteries, the idea of anticoagulation—using drugs to “thin” the blood to break up existing clots and prevent new ones—wasn’t accepted. The authoritative authors in Harrison’s said: “The lack of any statistically clear-cut demonstration of a lower mortality rate in the first few weeks following myocardial infarction suggests benefit of anticoagulant therapy, if any, is small.” In the late 1970s, we had moved on to some drugs in attempts at preserving heart muscle during a heart attack. Aspirin and beta blockers (drugs that block the effects of adrenaline on the heart) were found to be beneficial.

For decades after Dr. Herrick’s landmark paper, doctors thought that once a coronary artery was totally occluded, all of the muscle cells supplied by that vessel would die instantly and simultaneously. In the mid-1970s, animal studies suggested that this was not the case. These experiments showed that the death of the muscle cells develops at different time-related stages. A “wave” of cell death begins at the inside part of the muscle wall and progresses to the outside part of the wall. So even though the inner wall dies early, the outer wall can survive for up to six hours, or sometimes even longer, following the total blockage of blood flow. Further animal studies at that time suggested that if coronary blood flow is promptly restored in the setting of a heart attack, a substantial amount of heart muscle can be preserved. Restoring the blood flow is called reperfusion. Experiments also showed that the sooner the blood flow was restored, the more muscle would be preserved. These observations also suggested that a substantial amount of heart muscle could be salvaged over a period lasting up to many hours after the start of the heart attack. These findings can be summed up in a phrase we cardiologists use a lot: Time is muscle. The findings also provided an incentive to look for prompt treatments that would restore coronary blood flow as soon as possible as a way to try to limit the amount of the heart muscle damage and save lives. This was the beginning of the Reperfusion Era. Coronary Artery By Grafts (CABG) One way to restore coronary blood flow is to surgically reroute the arteries to go around the blockage. This requires a type of heart surgery known as a coronary artery by graft, or CABG (called “cabbage” for short). Emergency coronary by surgery was first reported as a treatment for heart attacks in 1972 by Dr. Lawrence Cohn, a pioneering cardiac surgeon at Harvard Medical School. He reported on eight patients who were all in the hospital at the time of their heart attacks. Seven of the heart attacks were the result of a complication during coronary angiography. Because the patients were already in the hospital, the surgery could be performed within three hours. There were no deaths.

A much larger group of patients was studied by Dr. Ralph Berg and his surgeons in Spokane. He reported on 1,295 surgeries done between 1969 and 1975. There were four deaths, or 5.2 percent mortality—a figure that proved the safety of the surgery. Even so, the use of CABG in the treatment of heart attacks did not become widespread because of its limited availability and the complexity of organizing it as a therapy.

Clot Busters In the late 1970s, however, a radical change occurred in the treatment of heart attacks. Before that time, it was still controversial as to what actually caused heart attacks. Most doctors thought that the plaque in the artery just become progressively worse until it finally obstructed the blood vessel to the point where blood flow was simply cut off. The blood clot found in the artery at autopsy was thought to have occurred after death, not as the cause of it. In the 1970s, Marcus DeWood of Spokane, Washington, boldly began performing coronary angiograms on people during the early hours of a real heart attack. His work revealed that almost all heart attack victim—87 percent—had a blood clot clogging up the artery. Also, when some of these patients underwent emergency by surgery as treatment for their heart attack, a blood clot was almost always found within the blood vessel. This discovery stimulated the revolutionary idea that it might be possible to dissolve a life-threatening blood clot with potent clot-busting medications. Doing this would lead to the restoration of blood flow (reperfusion), limit the heart muscle damage, and ultimately save people’s lives. Doctors could use a drug to stop a heart attack while it was happening. The first clot-busting drug to be tried was one that dated all the way back to 1933. William Tillet and R. L. Garner discovered that a certain bacterium, Group A beta streptococci, produced a substance that could actually dissolve human blood clots. This substance was named streptokinase. Animal studies performed during the 1940s showed the feasibility of dissolving blood clots in the blood vessels of living beings. In the late 1950s and early 1960s, isolated reports appeared describing the use of intravenous streptokinase in human subjects experiencing heart attacks. The benefits were controversial, and excessive

bleeding complications were common. In 1979, Peter Rentrop in Munich, , directly injected streptokinase into the coronary artery of a person actually having a heart attack. This dissolved the blood clot in the affected artery, restoring blood flow to the muscle of the heart. For the first time, a heart attack was actually stopped in progress. This was the beginning of the reperfusion era. Selected medical centers around the world developed programs to offer thrombolytic (clot-dissolving) treatment. The limitation, however, was that the majority of people with heart attacks did not have access to hospitals capable of performing emergency angiograms to show the blocked artery. Studies were then performed to see if the istration of clot-busting medication by an intravenous route (IV), instead of directly into the affected coronary artery, was effective in treating heart attacks. These clinical trials clearly showed that IV thrombolytic therapy saved lives. Once the safety and effectiveness of the IV method was shown, extensive treatment with clot-busting agents began worldwide. Hundreds of thousands of lives were saved. In the 1980s, streptokinase was the thrombolytic agent commonly used. A second-generation agent, tissue plasminogen activator, better known as tPA, was developed in the mid-1980s. In clinical studies, tPA was found to be superior to streptokinase in its effectiveness. Third-generation drugs, mostly chemical derivatives of tPA, were later developed. They are more convenient to give to the patient, but they don’t work any better than tPA. Thrombolytic therapy has many advantages in the treatment of heart attacks. It has been shown to save a significant number of lives—patients who get clotbusting drugs have a much better thirty-day survival rate than those who don’t. It’s easily available and can be given in any emergency facility throughout the world. It can also be given very early in the heart attack—and , time is muscle. In some places, paramedics ister these medications at the patient’s location soon after the onset of symptoms and only then begin immediate transport to the hospital. Thrombolytic treatment, however, is far from perfect. Several disadvantages limit the value of thrombolytic treatment. The concept of istering this therapy in the early stages of a heart attack is ideal and is currently being done in some parts of the world. Sadly, however, this is the exception rather than the rule. In a significant number of cases, istration of the therapy is delayed

too long. Often, thrombolytic therapy doesn’t completely restore the blood flow to the heart. Cardiologists rank how well the blood is flowing according to the TIMI scale (this stands for Thrombolysis In Myocardial Infarction, a scale that was established in 1984). Excellent blood flow, also called complete perfusion, is called TIMI 3 on the scale. It’s associated with the best clinical outcomes. TIMI 3 flow can only be achieved with thrombolytic therapy, at best, about 60 percent of the time. At worst, however, it can be as low as 30 percent of the time. Because complete perfusion isn’t usually achieved with clot-busting therapy, patients have a high risk of developing angina or even another heart attack later on. Serious complications are not uncommon with thrombolytic therapy. Bleeding can occur from a variety of different sources, such as the IV site, the digestive tract, the urinary tract, or the lungs. Allergies to some of the older thrombolytic agents are a potential complication of treatment but are fairly uncommon today. The most devastating potential complication of thrombolytic therapy is bleeding into the brain, causing a stroke. Luckily this is quite rare and affects fewer than one in one hundred people.

Angioplasty: Clearing Out the Clog Angioplasty is a process where an atherosclerotic blockage—artery-clogging plaque—is molded back into the walls of a blood vessel using a catheter (a very thin tube) with an inflatable balloon tip. The procedure is also known as percutaneous coronary intervention (PCI) or coronary angioplasty. If the blockage is flow-limiting, angioplasty widens the lumen of the blood vessel and can improve the circulation by letting more blood through. The word comes from the Greek word angeion, meaning blood vessel, and the Greek word plastos, meaning molded or formed. The catheter is snaked into the body through an artery in the groin or arm; from there, it is guided to the blocked artery in the heart. When the catheter reaches the blocked area, the balloon is inflated. It pushes open the blockage by pressing the fatty material within the plaque back into the artery wall.

Doctors long believed that inserting a catheter directly into the heart or its arteries would result in immediate death. A German doctor named Werner Forssmann didn’t share this belief, and in 1929 he proved it by experimenting on himself. He pushed a catheter into the right side of his heart through a vein in his arm. He then walked down to the basement of his hospital and X-rayed himself to prove he had done it. Forssmann was fired for recklessness by the hospital, but in 1956 he shared a Nobel Prize for his pioneering work. The next step took a long time. In the 1960s, Dr. Charles Dotter at the University of Oregon proposed using angioplasty to open clogged arteries. At the time, the idea seemed radical, even dangerous. He performed his first angioplasty in 1964, using a catheter to open the femoral artery (the main artery in the upper leg) of a woman who was facing leg amputation because the blood flow was so blocked. The procedure worked well and saved her leg. Today, angioplasty to open blocked arteries, deliver stents to keep them open, and to perform heart procedures that once required open-heart surgery, is very common. Dr. Dotter and his colleagues used a coaxial double-catheter system. This had some major drawbacks, and many of the procedures resulted in significant complications such as bleeding, blood-clot formation, or tearing of the blood vessel, which sometimes led to emergency surgery and even, at times, to amputation. As a result, Dr. Dotter was severely criticized, especially by his surgical colleagues. Because of the serious risk of poor outcomes, there was little acceptance of the technique in the United States. In Europe, however, it was looked upon much differently. Dr. Eberhart Zeitler, a radiologist in Nuremberg, , began imitating Dotter’s work, performing a large number of procedures with favorable outcomes. Dr. Zeitler’s success stimulated the thinking of a young, German-born cardiology fellow, Andreas Gruentzig, who had immigrated to Zurich, Switzerland, for his training at a large university hospital. In 1969, Gruentzig developed an inflatable, balloon-tipped catheter, which replaced the rigid dilators used by Dotter. He made the prototypes of these devices while working evenings in his own kitchen. Dr Gruentzig first performed angioplasty on an iliac (leg) artery of a human being in 1975. In line with his cardiology training, Gruentzig had an early interest in reducing the size of the catheter so it could be used in the

smaller coronary arteries. He soon perfected a catheter small enough for animal work in these vessels. The first canine coronary artery dilation was performed in September 1975. In November 1976, Gruentzig came to the United States for the first time and presented his animal data in a poster session at the American Heart Association conference in Miami Beach. Most observers of his studies were quite skeptical, as they had been previously with Charles Dotter. This, however, did not stop Dr. Gruentzig. In 1977, he and Dr. Richard Myler performed the first angioplasty procedure in a human heart. This was done while the patient was under general anesthesia undergoing coronary artery by surgery by Dr. Elias Hanna, a cardiac surgeon at Saint Mary’s Hospital in San Francisco. The first awake patient on whom angioplasty was attempted was a person who was too sick to have coronary by surgery. The angioplasty did not go well. The catheters couldn’t be advanced to the blockages, and the procedure had to be abandoned. The patient went on to die a few days later of a massive heart attack. In 1977, however, Dr. Gruentzig had his first major success. Back in Zurich, he found the ideal patient, a 38-year-old insurance salesman from Zurich with severe angina. A coronary angiogram showed that he had a high-grade blockage of the left anterior descending (LAD) artery, the artery that supplies the front wall of the heart. On September 9, 1977, Dr. Gruentzig performed the first successful angioplasty on an awake patient. Ten years later, the patient’s artery was still open and he was symptom-free. In 1979, Gruentzig published the results of his first fifty patients in a landmark article in the New England Journal of Medicine. Later that year, he returned to the American Heart Association’s annual conference. This time, after presenting his experience with angioplasty, he received a standing ovation. This was the birth of interventional cardiology. Previously, a cardiologist, an internal medicine physician with special training in the diseases of the heart, would mainly be responsible for the diagnosis and medical treatment of coronary artery disease. Once diagnosed, the patient would either be treated with aspirin, nitrates, beta blockers, and/or calcium channel blockers. If this failed, the next step would be coronary artery by surgery.

With the advent of angioplasty, also known as percutaneous coronary intervention (PCI), the cardiologist could now intervene by dilating (opening up) clogged coronary arteries, restoring normal blood flow to the heart’s muscle, and improving the symptoms of angina pectoris. It was a third option in the treatment of CAD. Angioplasty took the medical community by storm. It evolved rapidly, with innovations such as the intracoronary artery stent and improved blood-thinning medications, which have made it a safe and reliable procedure. It has now become one of the most common medical interventions. In fact, over the past few years, angioplasty, usually to place one or more stents, has overtaken coronary by surgery in the number of procedures performed.

Angioplasty to Treat Heart Attacks Geoffrey Hartzler was an interventional cardiologist at the Mid-American Heart Institute in Kansas City, Missouri. Dr. Hartzler was a pioneer of angioplasty. Not only was he known for his superior technical skills in the cath lab (he was known as the Michael Jordan of angioplasty), but he also was an incredible teacher, responsible for the training of many interventional cardiologists of the day by organizing courses attended by physicians from all over the world. In the late 1980s, Dr. Hartzler performed a coronary angiogram on a patient with severe angina. The patient was found to have a single blockage in the artery supplying the bottom part of his heart. After the angiogram, Dr. Hartzler explained the treatment options to this individual. Medical therapy and coronary artery by graft (CABG) surgery were possibilities. However, Dr. Hartzler also told the patient that he met all the criteria for being a good candidate for a new procedure, angioplasty. They decided to proceed with angioplasty the following morning. One hour before the procedure, Dr. Hartzler got a call from the lab saying the angioplasty had to be cancelled. The patient had suddenly developed a massive heart attack. This didn’t seem logical to Dr. Hartzler. Until just an hour before the procedure, the patient was a good candidate. He wondered, “What could have occurred with substance to negate that now?” Hartzler was not a big believer in thrombolytic therapy, stating that “It just didn’t work that well.” He

felt that his best option was to take the patient to the cardiac catheterization lab and try to perform an angioplasty in the setting of a heart attack. This was the first time this had ever been attempted. When the initial angiogram was performed, it showed, as expected, a totally occluded vessel. Hartzler then was able to the balloon to that occluded area and open up the blockage. This promptly restored blood flow to the bottom part of the heart. The patient’s chest pain immediately and completely resolved. The EKG returned to normal. Hartzler was astonished and described it as the most amazing thing he had ever seen. This ground-breaking discovery led to the belief that immediate angioplasty was the optimal treatment for acute myocardial infarction. When Dr. Hartzler presented the results of treating 250 patients with angioplasty at a conference of the American College of Cardiology in 1983, the audience was skeptical. His hypothesis went on to be proven in multiple clinical trails on thousands of patients. Despite some resistance, by the early 1990s, angioplasty was the accepted standard of treatment for heart attacks. When Dr. Hartzler ed away in 2012, he was responsible for saving millions of lives around the world. These studies showed that there are significant advantages of treatment with angioplasty over thrombolytic therapy. One advantage of angioplasty is that the anatomy of the coronary arteries is immediately known, because the first step is to image the heart vessels with an angiogram. This information is crucial because it determines the best choice of treatment. If the culprit blockage is suitable for angioplasty, the procedure can be performed immediately and stop the heart attack. If the patient turns out to have complicated triple vessel disease that is diffuse and calcified, the surgeon can see at once that emergency coronary artery by graft surgery may be the better treatment choice. Sometimes, the blood vessel responsible for the heart attack is too small to intervene—its diameter is smaller than the smallest balloon available. These blood vessels are best left alone. In such cases, the amount of heart damage done is usually quite small, and the patients usually have a good recovery and a favorable outcome. With angioplasty, the surgeon can see this at once and know that the patient does not need potent clot-busting medications, which are given blindly without knowledge of the coronary anatomy. Many serious

complications of these agents can thus be avoided. A major advantage of angioplasty is that the most devastating complication of thrombolytic therapy, intracranial bleeding leading to a stroke, is almost unheard of. Another great thing about angioplasty is that it almost always restores the full flow of blood through the artery. Clinical trials have shown that angioplasty consistently establishes TIMI 3 flow in greater than 90 percent of patients. Recurrent heart attacks, recurrent angina, and the need for further procedures is also considerably less than with thrombolytic therapy. By far the most important benefit of angioplasty is that it saves more lives than any other form of treatment for heart attacks. Of course, no treatment is perfect. There can be downsides to any form of therapy. The main limitation of angioplasty in the treatment of heart attacks is that its availability is profoundly limited. Fewer than 20 percent of the hospitals in the United States are capable of performing this life-saving procedure. Even fewer are capable of performing it in a suitable and timely fashion with adequate technical abilities. Outcomes for angioplasty are not only center-dependent, but much depends on the skill of the interventional cardiology team as well. Hospitals and interventional cardiologists who have the most experience have the more desirable outcomes. Time delays are also significant obstacles in providing optimal care. This is especially true if transport to another hospital is required. (I’ll discuss this in more detail in chapter 8.)

Strategies for Treating Mini-Heart Attacks Mini-heart attacks and unstable angina are technically referred to as non-ST elevation (non-STEMI) acute coronary syndromes (ACS). Mini-heart attacks and unstable angina are caused by coronary blood vessels that are tightly blocked, but still allow enough flow to keep most of the heart muscle alive. Mini heart attacks and unstable angina are almost as dangerous as fullblown heart attacks. If only treated conservatively, these disorders can progress to a major heart attack about 40 percent of the time in only a few months. The chance of dying of that heart attack is about 15 to 20 percent.

In the 1980s and most of the 1990s, treatment for non-STEMI acute coronary syndromes was conservative. Patients would undergo a coronary angiogram only if they either continued to have symptoms or failed a stress test done just prior to discharge from the hospital. In most cases, their symptoms were managed medically by drugs and lifestyle changes (stopping smoking, for instance). With the increasing use of angioplasty as a treatment for these syndromes, a new approach to patients became popular. Doctors starting being more aggressive in treating these patients. We began performing early coronary angiograms with angioplasty, or by surgery if necessary, between four and forty-eight hours after the patient was itted to the hospital. This approach is considered aggressive because it involves an invasive procedure, one where tubes must be placed inside the body. Invasive procedures always can carry inherent risks, such as catheter-induced damage to the vessels, bleeding, allergies and kidney problems related to the dye, and even the need for emergency heart or vascular surgery. For a procedure to be the treatment of choice, the benefit must significantly outweigh the risk associated with it. Fortunately, complications from angioplasty are rare. To test the two strategies—conservative medical treatment versus aggressive angioplasty—a major clinical trail comparing the two was conducted during the early 1990s. In 1994, the results were published in Circulation, a leading cardiac journal. The study showed that outcomes from early angioplasty weren’t any better than outcomes from more conservative medical treatment. This study and an additional major study known as the VANQWISH Trial, published in the New England Journal of Medicine in1998, showed no clinical benefit to the patients undergoing an aggressive approach. Soon after these studies appeared, however, the angioplasty procedure underwent major changes that made it a much safer, more reliable, and more durable procedure. The increasing use of coronary artery stents and better anticoagulation regimens dramatically reduced the risk of heart attacks and restenosis (recurrent blockage of the artery). As a result of these improvements, follow-up studies were performed in the late 1990s. This time, the aggressive approach was shown to significantly improve outcomes over the conservative approach. A good example is an article about a five-year follow-up on a study known as FRISC-II that appeared in the

prestigious British journal Lancet in 2006. The authors concluded: “The 5-year outcome of this trial indicates sustained benefit of an early invasive strategy in patients with non-ST-elevation acute coronary syndrome at moderate to high risk.”

Why Is an Aggressive Approach Better? In the early day of angioplasty, interventional cardiologists could only open up blockages with balloons. Sometimes, after dilating the artery, instead of seeing an improvement in the blockage, we would see the exact opposite—a totally closed blood vessel. This complication of angioplasty is called abrupt closure. It is caused by a tear in the intima, the inner lining of the blood vessel. This tear, called a dissection, then causes blood clot formation and cuts blood flow to that wall of the heart. Does that sound familiar? An intima dissection is essentially a balloon-induced heart attack. It is a devastating complication of angioplasty that happens between 2 and 8 percent of the time. Abrupt closure is analogous to what occurs in a STEMI. With abrupt closure, the chance of dying is five times higher than if there were no closure of the artery. The risk of a heart attack and emergency by surgery is ten times higher.

Stents Enter the Scene In 1987, the invention of the coronary artery stent meant we were able to prevent the damage from abrupt closure. A stent is a tiny mesh tube made of stainless steel wire that can be inserted into an artery of the heart using a catheter. It acts like a scaffold to keep the artery open. If someone is having abrupt closure due to an intima tear, we can insert a stent into the area to prop it open and stabilize it. The success of stents for treating abrupt closure led to their use to prevent restenosis. This happens when an artery clogs up again after it has been opened

with balloon angioplasty. Until we started using stents to prop these arteries open, restenosis was a big problem. It would sometimes occur just days to weeks after the artery had been opened. By the late 1990s, stents had become safe and effective and were being used in almost all angioplasties. At the same time, improved anti-clotting and anti-platelet drugs became available. The combination of stents and the new drugs reduced the number of restenosis cases. Even so, an artery with a stent could still clog up again. In 2002, the first drugcoated stents became available. Known as drug-eluting stents, these stents are coated with a drug that is then slowly released over several months after they are put into place. The drug prevents cell growth around the stent and sharply reduces the risk of restenosis. Today, about 80 percent of all the stents we put in contain these drugs. The sooner you can secure the heart’s circulation during an acute coronary syndrome, the better the clinical outcome will be and the more lives will be potentially saved. The use of stents allows us to open up the arteries quickly and get the blood flowing again. A number of large clinical studies have shown that the concept of “time is muscle” not only applies to major heart attacks but also to mini-heart attacks and unstable angina. Many interventional cardiologists feel that an even more aggressive approach may benefit the patients even further. In the standard aggressive approach, the patient with a mini-heart attack or unstable angina is first “cooled off” in a coronary care unit with potent blood thinners and other medications to protect the heart. The diagnostic angiogram is then performed in the next twenty-four to forty-eight hours. In the ultra-aggressive approach, the patient is taken directly to the catheterization laboratory, and diagnostic angiography is performed right away. This concept was studied in in 2002 in a study known as ISAR-COOL. The results suggested that the ultra-aggressive approach may be even more beneficial than the standard aggressive approach in treating these patients. ISAR-COOL was a small study, and additional larger clinical trials are needed to these findings. It is very encouraging, however. It makes sense that the approach well proven to save lives in a major heart attack would also benefit those with mini-heart attacks and unstable angina.

The benefits of modern therapy have been dramatic. There has been a 30 percent drop in mortality due to heart attacks in the last thirty years as a result of these new therapies. If you count heart attacks and strokes, however, atherosclerotic vascular disease is still the No. 1 killer. It is clear we have a long way to go, but at least we now have the tools to fight this disease hard. Our goal must be to aggressively attack the problem so that as many lives as possible can be saved.

5. Know Your Risk Factors

You have about a 50 percent chance of dying of heart disease, most likely from a heart attack. That doesn’t mean you’re randomly at risk, however. You can take a number of crucial steps that will sharply decrease your risk of having a heart attack at all. And if you do have a heart attack, there are important steps you can take that will help you survive it. You can save your own life in four simple steps: 1. Assess your personal risk of having a heart attack. 2. Recognize the symptoms of a heart attack. 3. Know who to call for help. 4. Know where you need to be taken. Having a nearby cardiac center of excellence and state-of-the-art emergency medical services is crucial for getting the ultimate care in the treatment of a heart attack. However, you can have the best system in existence available to you and still needlessly die of The Big One. This is because we are our own worst enemy. Time after time, people having every obvious symptom of a heart attack still don’t realize it is happening to them. Why? Because all too often, they don’t realize—or don’t it to themselves—that they are at risk of having a heart attack. “This can’t be happening to me,” they think. If you don’t know you’re at risk, you are much more likely to fail to recognize or it your heart attack symptoms. This leads to delay in getting the right treatment. Assuming the delay isn’t fatal, as it can be, delaying treatment can lead to much more serious damage from a heart attack. That, in turn, means a far greater risk of disability and death going forward. If, on the other hand, you know that you have at least some risk factors for a heart attack, you’re more likely to recognize the symptoms and take appropriate action. That could well be the difference between life and death.

We are now at the point where the ultimate question arises: what should you do to prevent yourself from dropping dead of a heart attack? You must take responsibility for yourself. You must become proactive. You must know your risk. Assess Your Personal Risk Your first step toward learning how to prevent a heart attack is to assess your personal risk of having a heart attack. To prevent something from killing you, you must completely understand the enemy so you can learn to fight it. To assess your personal risk of dying of a heart attack and learn what you can do to prevent it, you must first understand your personal risk factors.

The Framingham Study Even as the death rate from heart disease rapidly increased in the first part of the twentieth century, investigators of the time debated why. A definitive answer required data, but it wasn’t until the early 1960s that solid information became available. Between 1948 and 1951, 5,209 men and women between the ages of 30 and 62 in the community of Framingham, Massachusetts, were enrolled in a study sponsored by the National Heart Institute (now known as the National Heart, Lung, and Blood Institute or NHLBI). The Framingham Heart Study, as it was unimaginatively called, was geared to observing possible factors contributing to the development of heart disease. In 1961, after six years of data collecting, the initial results were published in the Annals of Internal Medicine. This seminal article showed, for the first time, that high blood pressure, smoking, and high cholesterol levels were major risk factors in the development of heart disease. From this first report, the concept of cardiac risk factors emerged. (The Framingham Heart Study continues to this day, tracking the offspring of the original participants.) The list of risk factors for heart disease developed from the Framingham Study has become a valuable tool for health care professionals. It allows us to determine the risk of heart disease for our patients by determining the presence

or absence of risk factors. The more risk factors that apply to you, the greater your risk of disease. Some risk factors are nonmodifiable—there’s not much you can to do change them. Others, however, are modifiable—you can do a lot to change them and reduce your risk.

Nonmodifiable Risk Factors Age is a major nonmodifiable risk factor. Growing old is inevitable. The only alternative is to die young, obviously not a desirable option. The rate at which people age varies with the individual. Some people seem to age very slowly. Old Tom Parr, supposedly born in England in 1483, didn’t marry until he was 80, committed a sexual offense at the age of 102, and ed away in 1639 at the tender age of 152. OK, that’s legend. Now let’s discuss facts. Many explanations of why we age have been formulated. These include degradation of bodily proteins due to free radicals, cellular toxic waste buildup, genetic mutation, and autoimmune reactions (when the body becomes allergic to itself). A number of other theories exist, such as those that view aging as a progressive response to stress, a change in a person’s metabolic rate, or gradual deterioration of the nervous system. There is little evidence to prove any of these concepts. Ultimately, the causes of aging are still mysterious. What we do know for sure is that your risk of a heart attack rises with age—and that you can do nothing about getting older. Aging is as unmodifiable as it gets. Just being young doesn’t completely protect you from a heart attack, however. We are seeing more people with heart attacks in their 50s, 40s, and, not uncommonly, even in their 30s. In fact, 150,000 people who die every year of a heart attack are younger than 65. The youngest person I took care of with a true heart attack was 27. Today, the baby boomers are a particularly high-risk age group for heart attacks. After World War II, there was a period of dramatic increase in the birth rate in the United States—the baby boom. The most accepted definition of a baby

boomer is anyone born between 1946 and 1964. That means there are 78 million baby boomers living in the United States today. This group’s size alone dwarfs other groups born before and after the baby boom years. Their sheer numbers will profoundly tax the health care system for many years to come. Simply because they are getting older, baby boomers are at very high risk of having a heart attack. In addition, the boomers aren’t very healthy. About 49 percent of them have hypertension. Many of them aren’t getting adequate treatment for this condition. Even worse, many are undiagnosed and aren’t getting any treatment at all. About 78 percent of baby boomers are overweight; 39 percent are obese—that is, their body mass index is greater than or equal to 30. Twenty-five percent of baby boomers still smoke tobacco. The metabolic syndrome (I’ll explain more about that later in this chapter) affects a large number of people in this age group, making them much more vulnerable to a heart attack. Baby boomers are under a tremendous amount of stress. Their parents are living longer as a result of modern technology, while their children, the echo boomers, are finding it difficult to maintain jobs and provide for themselves. Many of the echo boomers are still living at their parents’ home even though they are in their late 20s and early 30s. As a result, the baby boomers are trying to care for elderly parents and their children at the same time, while also working and trying to care for themselves as the inevitable diseases of age start to affect them. Some have called the boomers the sandwich generation, caught between two very stressful demands. As a result of all of this, the baby boomers are the highest risk group of people ever to have heart attacks. A baby boomer dies every 53 seconds. That’s about 600,000 people per year. Half of those deaths are due to heart attacks. Of those 300,000 people, 30 percent will die before they reach the hospital.

Gender What is the most common cause of death in women? When asked this question, most people will say breast cancer. This answer is wrong. Breast cancer isn’t even the most common cancer among women or the one that kills the most women—that dubious honor goes to lung cancer.

The most common cause of death in women is heart attack. Heart attacks kill more than half a million women every year, ing for 45.2 percent of all deaths in women. One out of every two women will eventually die of heart disease or stroke, compared with the one in twenty-five who will eventually die of breast cancer. There are a lot of reasons for this—and I will go into them in detail in chapter 7. At younger ages, men have a significantly higher risk of heart attack than premenopausal women. After about age 55, though, when most woman have reached menopause, the odds even out and women are just as likely as men to have heart attacks. Men are also more likely to have premature heart disease—coronary vascular disease that strikes before age 65, which is the average age for a heart attack in men. Somewhere between 4 and 10 percent of all heart attacks happen before age 45; most of those victims are men. The outlook for young men having a heart attack isn’t great. In one study of young men with heart attacks, the average age was just 36, but 30 percent of those men were dead within fifteen years.

Family History It has always been said that you can’t choose your family, which, at times, is too bad. You can’t change your family history of heart attacks, but it is important to be aware of it so you can use it to assess your own risk. If indeed your father died suddenly of a heart attack at age 46, your chance of having a heart attack at an early age is quite high. A family history of heart disease, especially early heart attacks, is related to genetics. You’re stuck with the genes you’ve inherited, but environmental factors can contribute greatly to whether those genes kick in. Doctors often say that genes load the gun but environment pulls the trigger. Your father or grandfather might have had a genetic tendency toward a heart attack at a young age, but by smoking, drinking a lot, or abusing fast foods, they weighted their genes toward disease. You might have those same genes, but you can tilt the scale away from disease with a healthy lifestyle.

Ethnicity African Americans have more severe high blood pressure than Caucasians and a higher risk of heart disease. Heart disease risk is also higher among Mexican Americans, American Indians, native Hawaiians, and some Asian Americans. This is partly due to higher rates of obesity and diabetes among these ethnic groups. Whether this is due to actual genetic differences, environmental and cultural differences, or perhaps a combination of factors is certainly not clear. In the past, death rates from atherosclerotic vascular disease in Sweden, Italy, and Switzerland were half that of the United States. These comparisons are even more amazing when certain age groups are studied. In the United States, mortality rates in men between ages 35 and 64 have been six times higher than men in the same age group in Japan. However, Japanese who move to the United States acquire the same predisposition to atherosclerosis as people born and raised in the United States.

Modifiable Risk Factors The impact of aging, gender, ethnicity, and family history on the risk of heart disease can’t really be changed. Fortunately, many of the other risks for heart disease are things we can modify, some more easily than others.

Hypertension In 1905, the Russian surgeon Nikolai Korotkoff developed the modern technique of using a stethoscope to listen for the sounds of blood flowing through the artery. His method proved to be extremely accurate and led to the discovery of hypertension, also known as high blood pressure. Blood pressure is the force exerted by the flow of blood on the arterial wall. It is generated by contraction of the left ventricle of the heart, which pumps blood out to circulate throughout the body. Blood pressure is measured in millimeters of mercury, units that refer to the height to which a column of mercury is raised by an equivalent pressure. (Old-fashioned blood pressure machines actually used a

tube of mercury to measure the pressure, much as a barometer does.) Your blood pressure reading has two parts, expressed as systolic over diastolic pressure. So, when your blood pressure is taken, you might be told it’s 135 over 80. The first number is the systolic pressure, measured while the heart is contracted and pushing blood out. The second number is the diastolic pressure, measured while the heart is relaxed. Normal blood pressure is below 120 over below 80. If your blood pressure is 120 to 139 over 80 to 89, you have prehypertension—not quite high blood pressure, but heading in that direction. If your blood pressure is 140 to 159 over 90 to 99, you have Stage 1 hypertension. And if your blood pressure is 160 or more over 100 or more, you have Stage 2 hypertension. Blood pressure that is higher than normal causes damage to blood vessels throughout the body. Hypertension causes heart attacks, strokes, and kidney disease. It’s a great idea to get yours checked. Hypertension has been causing vascular disease for thousands of years. Autopsies of Egyptian mummies have shown evidence of this process even at that time. As early as the 1700s, scientists working with animals recognized the concept of hypertension. However, it was not until the beginning of the twentieth century, when the blood pressure cuff was invented, that physicians could accurately measure blood pressure over a long period of time. It then took another fifty years for medical science to make the association between hypertension and vascular disease. The effects of hypertension are profound. For every increase of diastolic blood pressure of only 7 mm, the risk of stoke increases by 42 percent! The risk of heart attack goes up by 27 percent. Over 70 million people in the United States have high blood pressure, almost one out of every three adults. Of these, 30 percent don’t even know that they have it. Only 60 percent of people who know they have high blood pressure are getting treatment. And of that group, only about one-third are adequately controlled. The first step in treating high blood pressure is to begin health-promoting lifestyle changes.

Weight reduction alone can have a dramatic effect on blood pressure, to the point of a cure in a significant number of people. Salt and fluid restriction can also help quite a bit. A regular aerobic exercise program can not only help with weight reduction but can also contribute to lowering blood pressure in and of itself. If these measures alone are not successful, then consider taking medication to get your blood pressure under control. There are a huge number of choices when it comes to blood pressure medicines. Each drug has its own benefits and potential side effects. What must be kept in mind is that everyone is different. The best drug for one person may be totally wrong for the next, so you need to work with your doctor to find the best treatment for you. This can take some time and, frankly, some trial and error. Finding the right dosage for you can take a few months, and often people need to take more than one drug. It’s almost impossible to predict what side effects you might have. Be patient, because the benefit you get is well worth the wait. If you normalize your blood pressure, you reduce your risk of having a heart attack by about 20 to 25 percent. The risk of having a stroke is decreased 35 to 40 percent. The risk of going into heart failure is lowered about 50 percent.

Diabetes Diabetes is defined as elevated levels of sugar (glucose) in the blood. About 18 million people in the United States, or about 6 percent of the population, have been diagnosed with diabetes. About 5 million of these people don’t even know they have the disease—many of those individuals will learn they have it only after they’ve had a heart attack. Most people with diabetes have type 2 diabetes, which is caused by insulin resistance. The rest have type 1 diabetes, which occurs when, for reasons that are unclear, the pancreas stops producing insulin, usually in the early teen years. Insulin is a hormone produced by the pancreas. Your body uses insulin to carry glucose from your blood into your cells, where it can be burned for energy. People with type 2 diabetes have become resistant to the effects of insulin. They still produce plenty of insulin, but their cells have stopped responding to it properly. Some glucose still makes it into the cells, but insulin resistance means that a lot of glucose remains in the blood. All that extra glucose is damaging to

the blood vessels, especially the smaller ones in the heart, kidneys, eyes, and toes. What causes insulin resistance? It is a combination of genetics, being overweight, and having a sedentary lifestyle. Put all three together and type 2 diabetes is a near certainty as you age. You have type 2 diabetes if your fasting blood glucose level is 126 mg/dL or higher (normal would be 100 mg/dL or less). You have prediabetes if your fasting glucose level is between 100 and 125 mg/dL. Without lifestyle changes such as weight loss and more exercise, most people with prediabetes will progress to type 2 diabetes within ten years. As with hypertension, we have known about diabetes for quite a while. The first record of its existence dates back to 1552 BC, the Third Egyptian Dynasty, when a physician by the name of Hesy-Ra mentions polyuria (frequent urination) as a symptom of this disorder. In the first century AD, Arateus described diabetes as “the melting down of flesh and limbs into urine.” These ancient authors were probably describing type 1 diabetes, which is an autoimmune disease that usually strikes in early adolescence and destroys the ability of the pancreas to produce insulin. Type 2 diabetes, caused in adults by obesity and lack of activity, was probably unknown to them. Even so, the descriptions apply—increased urination is a common symptom of type 2 diabetes as well. Diabetes causes profound damage to blood vessels and compromises the delivery of blood, leading to severe organ damage. It’s an independent risk factor for coronary artery disease. People with type 2 diabetes are also at extremely high risk of a stroke. In fact, having type 2 diabetes makes you two to four times more likely to have heart disease or a stroke than someone without diabetes. At least 65 percent of people with diabetes die from some form of heart disease or stroke. In the United States, type 2 diabetes is also the leading cause of end-stage renal disease (ESRD), nontraumatic lower extremity amputations, peripheral artery disease, and adult blindness. Because type 2 diabetes is rapidly becoming more prevalent worldwide, it will be a leading cause of morbidity and mortality for a very long time. Even when someone has the high blood sugar of type 2 diabetes under control,

the risk of heart disease, stroke, and other complications is still much higher than for people without diabetes. That’s because most people with type 2 diabetes also have other health issues, such as hypertension, high cholesterol and high triglycerides, and obesity, which all contribute to heart disease even if someone doesn’t have diabetes.

Dyslipidemia Dyslipidemia (also known as hyperlipidemia) is the term cardiologists use for high levels of cholesterol and triglycerides in the blood. Cholesterol is a waxy substance your body produces naturally. We tend to demonize cholesterol as always a bad thing, but you need it for many crucial body functions, such as making many hormones (including the sex hormones estrogen and testosterone), for making the membranes of the body’s cells, and for converting sunlight to vitamin D in the body. You have some cholesterol in every cell of your body; it also circulates in your bloodstream. About 75 percent of the cholesterol in your body is made in your liver. The rest comes from your diet. Triglycerides are tiny droplets of fat that circulate in your blood before eventually being burned for energy or stored as body fat. During the 1800s, as result of observations made during autopsy, it was well known that human blood vessels were prone to becoming blocked as a result of atherosclerosis. During the early 1900s, Russian scientists found that if they fed milk and eggs to rabbits, they could induce atherosclerosis in the blood vessels of these laboratory animals. In 1913, Nikolai Anichkov showed that the material responsible for the blockage was pure cholesterol. In the 1930s, the ability to measure cholesterol levels in the blood became available. In the 1950s, John Gofman discovered low-density lipoproteins (LDL) and highdensity lipoproteins (HDL), the two main components of cholesterol. His work included the first prospective studies demonstrating that high LDL levels were present in almost 90 percent of people who had suffered heart attacks. Thereafter, LDL cholesterol became known as “bad cholesterol.” He also found that low HDL levels represented another risk factor for coronary heart disease, because high HDL cholesterol was found to protect against blocked arteries. Thus the concept of HDL being the “good cholesterol” evolved.

Definitive proof that high total cholesterol levels, and especially high LDL levels, are a major risk factor for heart disease came in 1961, when the results of the Framingham Study were published. According to the experts of the National Cholesterol Education Program (part of the National Heart, Lung, and Blood Institute), most people should aim for an LDL cholesterol level below 130 mg/dL (3.4 mmol/L). If you have other risk factors for heart disease, such as high blood pressure, your target LDL should be below 100 mg/dL (2.6 mmol/L). If you’ve already had a heart attack, or have type 2 diabetes, or are at very high risk of heart disease for any other reason, you should aim for an LDL level below 70 mg/dL (1.8 mmol/L). Generally speaking, the lower your LDL cholesterol level is, the better. High triglycerides mean you have a lot of tiny fat droplets floating around in your bloodstream. This contributes to atherosclerosis and may also be a sign that you have type 2 diabetes. According to the American Heart Association (AHA), the optimal triglyceride level is 100 mg/dL (1.3 mmol/L) or lower. Numerous clinical trials over several decades have clearly shown that getting your cholesterol to desired levels not only reduces the risk of a first heart attack (primary prevention), but, if you’ve already had a heart attack, it also will reduce your risk of having another (secondary prevention). Diet and exercise are a great start for lowering cholesterol, but with this risk factor, it isn’t usually that simple. While lifestyle changes can usually reduce your LDL cholesterol by up to 20 percent, the problem is that often just reducing the LDL cholesterol isn’t enough. If you have an LDL of 180 and you need to get to less than 70, lifestyle alone obviously will not get you where you need to be. For people with previous heart attacks or who are at high risk of having heart attacks, cholesterol-lowering medication is necessary and important. A variety of medications are available, but the only drugs that have been proven to save lives over and over again are the statins—drugs such as Lipitor (atorvastatin), Mevacor (lovastatin), Pravachol (pravastatin), and Zocor (simvastatin). These drugs can reduce LDL levels by between 30 and 50 percent. They work by inhibiting the action of an enzyme in the liver, HMG-CoA reductase, which blocks the production of this type of cholesterol. Statins also work by acting as an anti-inflammatory agent. This effect contributes to stabilization of the plaque, lowering the risk of it rupturing and causing a heart attack.

A 2006 trial called ASTEROID has shown that if LDL cholesterol levels are reduced to very low levels by taking a powerful statin drug, the process of atherosclerosis can be halted—and the plaque embedded in the arteries can actually be absorbed. This is the first time a drug has been shown to cause regression of the disease. As with all medications, there can be side effects with statins. Muscle pain and cramping are commonly reported, but in the large clinical trials, these complaints were equally reported in the placebo groups as well. Mild elevation of liver enzymes can occur in about five people in a thousand. Routine blood testing of liver function is crucial for everyone taking these medications. Some people, especially postmenopausal women, can develop elevated blood sugar from statins, perhaps to the point where the drug causes type 2 diabetes. The value of the drug needs to be weighed against this slight risk. The major safety concern of therapy with statins, however, is severe muscle inflammation that can lead to kidney failure. This event can be life-threatening, but it’s also very rare. Overall, the benefits of treatment in the majority of situations far outweigh the potential risk. Thousands of lives are saved every year. HDL, the “good cholesterol,” also plays a prominent role in the clogging of arteries. HDL carries fat from the blood vessels to the liver, which then disposes it. The higher your levels of HDL, the more you are protected from heart attacks. On the other hand, the lower your HDL level, the higher your risk of a cardiac event. It is difficult to raise your HDL level. Exercise can help a bit, but so far, no drugs have really been effective. Large doses of niacin can help some people, but the side effects, especially flushing, make this drug hard to take. Based on recent research, it’s also unclear if raising your HDL level really has an impact on reducing your risk of a heart attack. How low should you go with your cholesterol? That depends on your clinical situation. If you’ve had a heart attack, mini-heart attack, or unstable angina, you want to get your total cholesterol to less than 200 and your LDL cholesterol to less than 70, or maybe even lower. You want to get your HDL as much over 40 as you possibly can and your triglycerides to less than 150. If you have never had a cardiac event but have significant risk factors, you probably want to get

your LDL to less than 100. Despite all the evidence that these measures are hugely successful in helping people with atherosclerosis, it is shocking that of the 105 million people in this country with hypercholesterolemia, 92 million are untreated. Understanding this makes it clear why heart attacks are such a major problem.

Obesity What is the No. 2 preventable cause of death in the United States? When asked this question, most people will say accidents, murder, suicide, or anything else except for the right answer. It’s obesity. Obesity is a disease caused by having too much body fat. In general, you are obese and at high risk for heart disease if your body weight is about 30 pounds heavier than your ideal weight. According to a formula devised in the late nineteenth century and modified in the 1970s and 1980s, a man’s ideal body weight is usually estimated as about 106 pounds for the first 5 feet in height plus 6 pounds for each additional inch over 5 feet. So if you’re 5 feet 8 inches tall, your ideal body weight would be 106 plus 48, or 154 pounds. A woman’s ideal body weight is about 100 pounds for the first 5 feet in height, plus 5 pounds for each additional inch over 5 feet. Note that in the last quarter of the twentieth century, this ideal body weight calculator was discredited by all major medical institutions as way to measure obesity. A more realistic, though also discredited way to think about body weight is the body mass index (BMI), which is calculated from your height and weight. To find your personal BMI, use one of the many charts available on line. According to The National Heart, Lung, and Blood Institute: If your BMI is below 18.5, you’re underweight. If your BMI is between 18.5 and 24.9, you’re normal weight. If your BMI is between 25 and 29.9, you’re overweight—your weight is about 10 to 30 pounds more than is healthy.

If your BMI is over 30, you’re obese. And if your BMI is over 40, you’re extremely obese, also sometimes called morbidly obese. When looking at the BMI charts, it’s important to that they represent a range of weight. If you have a muscular build, your BMI could be on the high side, but you probably don’t have excess body fat. More worrisome is that the BMI number may underestimate body fat in older persons and others who have lost muscle. So you could be an older person who’s had a serious illness recently but still fall into the normal weight BMI range even though you’re really underweight. Overall, however, many believe that the BMI is a pretty good indicator of where you are with your weight. There are about 300 million people in the United States today. About 65 percent of Americans are overweight—about 130 million people. About 35 percent of Americans are obese—about 60 million people. About 4 percent of Americans are extremely obese—about 9 million people. About 16 percent of American kids between the ages of 6 and 18 are overweight or obese—about 9 million young people More people are overweight in this country than are not! It should be no surprise, then, to learn that we are the fattest people in the world. It should also be no shock that we have the most heart attacks. Obesity is strongly associated with increased risk of illness, disability, and death. It places enormous strain on the cardiovascular system and sharply increases the risk of diabetes, hypertension, and elevated lipid levels. This is clearly a problem of extreme magnitude. In the past few decades, the incidence of obesity has accelerated to the point where today, almost 400,000 people die every year in the United States as a result of diseases due to obesity. Morgan Spurlock, creator of the documentary film Super Size Me, describes the problem very clearly: “We are eating more food than ever before—way more.” “We are eating more food that’s bad for us—way worse.” “We are getting less physical exercise—way less.” A huge thing that many don’t even realize is that a lot of people are making a

whole lot of money on us getting fat! In fact, a large part of the profits made every year by Big Corporate America is based on how much food we stuff into our bodies. These corporations spend obscene amounts of money—billions and billions—on ads that show us food, that stimulate our hunger, and make us want to eat much more than we need. McDonald’s all by itself spends close to a billion dollars a year on advertising. A large portion of this money is focused on advertising to children. A lot of kids’ first words include Ronald McDonald or Happy Meals. We are constantly exposed to this propaganda. Radio, television, magazines, newspapers, the Internet—it gets to the point where you can see a food item and know what it is without even reading its name. I was watching a Lakers game on TV recently and was shown commercials for McDonald’s, Jack in the Box, Taco Bell, Pizza Hut, Domino’s Pizza, KFC, Burger King, and a number of other fastfood places. And that was just in the first quarter of the game! As a result of this barrage, American eating habits have become abysmal. Almost a quarter of the food we consume comes from junk food—prepared or packaged foods that are high in calories and low in nutrition. We are putting too much food into our bodies, and we are constantly being reminded to do so by the media. We stuff ourselves with so many excess and empty calories that every year we put on pounds that we certainly do not need! We do this without giving much thought to the number of calories we actually consume. It’s like going on a shopping spree with no knowledge of your bank or credit card balance. It adds up more quickly than you expect. The next thing you know, you have a $15,000 bill. With food, we are on an eating spree, and the next thing you know, we are 10 to 20 pounds heavier than we should be. If we’re not careful, eating can get out of control. We are in love with food. And why not? It satisfies our hunger, it tastes great, and it can be comforting. We are incredibly lucky, because for us, food of all sorts is abundantly available and affordable. Many in this world are far less fortunate. The main problem is that food has become a substance that, like so many others, we abuse. We find comfort and solace in eating. We get a certain degree of

euphoria from eating something delicious. And the short-lasting effects cause us to eat even more. And it is making us really sick.

Sedentary Lifestyle Lack of exercise compounds the detrimental effects of eating too much. According to the U.S. Department of Health and Human Services, adults aged 18 years and older need forty minutes of physical activity five or more days a week to be healthy; children and teens need sixty minutes of activity a day for their health. Only three in ten adults get the recommended amount of physical activity. Among adults, 37 percent report they are not physically active. Only 33 percent of American students exercise for more than two hours per week! In Austria, , and the Slavic Republic, 80 percent of students exercise for more than two hours per week. Kids would rather watch TV, surf the Internet, or play video games! Adults would rather do the same.

Tobacco Abuse What is the top preventable cause of death in the United States? Tobacco abuse, particularly cigarette smoking. Tobacco is a plant in the nightshade family. It is indigenous to North and South America. Tobacco contains nicotine, which is a potent, short-acting stimulant of the brain and which is highly addictive. For hundreds of years before the Europeans arrived, Native American used tobacco for ceremonial purposes and for pleasure. In the 1500s, early settlers learned about smoking tobacco and took it back home to Europe, where it became extremely popular. The huge demand for tobacco was one of the major forces that drove the colonization of the Americas. The demand continues today around the world. In the United States, an

estimated 25.6 million men (25.2 percent of the population) and 22.6 million women (20.7 percent of the population) are smokers. That number is down quite a bit from the time in the early 1960s when nearly half the population smoked, but it’s still far too high. The list of diseases linked directly to smoking is very long. The cardiovascular diseases alone include heart attack, angina, abdominal aneurysm, peripheral artery disease, and stroke. The well-known risk of lung cancer is ed by other cancers, including cancer of the mouth, larynx, esophagus, throat, bladder, cervix, colon, stomach, kidney, and pancreas—and also acute myeloid leukemia. Smoking causes gum disease, makes asthma worse, increases the incidence of pneumonia and bronchitis, and causes emphysema and chronic bronchitis. About 440,000 people die prematurely from these diseases every year in the United States. Adult men lose 13.2 years of life and adult women lose 14.5 years as a result of smoking. That’s the difference between dying in your early 60s and dying when you’re in your 80s. Smoking has severe economic consequences for the nation, estimated at a staggering $53.7 billion in total annual costs. Despite the massive amount of direct evidence showing that tobacco not only causes disease but is also strongly addicting, it is perfectly legal to sell tobacco throughout the world. And why is this? For the same reason we are allowed to be sold junk food. The tobacco industry sells $100 billion of product every year and obviously wants to continue profiting. Our government receives a lot of tax money from these profits; states, too, receive a lot of money from taxing the sale of cigarettes. Every year, the tobacco industry spend between $5 billion and $10 billion on advertising. Their primary goal is to stimulate worldwide demand for tobacco, that is, to get more and more people addicted so that more money can be made. Much money has been invested in the movie industry since the early 1920s with the intent of making cigarette smoking hip, cool, glamorous, and sexy. In the 1950s and 1960s, tobacco companies were frequently sponsors of television and radio shows. Tobacco advertising has been banned from TV and radio since 1971. Over the years, increasing restrictions on tobacco advertising have been put into place. In 2010, new regulations came into effect forbidding tobacco companies from sponsoring sports, concerts, and other events. Tobacco companies are now prohibited from putting their logos or ads on hats, T-shirts,

and other clothing. Despite all the restrictions, tobacco companies continue to find ways to promote their products. They make special efforts to target women and young people. These efforts are necessary to be able to sell a product that kills so many of its customers every year—new smokers must be recruited constantly, preferably while they are still young and impressionable and many years of smoking away from the tobacco-related diseases that will eventually kill them. The efforts have been successful. Every day in the United States, more than three thousand young people become regular smokers. That is more than 1 million new smokers every year. People addicted to tobacco are no different than any other type of drug addict. It is incredibly difficult to break the smoking habit. During my training at LAC/USC Medical Center, I ran across a number of former junkies, crack heads, and a variety of other former drug addicts. Almost every one of them told me that quitting the drug they had abused was far easier than quitting tobacco. The majority of the people that I met then are still smoking tobacco. They’ve traded one addiction for another. At least cigarettes are legal. Tobacco’s adverse effect on health was suspected as early as the 1600s when King James I of England warned his subjects of this. Nobody listened. In the United States, it took until 1964, when the U.S. Surgeon General released a report based on scientific research that linked tobacco use with cancer and cardiovascular disease. Because of this report, laws were ed requiring warning labels on tobacco products and restrictions on tobacco ments. In April 1970, Congress ed a law banning the advertising of tobacco products on television and radio, effective January 2, 1971. Since then, most tobacco advertising is done in magazines, billboards, racecar sponsorships, concert tours, and the Internet. Performers such Madonna and Paula Abdul have done concert tours sponsored by tobacco companies. What is frightening is that cigarettes are becoming even more addictive. Since 1998, tobacco companies have been breeding tobacco plants to have even more nicotine and thus make smoking even more addictive. The average cigarette today has between 10 and 30 percent more nicotine than it did in 1998.

The consistency of the increase leads many to believe that it is a conscious and deliberate act by the tobacco companies. The companies can do this because no federal agency regulates tobacco products, even though the FDA has suggested that cigarettes are nicotine-delivery devices and should be regulated. The majority of the patients I take care of are or were smokers. The motivation for them to quit has usually been that they have suffered a heart attack and nearly died. Once these patients have gotten through the withdrawal period, they then become the most ardent antismokers. Many of them are disgusted with the sight and, even more so, the smell of cigarette smoke. Most people who try to quit smoking cigarettes fail at least once and often several times before they kick the habit. There are countless ways to quit. You can try nicotine patches, gum, or lozenges; hypnosis; acupuncture; antismoking group therapy; the antidepressants Zyban (bupropion) or Chantix (varenicline); or going cold turkey. Try them all until you find the way that works for you. You can count on the fact that if you truly want to quit, it will get a little easier every day. In of your risk of having a heart attack quitting tobacco significantly decreases your risk. The longer you have stopped smoking, the lower your risk of having a heart attack. In addition, your risk of other smoking-related illnesses, including asthma, bronchitis, emphysema, and lung cancer, goes down as well.

The Metabolic Syndrome The metabolic syndrome is basically the end result of the combination of some or all of the risk factors we have just discussed. The definition of the metabolic syndrome (sometimes called Syndrome X in older material) varies, but most doctors accept the definition given by the American Heart Association and the National Heart, Lung, and Blood Institute. You have the metabolic syndrome if you have three or more of these factors: Elevated waist circumference. In men, this is equal to or greater than 40 inches (102 cm); in women, it is equal to or greater than 35 inches (88 cm). This is known as central obesity or having an apple shape—you carry your excess weight in your belly.

Elevated triglycerides. Equal to or greater than 150 mg/dL. Low HDL (“good”) cholesterol. In men, less than 40 mg/dL; in women, less than 50 mg/dL. Elevated blood pressure. Equal to or greater than 130/85 mm Hg. Elevated fasting glucose. Equal to or greater than 100 mg/dL. About 25 percent of the adult U.S. population probably has the metabolic syndrome, although many don’t know it. Having the metabolic syndrome dramatically increases your risk for heart attack, stroke, and diabetes. Your risk of type 2 diabetes is increased ten to thirty times over the risk for someone without the metabolic syndrome. Your risk of heart disease and stroke may be up to five times higher. The metabolic syndrome is also associated with fat accumulation in the liver (nonalcoholic fatty liver disease). This can commonly lead to inflammation of the liver (hepatitis) and frequently to irreversible damage with scarring (cirrhosis). The cause of the metabolic syndrome is quite controversial. There are many different theories, but most researchers now believe that it is caused by a combination of genetic factors along with poor diet and lack of exercise. Earlier I mentioned the movie Super Size Me, produced, directed, and written by Morgan Spurlock. If you haven’t seen it, I highly recommend you do so—it is frightening and very enlightening. For the movie, Morgan committed himself to eating only McDonald’s food for breakfast, lunch, and dinner for a whole month. In addition, if he was asked to supersize his meal, he could not refuse. His personal physician closely monitored him. The outcome was dramatic. In just one month, his health deteriorated rapidly. He gained almost 40 pounds. He became profoundly fatigued and short of breath with minimal exertion. His blood pressure increased, as did his waistline. What is even scarier is that on routine blood testing, not only did his triglycerides, blood sugar, and bad cholesterol all go up, but his liver functions tests also began to show signs of hepatitis! His doctor actually accused him of drinking excessive amounts of alcohol. It is clear that by eating only junk food, Morgan Spurlock gave himself the metabolic syndrome.

His experience is a model for what is actually occurring not only in the United States but also throughout the world. It explains why heart attacks are now a problem of such international magnitude.

Exercise As we get busier in our lives, we tend to exercise less and less. At the end of a twelve-hour workday, the choice can come down to either an hour of exercise or a glass of wine and relaxing on the couch. The latter seems to win out more and more. We must keep in mind, however, that exercise has a profound and substantial beneficial effect on heart disease. Exercise improves your cardiovascular risk even if you lose no weight. In the Health Professionals’ Follow-Up Study (HPFS), an ongoing study of 44,452 U.S. male health professionals were followed in two-year intervals from 1986 through 1998. The objective was to assess the amount, type, and intensity of physical activity in relation to risk of coronary artery disease among these men. The results were startling. One hour of running per week reduced the risk of coronary heart disease by 42 percent. Half an hour a day of brisk walking brought the risk down by 18 percent. We know from this study and many others that exercise can have all of the following beneficial effects on cardiac risk factors: Weight loss and percentage of body fat reduction Lower blood pressure Increased HDL cholesterol Decreased LDL cholesterol Improved glucose control and insulin sensitivity Decreased blood coagulability (less risk of clotting)

Increased skeletal muscle mass Improved aerobic capacity Improved lung function Increased bone mineral density and decreased osteoporosis Your exercise goal should be forty minutes of moderate continuous aerobic activity at least five times a week. It can be as easy as walking twenty minutes away from your home or work and walking twenty minutes back. Exercising at a moderate level should leave you warm and a little winded, but not gasping for air. You should be able to carry on a conversation, but not sing a song.

Assessing Your Risk Factors If you want to avoid a heart attack, you must assess your risk of having atherosclerosis. You must look at your risk factor profile for having clogged arteries and see where you stand. The more risk factors you have, the more likely it is that you may have a heart attack. So, if your mom and dad lived until their 90s, you’ve never been a smoker, you are not unhealthfully overweight, you do not have high blood pressure or diabetes, your good cholesterol is high and your bad cholesterol is low, and you just completed your sixth marathon last week, you are at a fairly low risk of having a cardiac event. On the other hand, if your dad dropped dead at age 53, you’ve smoked a pack a day since high school, your blood pressure is high, your cholesterol is high, you have diabetes, and your profile looks like Homer Simpson, you are at extremely high risk and should get thoroughly evaluated by a health care professional as soon as possible. If you’re a fan of the show The Simpsons, you that Homer needed by surgery when he was in his mid-40s. You must also understand that an assessment of risk is merely looking at your odds of having a heart attack. You may be at high risk and never have a problem. You may, however, be at low risk and still go on to have The Big One. The reality is that most of us stand in the middle. We are all at risk.

6. The Gold Standard

The optimal treatment of acute myocardial infarction can be summed up easily: Time is muscle. If you are having a heart attack, prompt therapy to restore blood flow to the culprit coronary artery, as soon as possible, limits the size of heart muscle damage and will save your life. This central concept was first proven through large clinical trials of clot-buster medications in the 1980s. Hundreds of thousands of patients were studied. The studies showed conclusively that the shorter the time from the beginning of the heart attack to the initiation of treatment, the more lives were saved. Similarly, the clinical studies evaluating angioplasty as a treatment for heart attacks, again performed on thousands of patients, clearly showed that the time to treatment significantly reduced the patient’s risk of dying. It’s clear that the focus for heart attack treatment in the twenty-first century should be on the early recognition of heart muscle in jeopardy and the prompt initiation of treatment that has been proven to save people’s lives. Today the “gold standard” approach to treating heart attacks is the rapid restoration of normal coronary blood flow to the clogged artery that is causing the heart attack. The faster and more efficient the delivery of this care, the more lives will be saved. When a coronary artery closes, an aggressive system must be in place that can be immediately activated and that will respond rapidly to provide the optimal treatment. Ideally, this system will mean treatment is given within the first ninety minutes. If treatment is istered within this time frame, the risk of dying is reduced by 40 percent! The system must always be on the clock, striving to minimize the time necessary to provide this ultimate care. Every minute counts.

The Gold Standard of Care The gold standard of care for someone having a heart attack is ninety minutes from the first medical to an open artery. The standard was set in 2004 by the American College of Cardiology and the American Heart Association. The gold standard of care must exist at three critical levels: Level one is the time from the onset of symptoms to the 911 call for help. Level two is the time from the arrival of the emergency medical services (EMS) to the patient location and the time to arrival at the hospital. Level three is the time from the arrival at the hospital to attaining an open artery in the heart. In medical shorthand, this is called the D2B time—the time it takes to get the patient from the door of the emergency to having an angioplasty in the cath lab. Achieving the gold standard of care for a heart attack starts with the patient. The person experiencing the heart attack, or someone nearby, must immediately call 911 for help. Next, emergency medical services must rapidly respond to the scene, stabilize the individual, and transport him or her to the hospital. Finally, the hospital must be able to receive the person and transport him or her immediately to a cardiac catheterization laboratory, where the occluded coronary blood vessel can be opened with emergency angioplasty. The gold standard of care is to do all of this within 90 minutes or less. If all three steps are followed, study after study has clearly shown that many lives are saved.

Barriers to the Gold Standard Even though the gold standard is the ideal situation, in reality, it is far from being accomplished the majority of the time when someone has a heart attack. Treatment that saves lives is dependent on the time and access to acute state-ofthe-art medical care. Although the “time is muscle” concept is well recognized, rapid access to emergency medical care remains a major problem.

Despite an enormous amount of evidence ing an aggressive approach to heart attack treatment, too many studies have shown the common failure to deliver this gold standard of care. A significant number of people with heart attacks who would be candidates for treatment with angioplasty are not receiving this type of care.

Causes of Delay These life-threatening delays have multiple causes: Patients delay seeking care. On average, heart attack patients wait one and a half to two hours from the onset of symptoms to call for help. Sometimes they don’t call 911. Instead, they self-transport to the hospital, either driving themselves or having someone take them. Patients go to a hospital without state-of-the-art care. Whether they arrive by ambulance or by self-transporting, patients usually go the nearest hospital, not the one that can provide state-of-the-art care. The time to treatment is delayed, sometimes fatally, while the patient waits for transport from the first hospital to another that can provide adequate treatment. Delays occur at the hospital. Once at the hospital, treatment for someone having a heart attack is often delayed by a series of time-consuming steps. The time from arrival in the emergency to evaluation (triage) is delayed by insurance verification. It can also be delayed if the ER is busy. The lack of adequate triage and treatment protocols frequently leads to delay in immediately seeing patients with chest pain. Delays can also occur in getting an EKG on the patient, having that EKG read by the ER doctor, and calling in a cardiologist for a consultation. If clot-busting medications are needed, they may not be immediately available in the ER. More time is lost in ordering them from the pharmacy. Ordering, performing, and getting the results from lab tests takes additional time. When the time to diagnosis is significantly delayed by not getting appropriate tests in a timely fashion, the patient is likely to have a bad outcome. If the patient is found to need angioplasty, the cath lab has to be notified. Assuming the cath lab is in the same hospital (likely only about 20 percent of the time), the lab must then bring together all the staff needed for the procedure, which may take some time. The interventional cardiologist must then be able to

promptly open the blocked vessel.

Delays in Angioplasty The scary thing is that a large number of people are not receiving any reperfusion treatment at all. Of the five thousand or so hospitals in the United States, less than 20 percent are capable of performing emergency angioplasty. Of these hospitals, many do not treat a high volume of cases every year, which means their medical teams don’t have as much experience. Outcomes at hospitals that do angioplasties all the time are better than at hospitals that don’t do them often. Many hospitals adequately treat heart attacks during business hours, but after hours, they experience serious logistic difficulties in performing emergency angioplasties. Too often, this leads to care that falls below the gold standard— and suboptimal care leads to higher death rates. The relationship between the emergency room physician and the consulting cardiologist is critical in providing optimal care. A good relationship leads to prompt involvement of the cardiologist, ideally in the first ten to fifteen minutes after the patient arrives at the emergency room. This provides rapid confirmation of the diagnosis and initiation of care. Too often, there are substantial delays. Callbacks from the cardiologist can frequently be delayed, putting diagnosis and care beyond the ten- to fifteen-minute goal. Sometimes the cardiologist on call cannot be reached at all, for a variety of reasons, and the ER physician must scramble to find an appropriate replacement. The convenience of the consulting cardiologist can be an issue in deciding which therapy to ister. A three o’clock in the morning, some cardiologists have been known to order thrombolytic therapy by phone from their beds rather than go out into the cold and dark night to do an emergency angioplasty. When lecturing at an emergency room in Northern California, I was told of one cardiologist who would not cancel his afternoon office patients to perform an angioplasty on one of his patients who was having a heart attack. He ordered thrombolytic therapy and saw the patient four hours later, once his office patients were seen. The cardiologist’s office was across the street from the hospital!

As a result of all these issues, fewer than 35 percent of blocked arteries are open in less than ninety minutes. The risk of dying increases by over 40 percent if care is delayed as little as thirty minutes.

How to Achieve the Gold Standard To achieve the gold standard of heart attack care, a transformation is required in the care that is presently being given. A 2006 article in the New England Journal of Medicine showed the median door-to-balloon (D2B) times among a group of 365 acute-care hospitals that followed the recommended guidelines and performed at least twenty-five angioplasties a year. The median door-to-balloon time was calculated for each hospital in the study. The median times was 100.4 ± 23.5 minutes, which is considerably longer than the 90-minute interval recommended in the 2004 guidelines of the American Heart Association and the American College of Cardiology. This shows that even the better hospitals with a high volume of angioplasties have difficulty attaining the gold standard. The gold standard is not an impossible standard. We now have ample evidence to show that it can be consistently attained. Achieving the gold standard takes a coordinated effort on the part of emergency medical services, doctors, hospitals, and the community. The payoff is greatly improved survival for heart attack patients.

Heart Attack Centers of Excellence To widely implement the gold standard, the establishment of Heart Attack Centers of Excellence is essential. These centers of excellence must provide state-of-the-art care of heart attacks to an entire region. To qualify as a center of excellence, a hospital must meet stringent requirements: - The hospital must be able to consistently diagnose and treat heart attacks in a timely fashion.

- The hospital must provide true 24/7 coverage, throughout the year, without lapse. - The hospital must have a well-established set of procedures geared to making a rapid diagnosis of a heart attack and providing effective, prompt therapy. - A center of excellence must strive to attain a D2B of ninety minutes or less as often as is humanly possible. The system must be highly efficient so that the time from first clinical with the individual (the 911 call) to an open, stable artery is maximally minimized. - A center of excellence must perform a high volume of angioplasties and other heart procedures. The interventional cardiologist should perform at least seventy-five interventions a year. The greater the experience and skill of the cardiologist, and the greater the skill and experience of the catheterization team, and the more patients the center of excellence treats, the better the outcomes, with more lives saved and fewer complications. - The cardiac catheterization laboratory must provide state-of-the-art equipment with high-quality digital radiographic imaging, hemodynamic monitoring systems, and a full inventory of guide wires, guiding and balloon catheters, and stent sizes. - A center of excellence must have the capability to perform emergency coronary artery by surgery if angioplasty can’t open the blocked artery. - A center of excellence must be able to provide devices that can circulation to the body while the heart is given a chance to recover or as a bridge to a heart transplantation.

Creating a Center of Excellence A center of excellence must continuously monitor quality assurance. Door-to-balloon times must be continuously monitored. If goals are not met, the cases must be reviewed so that mistakes can be learned from and not made again.

Morbidity and mortality conferences, where deaths and avoidable problems are discussed, need to be regularly scheduled and well attended. Rigorous standards for after-procedure care must be maintained. A patient education program is vital. Understanding the complicated schedule of drugs patients often need after a heart attack can be difficult. Patients frequently make mistakes in their medication that can result in complications and at times can even be fatal. As part of after-procedure care, patients and their loved ones need clear explanations of why and how to take medications, quit smoking, lose weight, and exercise regularly. They also need good follow-up to avoid rehospitalization. Development of a center of excellence requires a considerable amount of time and effort. Leaders from the multiple disciplines throughout the hospital have to start by organizing a team to set forth the primary goal: a state-of-the-art approach to the rapid diagnosis and treatment of heart attacks. Doctors, nurses, ER and cath lab personnel, medical technicians, paramedics, pharmacists, hospital s, and everyone else involved in patient care must be thoroughly educated about the latest developments and innovations in the diagnosis and treatment of heart attacks. As people know more about heart attacks, fewer mistakes are made and more people will live. Good organization is important. Crucially, standardized policies and guidelines must be in place. The same quality of care must be istered no matter which particular of the team are working on a given day or night. Standardization helps to assure that happens consistently. Communication is key to the success of a center of excellence. The more the of the team talk, the more efficient the care will be. In this day and age, technology is so advanced that the ability to communicate is at an all-time high. With cell phones, text messages, and pagers, there is no excuse for not being able to immediately get a hold of the medical team responsible for treating a heart attack. This will ultimately save people’s lives. Lastly, commitment to the aggressive treatment of the No. 1 killer of humanity in the world is of ultimate importance. The system will not be effective if the personnel involved do not take their roles seriously. A motivated and enthusiastic

team is critical if a center of excellence is to succeed.

Optimal Care of a Heart Attack Patient Heart attack receiving networks, also called STEMI receiving centers (SRCs), must be a coordinated effort between Emergency Medical Services (EMS) and a Heart Attack Center of Excellence. The primary goal of Emergency Medical Services is to make the diagnosis of a heart attack quickly and initiate early transport directly to a Heart Attack Center of Excellence. The mission of the ER doctor at the heart attack receiving center is to that a true heart attack exists. The first step in so ing is to get an EKG as soon as possible. The maximum time limit from the moment the patient arrives in the ER to the EKG should not exceed ten minutes, but the less time it takes, the better. The moment the EKG is completed, it must immediately be read by the ER physician. If the person is indeed having a heart attack, then the ER doctor must activate the cardiac catheterization laboratory and the interventional cardiologist on-call to perform angiography and possible angioplasty in an attempt to promptly restore flow to an obstructed coronary artery. Whether these personnel are in-house or not, they must be ready to receive transport of the individual to the lab in less than forty-five minutes. Optimal care of a heart attack patient must begin in the emergency department. All people presenting with chest pain must be evaluated immediately to see if the symptoms are due to a heart attack. All health care professionals—including doctors, nurses, technicians, secretaries, and anyone else in with patients within the ER—need to be fully aware of a potential emergency and must be meticulously educated and trained to understand, recognize, and react to it. The Role of Emergency Medical Service (EMS) The center of excellence concept is crucial in the optimal treatment of a heart attack, but it is obvious that there is no way a center of excellence can stand alone. An aggressive and efficient Emergency Medical Service (EMS) must also be in place to allow the gold standard of care to be delivered.

Emergency medical services play a crucial role in the pre-hospital treatment of heart attacks. Lives are saved if paramedics can get to the scene promptly and then rapidly transport the individual to a facility that can ister the best care. The shorter this pre-hospital phase, the more lives are saved If someone is having a heart attack at home and calls 911, the paramedics need to be on the scene in a minimal amount of time. They must have the capability to perform an EKG in the field to try to establish the diagnosis of a heart attack right away. If a heart attack is positively identified, then the paramedics can alert the emergency room physician at the nearest Heart Attack Center of Excellence that a heart attack is in progress. The ER doctor can then quickly notify the interventional cardiologist and the cardiac catheterization laboratory. By the time the patient arrives, he or she can immediately be taken for an emergency angiogram and possible emergency angioplasty. This is the gold standard of care. To provide this level of care, an aggressive and well-coordinated system must be in place. A state-of-the-art system must be reliable and consistent to provide this care as soon and as quickly as possible, every single time. The key to providing this standard of care is to combine the efforts of the Heart Attack Center and Emergency Medical Services. This combination is the heart attack receiving network. Regional heart attack receiving center networks must be established throughout the country. The goal of these networks is to maximize access to lifesaving care for the treatment of heart attacks to as many people as possible. However, very few people have access to state-of-the-art care. Less than 25 percent of hospitals in the United States have the capability to perform emergency angioplasty. Even fewer attain reperfusion within ninety minutes. Only 50 percent of heart attack patients call 911. In many areas, EMS will automatically transport to the nearest hospital, even though the majority of these institutions cannot perform emergency angioplasty. That means a large number of people eligible for reperfusion therapy receive neither angioplasty nor clotbuster therapy within the ninety-minute window that could save their life. Fifty percent of patients self-transport to the hospital. They usually take themselves to the closest hospital. As is the case with most patients who arrive at the ER in an ambulance, the closest hospital is not necessarily the best hospital

for a heart attack patient. Delay can mean death. The first huge step in improving heart attack survival rates is taking people with suspected heart attacks directly to the nearest center of excellence. The current practice of transporting patients with heart attacks to the nearest hospital must be eliminated! If a patient is having a heart attack and ends up at a facility without the capacity to perform emergency angioplasty, a system must be in place to quickly transport that person to a center of excellence to receive the appropriate care. The more efficient the system, the more lives will be saved.

Building a Receiving Network Many leaders in cardiology have called for the increased national organization of heart attack receiving center networks. But in reality, this has only just begun to happen. Today, we have only a handful of organized regional heart attack treatment systems in the United States. The first EMS system to by the nearest hospital and go instead to a heart attack center was in Boston in the mid1990s. Interhospital transport systems have been in existence in Minneapolis and in Covina, California, since early 2000. The programs in existence show that large heart attack receiving center networks can be very effective. Recent data from the Mayo Clinic hospital network showed that the goal of door-to-balloon time of less than ninety minutes could be achieved in more than 75 percent of patients. An organized system in North Carolina has recently reported data involving sixty-five hospitals in five geographic regions. They showed that 72 percent of patients had door-toballoon-times of less than ninety minutes, which is close to the goal of 75 percent set up by the D2B Alliance. (The D2B Alliance is a nonprofit network of hospitals, physicians, and strategic partners who have come together as a nationwide community of committed organizations and individuals to address the challenge of lowering D2B times.) One of the first large areas to organize a heart attack receiving center network is in Southern California. Orange County was the first such center to function, starting in February of 2005. Los Angeles County began their program in December 2006. Programs in San Diego and Ventura Counties soon followed, beginning operations in January 2007. By

October of 2007, these four counties, with a total population of about 16 million people, reported a combined door-to-balloon time of under ninety minutes more than 85 percent of the time. This achievement makes it clear that attaining an effective nationwide program is absolutely possible. It is imperative that these systems be rapidly implemented throughout the country so that more lives can be saved. The concept of a nationwide system that provides state-of-the-art treatment of heart attacks must become a reality. Efforts to improve treatment are currently underway. The American College of Cardiology (ACC) has launched a national program called D2B, for door-toballoon. The goal of this campaign is to help hospitals improve their performance by implementing the 2012 American College of Cardiology/American Heart Association guidelines. The guidelines specify that the optimal time from the first medical to open artery time should be under ninety minutes in 75 percent of identified heart attack patients. Earlier in this chapter, I mentioned an influential 2006 article in the New England Journal of Medicine that showed that even at high-volume hospitals, the median door-to-balloon times were often one hundred minutes or more. The article provided a number of valuable recommendations for improving performance and save time. Allowing the ER doctors to activate the cardiac cath lab, instead of waiting for the cardiologist, improved times by about eight minutes. The establishment of a “one-call” system, where a central operator pages the interventional team, rather than calling the individuals separately, saved about fourteen minutes. Expecting the cath lab staff to present within twenty minutes of being paged saved almost twenty minutes. Having a cardiologist on-site in the hospital saved almost fifteen minutes. Giving immediate to the staff on their performance saved almost nine minutes. About 1,250 hospitals are now participating in the ACC D2B program in the United States. Many hospitals in South America and Europe are showing interest in participating. It is hoped that adopting these simple and inexpensive strategies will allow more hospitals attain the goal of less than ninety minutes in more cases. To accelerate the development of heart attack receiving center networks throughout the country, efforts must made at a number of different levels.

Federal and state governments must mandate measurements to develop these networks as soon as possible. Probably the most powerful and most underused resource for change, however, is the community. Efforts must be made to organize local hospitals with interventional capabilities and local EMS so that a coordinated approach to care is developed. Every community in the United States must focus its attention on developing these networks. All of the community must be educated and trained to take advantage of them in a time of an emergency. Every member of the community must take this issue seriously and contribute to its formation. If all of this can occur, it will tremendously reduce someone’s risk of dying of a heart attack.

How Good Can It Get? Martin, a 56-year-old man with no previous history of heart disease, was preparing to go for a morning jog before going to work. He had no previous history of heart disease. He had never experienced any type of chest pain, shortness of breath, or palpitations. He had no history of smoking and no close family history of heart disease. However, he did have significant risk factors for coronary artery disease, including high blood pressure and high cholesterol. He took medication for both of these conditions and had them under control. His primary care doctor had told him he was prediabetic and suggested he follow a healthier diet, get more exercise, and lose 20 pounds. Martin’s morning jogging routine was part of his effort to comply with what his doctor had recommended. 9:00 a.m. While putting on his jogging shoes, Martin suddenly developed chest pain and shortness of breath. At first he tried to “walk it off” but did not get much relief. He drank some Alka-Seltzer; again, no improvement. He returned to his bedroom and lay down, hoping some rest would help. 11:02 a.m.: The Call for Help Martin continued to worsen. His chest discomfort increased, and he was more short of breath. He was experiencing increasing weakness. He finally called 911

for help, 122 minutes after the onset of his symptoms. 11:06 a.m.: The Paramedics Arrive EMS arrived at the scene in only four minutes. Martin was found lying on the ground in his yard, stating, “I’m having a heart attack.” His chest pain was 6 on a scale of 1 to 10. He was nauseous and had vomited twice. His vision was blurred, and he was sweating heavily. His blood pressure was 120/80, his pulse was 65, and he was breathing at a rate of 20 breaths per minute. 11:18 a.m.: The First EKG The only lucky thing Martin had going was that he happened to live in an area that had developed a heart attack receiving center network. As per protocol with people having chest pain, the paramedics performed an immediate EKG. The computerized readout stated: “acute MI suspected.” The paramedics then ed the ER doctor at the heart attack receiving center by cell phone and notified her that the patient was having an acute heart attack and that they were bringing him in. The ER physician then called a Code STEMI that immediately activated the cardiac catheterization lab and the interventional cardiologist on call. 11:34 a.m.: Arrival at the ER Because they had been alerted to a Code STEMI, the cardiac catheterization laboratory team, including the interventional cardiologist who was on call, was waiting in the ER for Martin to arrive. As he was rolled through the ER door, the cardiologist immediately evaluated him. He was completely awake, alert, and oriented. He stated that he was still having chest pain and now it was much more severe, rating it an 8 out of 10. He also complained of persistent nausea and dizziness. The cardiologist noted that Martin was sweating very heavily yet was amazingly cold to the touch. He could not feel Martin’s pulse or obtain a blood pressure reading. In fact, it was a miracle that Martin was able to communicate at all. Martin was breathing comfortably—his lungs were clear and the oxygen saturation of his blood was 100 percent on only room air. His heart rhythm on the cardiac monitor was regular, with a pulse rate of 76.

The cardiologist told Martin he was suffering from a massive heart attack and that he was in shock as a result of severe heart damage. Martin’s only chance of survival was an immediate emergency coronary angiogram with a possible angioplasty or coronary artery by surgery. These are the only treatments that have been shown to be lifesaving in a person with cardiogenic shock. Martin softly replied, “Do what you have to do, doc.” 11:38 a.m.: Arrival at the Catheter Lab The cath lab was set up and ready to receive Martin even before he arrived at the ER. His chest pain upon arrival at the lab was still an 8 out 10. He was immediately place on the X-ray table. His right groin area was shaved and cleaned with a sterile solution. He was covered with sterile drapes. The interventional cardiologist anesthetized the skin of Martin’s right groin with lidocaine and then placed a small plastic tube into the right femoral artery in order to gain access to Martin’s circulation. A catheter especially shaped to enter the left coronary artery was advanced through the femoral artery and up the aorta to where this artery branches off. A cannula, or very thin tube, was inserted into the artery. Dye was sent into the heart through the cannula, and an angiogram was performed. To everyone’s astonishment, the main portion of Martin’s left coronary artery was totally occluded with cholesterol blockage and a blood clot. The majority of individuals with this presentation die suddenly. Very few survive to the point where it is possible to save their life. An angiogram of Martin’s right coronary artery explained why. It was quite large and supplied blood to more then the usual amount of heart muscle. The priority for Martin’s treatment was to immediately reestablish blood flow to the left coronary artery. This was promptly done by inserting a very thin, steerable, stainless steel wire through the coronary catheter and into the left main coronary artery. The wire was pushed through the blood clot and blockage into the front branch of the left coronary artery, known as the left anterior descending artery. A second wire was then placed into the circumflex artery, the branch of the left coronary artery that supplies the back part of the heart. 11:54 a.m.: The First Balloon Inflation

An angioplasty balloon catheter was then advanced over the wire to the area of the blockage. The balloon was quickly inflated for only about twenty seconds. It was then deflated. A repeat angiogram was then performed. It showed restoration of blood flow to both branches of the left coronary artery. The emergency room door to open artery time—D2B—was twenty minutes. The first medical to open an artery was thirty-six minutes. With the restoration of blood supply to the heart muscle, Martin’s pain improved dramatically, dropping to a 2 out of 10. His blood pressure increased to 70/30, although that was due to intravenous drugs. The angiogram showed that both branches of the left coronary artery were diffusely diseased—Martin had extensive blockages. Attempts to improve his coronary circulation with stents wouldn’t be enough to help. In addition, it didn’t seem very likely that Martin would recover from his cardiogenic shock. In cardiogenic shock, the heart muscle is so stunned that it can no longer pump enough blood to meet the body’s needs. Martin’s heart was pumping so weakly that he barely had any blood pressure. An emergency cardiovascular surgery consultation was called. The surgeon decided to Martin’s circulation by placing a device called an intra-aortic balloon pump (IABP) into his descending aorta. The balloon inflated and deflated along with Martin’s heartbeats, sending more blood to the coronary arteries while also reducing the amount of work the heart had to do to send blood to the rest of the body. The heart surgeon, fortunately, was in-house and quickly came down to the cath lab. After assessing the situation, he agreed that that only hope of survival was to take Martin directly to the operating room for emergency coronary artery by surgery. 12:25 a.m.: Arrival in the Operating Room Martin remained fairly stable while being transported to the OR. He remained awake and alert. His blood pressure was 80/30 and his heart rate on the monitor was 90 beats per minute in a normal rhythm. He was breathing comfortably. In the operating room, however, Martin suddenly lost consciousness. The monitor showed a flat line. Cardiopulmonary resuscitation (R) was started

immediately. The surgeon then performed an emergency thoracotomy—he “cracked the chest” and began to perform direct open massage to Martin’s heart. While Martin’s heart was being pumped by the surgeon, the heart-lung machine was readied, and Martin was placed on cardiopulmonary by. The machine took over for his heart and temporarily stabilized his circulation. The heart surgeon performed a two-vessel coronary artery by graft surgery on Martin. He placed a left internal mammary arterial graft to the left anterior descending artery and a saphenous vein by graft (using a piece of vein taken from Martin’s leg) to his circumflex artery. The right coronary artery had no significant blockages and did not require bying. After the byes were placed, an attempt was made to wean Martin off the heart-lung machine. However, his heart still couldn’t meet his body’s needs sufficiently. Instead of contracting inwardly with each beat, the front and back walls of his heart moved outwardly in the complete opposite direction. This is a sign of profound heart weakness that is incompatible with survival. More and more heart strengthening drugs were added to try to get Martin off the pump. Multiple attempts were unsuccessful. It was clear that Martin’s heart was so weak that he would only survive if he received mechanical assist devices, small pumps that would his circulation and give his heart a chance to improve. Martin received both left ventricular and right ventricular devices. If Martin’s heart couldn’t recover enough, then he could be stabilized with the devices in the coronary care unit until he could be evaluated for a possible heart transplant. At first, Martin was kept under anesthesia in the coronary care unit (CCU) so that he could be stabilized. After a few hours, the sedation was lowered so his neurological status could be assessed. Unbelievably, Martin was able to respond to commands. His left arm and left leg were weak compared to his right side, suggesting that he may have had a stroke around the time of the surgery. Martin’s preserved mental status provided optimism that he still had a chance to survive in a meaningful way. Placing the mechanical assist devices stabilized Martin, but he had a number of postoperative complications. His coagulation system was compromised, which made him bleed from many different places; he needed transfusions and special blood products to stabilize the complication. His kidney function deteriorated to

the point where he needed dialysis to rid his body of excess fluid that had accumulated in the lungs. It was clear that Martin needed a heart transplant. After several days in the CCU, he was transferred, using a specialized mobile intensive care unit, to a nearby tertiary medical center that was a heart transplant center. The following morning, Martin was again taken to the operating room, where a different type of cardiac assist device, the HeartMate, replaced the ones placed previously. The new device was much smaller and portable. It could stay in place for long periods of time while Martin waited to see if his heart would strengthen. If that didn’t happen, the device would keep him stable while he waited for a heart to become available. Over the next few days, Martin dramatically improved. His kidney function returned to normal and he was able to eliminate the excess fluid in his lungs on his own. His left side strengthened, and he was able to get out of bed and sit up in a chair. Over the following days, he began walking the halls of the hospital, getting stronger every day. He is now patiently waiting for a new heart and is making plans to walk his daughter down the aisle at her wedding.

7. Women and Heart Attacks

Because I have lived with five beautiful women over the past thirty years, I feel confident and secure about making the statement that men and women are quite different. (The only other males in the house are my son and a cat named Bob.) The average number of words spoken each day by a woman is approximately twenty-one thousand. The average amount by a man is about three thousand. A woman thinks about having sex about once every day. A man thinks about it every thirty to forty seconds. There are also differences between men and women when it comes to heart attacks. For too long, physicians and researchers didn’t pay enough attention to women and heart attacks. When they did, they tended to think of women as just small men and didn’t take into the special and unique issues that affect women and how they have heart attacks. Today, the treatment of women with heart attacks has come a long way. Even so, women face the same basic issue as men: they fail to recognize that they are having a heart attack and fail to call for help quickly enough. The outlook for women who have had a major heart attack is actually worse than it is for men.

The Problem Is Real If you ask a woman what disease she is most likely to die from, she’ll probably say breast cancer. That’s what most women answer when asked that question, but in reality, breast cancer isn’t even the most common cause of cancer death in women—lung cancer is. Heart disease kills twice as many women as all forms of cancer combined. More women die from heart disease than men. In 1996, 505,930 women died from coronary artery disease (CAD). By comparison, in the same year, 453,297 men died from CAD.

Hormones and Heart Attacks The female hormone estrogen provides strong protection against a heart attack in women who are still menstruating and therefore still making the hormone in large amounts. Estrogen seems to help blood vessels stay flexible and helps to keep cholesterol levels down. However, once menopause occurs, usually when a woman is in her early 50s, the blood vessels stiffen, bad cholesterol levels go up and good cholesterol goes down, and other conditions, such as high blood pressure and having the metabolic syndrome (discussed in chapter 5), tend to start. The protection from estrogen means that blocked arteries are likely to develop in a woman about ten to twenty years later than they would in a man. By the time a woman is 70, her risk of heart disease is equal to that of a man of the same age. On average, women experience heart attacks about ten years later than men—in their 70s instead of in their 60s. At that point, simply because they are older, women are more apt to have other health problems, such as diabetes, high blood pressure, stroke, or frailty, that make it more difficult to diagnose and treat their heart attacks.

Heart Attacks Are Deadlier for Women While we have made progress in treating women with heart attacks over the past decades, the improvement for women isn’t as good as the improvement for men. Women who have acute myocardial infarctions have a much worse outlook than men. Their mortality rate is about twice as high. Overall, about 9 percent of the women being treated for a heart attack in a hospital die there, compared to only about 4 percent of men. For women with diabetes, the risk of death from a heart attack is nearly three times higher than it is for men with diabetes. We still don’t really understand why this is. We know that women take longer to call 911. On average, a woman with chest pain will wait an hour before calling for help, while a man waits only about 44 minutes. Time is muscle in heart attacks, and those 15 minutes or so can make a difference in survival. Also, we seem to take a little longer to get a woman with MI symptoms into the cath lab, about 45 minutes instead of 40 for men. Again, those few minutes may not seem very long, but time is muscle. It all adds up. The average woman with a heart

attack is more likely to have complications such as atrial fibrillation than a man and ends up spending a day more in the hospital than a man, probably because women having a first heart attack tend to be older and have more health problems. Finally, after a woman who’s had a heart attack is sent home from the hospital, she’s less likely than a man to get all the standard recommended treatments. We don’t fully know why heart attacks are more deadly for women than men. Women tend to be older and to delay treatment, which make the heart attack more dangerous, but delays within the medical system play a role as well. We all need to be more aware that women have heart attacks!

Heart Attack Symptoms in Women Making the diagnosis of ischemia (lack of blood flow) from a blocked coronary artery can be much more difficult in women than in men. First, and most important, women and men may experience heart attack symptoms quite differently. Men more typically experience crushing substernal chest pain that radiates down the left arm—the sort of pain that can only be from a heart attack. Many women don’t have that sort of pain. Instead, they describe a heaviness or discomfort in the shoulders, jaw, neck, back, throat, or teeth—and not in the chest. Women may experience intermittent pain or even no pain at all up to 25 percent of the time. Nausea, vomiting, and shortness of breath can be sometimes be the main symptoms. Often, feeling very fatigued is the primary symptom. In addition, unlike men, about half of all women who have heart attacks don’t have any symptoms of angina or chest pain before The Big One hits. Because many women don’t have angina and don’t realize that they are at risk of a heart attack for other reasons, they tend to brush off their symptoms. Many times, I’ve treated a female patient who finally came to the emergency room after spending hours at home thinking she had a stomach flu or even just indigestion. It was only when the pain got worse or she actually fainted that 911 was called. Women need to be aware that The Big One could be happening to them. Specifically, women should be aware that if any of the following symptoms last

for more than five minutes, it’s time to call 911: Uncomfortable pressure, fullness, squeezing, or pain in the center of the chest that lasts for more than a few minutes. The sensation may go away and then come back. Pain or discomfort in one or both arms, one or both shoulders, the back, neck, jaw, or stomach. Shortness of breath. Breaking out in a cold sweat. Nausea or vomiting. Lightheadedness or faintness. Women who have heart attacks tend to be older (69 versus 61 for men) and sicker than men who have heart attacks. They also tend to have atypical symptoms. Historically, that has meant that women tend to be treated less aggressively for heart disease. Today, we cardiologists are a bit more enlightened. We are far less likely to tell an older woman with atypical heart attack symptoms that it’s all in her head. However, for the most part, women still undergo less cardiac catheterization, less angioplasty, and less by surgery. If treatment with angioplasty or by surgery is required, women are at higher risk of complications and even of death.

Heart Attacks in Women Are Different Atherosclerosis in women is different from atherosclerosis in men. Women have smaller coronary arteries, so even a small blockage can be enough to affect a woman more severely than a similar blockage in a man. A the same time, when we do an angiogram on a woman with heart symptoms, we often find the arteries aren’t severely blocked. Instead, the blood flow is being restricted by endothelial dysfunction. The endothelium—the inner walls of the main coronary arteries and the smaller arteries that branch off from them—isn’t functioning properly, usually as a result of high blood pressure and/or diabetes. It isn’t letting oxygen and nutrients out from the blood to nourish the heart muscle. That causes

what’s called silent ischemia, meaning lack of blood flow without symptoms. When women have plaque in their arteries, it’s more likely to push outward, into the artery, rather than to protrude inward into the lumen of the artery, where it can interrupt the flow of blood. Outward remodeling, as this is called, is hard to see on an angiogram. So even when a woman does have chest pain, we often can’t see the reason for it. Plaque in the arteries of a woman also often behaves differently than plaque in a man. In men, the plaque tends to rupture suddenly, causing a blood clot, a heart attack, and an ambulance ride to the emergency room. In women, the plaque tends to wear away, not rupture, and cause a blood clot less dramatically. Plaque erosion is twice as likely to be the cause of a heart attack in women as it is in men.

Evaluating Heart Attacks in Women Detecting and evaluating heart disease in women is harder than in men. Aside from the higher rate of atypical symptoms, the standard tests for blocked arteries aren’t as accurate for women. Standard exercise stress testing, where we monitor the heart while the patient walks on a treill, has a fairly high false-negative and false-positive rate in women. This is especially true if they are older or have a lower capacity for exercise. We get more accurate results from doing a stress echocardiogram. If the patient can exercise on a treill, we use that to cause the stress. If not, we inject the patient with a small amount of a drug to stimulate the heart. An alternative is a nuclear stress tests, where the patient is injected with thallium while exercising on a treill. An X-ray picture of the heart then shows us areas that aren’t getting enough blood. These tests are about 90 percent accurate in women.

Treating Heart Attacks in Women Women are generally of smaller stature than men, with smaller coronary arteries. These small arteries make angioplasty more risky. There’s a greater chance that an opened artery will clog up again, and there’s also a greater chance of tearing an artery when inserting the catheter. That doesn’t mean women having heart

attacks shouldn’t get percutaneous coronary intervention (PCI) to clear the blockage. Studies show that women benefit as much as men do from angioplasty. Women do tend to have more complications from angioplasty than men, particularly if they have diabetes. Bleeding complications, however, are far less common today for both men and women, because we now try to use a vein in the wrist to insert the catheter whenever possible. Overall, women are at no greater risk for death than men are after undergoing an angioplasty, even though women having angioplasty usually are older and have more risk factors. When it comes to by surgery, women’s smaller blood vessels make the surgery technically more difficult, which usually means it takes longer to perform. The smaller vessels are also more likely to clog up over time. And, as with angioplasty, women having by surgery are usually older and have more additional health problems than men do.

Preventing Heart Disease in Women For the most part, the same steps to help prevent heart disease in men also help prevent it in women. Women are sometimes so concerned with the health of other family that they neglect their own. If you have any risk factors for heart disease, get yourself checked! Because estrogen is protective against heart disease, at one time supplemental estrogen was touted as a magic pill that would keep a woman’s heart (and the rest of her) young. We now know that this is very much not the case. While hormone replacement therapy (HRT) with estrogen can be helpful for women who have severe menopause symptoms, such as relentless hot flashes, it doesn’t reduce the risk of a heart attack. In fact, HRT can actually increase the risk of a blood clot that may cause a heart attack or stroke. The risk increases the longer you take the hormones. Women who want to use HRT for menopause symptoms should do so at the lowest possible dose and for the shortest possible time.

Cardiac Syndrome X (CSX) Cardiac syndrome X (CSX) is an unusual and atypical form of ischemic heart disease that is probably commonly undiagnosed. People with CSX are almost all

older women who have ed menopause. The main symptom of CSX is severe chest pain on exertion. The pain feels exactly the same as angina. And when we have the patient do an exercise stress test, it looks like angina on the EKG. Other types of tests also show reversible ischemia, just like angina. Despite this, when these people undergo cardiac catheterization or CT (computed tomography) coronary angiograms, they usually have normal coronary arteries that look nice and smooth. They also have no inducible coronary artery spasm. In the past, after looking at the angiograms and seeing nothing abnormal, cardiologists would often tell their female patients that their symptoms were noncardiac. They would suggest that stress or anxiety, not a heart problem, was causing the symptoms—a really bad example of the gender gap in heart care. It is now clear that many of these women have disease in the small arteries within the muscle of the heart. Their chest pain is caused by true ischemia, just as angina is. Women who are found to have clinical evidence of CSX are at high risk of being itted to the hospital for unstable angina over the next few years. They also have an increased risk of heart attack and death. The pain and inability to exercise as a result of CSX can be debilitating and can lead to poor quality of life. Unfortunately, at this point, it is still unclear how to treat these patients. While some women benefit from nitroglycerin to stop the chest pain, others do not. Likewise, some benefit from calcium channel blockers that lower blood pressure, while others do not. Does risk factor modification make a difference? How about cholesterol medications or blood thinners? What effects do diet and exercise have? Studies are currently underway to evaluate all of these issues and get the answers. In the meantime, it’s important to increase awareness of CSX and take it seriously as a medical condition and not just as anxiety.

The Broken Heart Syndrome I have a cousin who lives in Tarzana, California, a suburb of Los Angeles in the San Fernando Valley. She has no family history of premature ischemic heart disease. Both of her parents lived into their 90s. She does not need medication for high blood pressure, diabetes, or high cholesterol. She has never been a smoker. She eats a healthful diet and has had a regular exercise program for years. One night, their dog got into some kind of trouble in the kitchen and was put out for the night. The dog, unhappy about being outside, barked and scratched at the kitchen door for almost half an hour before he finally gave up. My cousin felt bad about leaving him out, but wanted to teach him a lesson. The following morning, to my cousin’s horror, she found her long-time pet floating dead in her swimming pool. She was, of course, totally freaked out and became hysterical as she attempted to pull the dog out of the pool. The dog was quite large, however, and my cousin is only about 5 feet 2 inches tall. All of a sudden, she developed severe substernal chest pressure, which radiated to her throat and left arm. She broke out in a sweat and became dizzy. After a few minutes, she felt a little better, but the chest pressure persisted. She had never experienced anything like this before and had no idea what to do. She then made a bad decision and drove to the office of her internist. (She should have immediately called 911!). Luckily, it was only a five-minute drive. The doctor, realizing that something was seriously wrong, did an immediate EKG. To his shock, it showed that my cousin was having a full-blown heart attack. The doctor immediately called 911, and my cousin was transferred to the local hospital. Luckily, this hospital was able to perform emergency angiograms and angioplasty. She was promptly seen by a cardiologist, who determined that she should immediately be taken to the cath lab. To the surprise of everyone involved, the angiogram showed that the coronary arteries were wide open and showed no evidence of any blockages whatsoever. They were equally surprised to find that when dye was injected into her left ventricle, it showed that the front wall was not moving at all. On the contrary, it was moving in the opposite direction, a condition called dyskinesis. In other

words, she had had a major heart attack with normal blood vessels. Because her arteries were open, no angioplasty needed to be done. She was transferred to the coronary care unit, where she could be closely monitored for irregular heart rhythms and congestive heart failure. The chest pressure didn’t completely go away until the next morning. A blood test showed significant elevation of troponin, an enzyme that indicates moderate to severe heart muscle damage. An EKG the next morning showed that the heart attack was over. She was surprised that she didn’t feel that bad. She was able to sit up in a chair that morning and was then transferred to a unit where she could be monitored while she walked around that afternoon and evening. The next day, she felt even better and was anxious to go home. Her cardiologist decided to get an echocardiogram prior to her discharge. He was astonished to find that the heart muscle had completely recovered and all the walls were now moving normally. It turned out that the heart muscle was not infarcted or dead, but was only stunned. This is a phenomenon usually seen in patients receiving early reperfusion with thrombolytic therapy or angioplasty. Today, my cousin is doing quite well with no residual effects from this frightening experience. What happened to her? The concept of being “scared to death” has been known for hundreds of years. It turns out that strong emotions—fear or grief, for example—can indeed impact the heart, though not usually to the point of death. Starting around 1997, doctors began to become aware of a syndrome consisting of all of the symptoms of full-blown heart attack, but with normal coronary arteries showing no blockages. It was first documented in Japan, where it came to be called takotsubo syndrome, named after a bulbous pot used by Japanese fishermen to catch octopus. The shape is similar to the appearance of the ballooning of the tip of the heart seen after one of these attacks. Takotsubo syndrome is also now known as broken heart syndrome. More technically, it’s called stress cardiomyopathy, stress-induced cardiomyopathy, or apical ballooning. It can happen as a result of an excess release of the stress hormone adrenaline, which is usually caused by some kind of severe physical or emotional stress. Almost all patients with broken heart syndrome are older women with no history of heart disease.

The good news is that the injury to the heart is usually reversible and is associated with a good outcome. The recovery of heart function is usually complete within two to three weeks.

8. How to Save Your Own Life

If you’re having a heart attack, swift action can save your life. Delay can kill you. Patient delay is an enormous obstacle to providing state-of-the-art care for heart attacks. When someone has a heart attack, he or she waits, on average, about 140 minutes before calling 911 or self-transporting to the nearest hospital. Public health agencies have made multiple attempts to try to change this. Pamphlets, seminars, websites, and radio and television spots—all explaining the signs and symptoms of hearts attacks and what to do if you are having one—have never been shown to make a difference in getting people to get to the hospital early. The big problem is denial. People don’t want to it that they could possibly be having a heart attack. They think heart attacks happen to other people, but not them. As Tommy Lasorda, outspoken former manager of the Dodgers, said after his myocardial infarction, “I don’t get heart attacks, I give them.” People also have tremendous anxiety about having to deal with the medical system. The bureaucracy at hospitals can be extremely burdensome. The thought of having to fill out lengthy forms and the possibility of having a prolonged wait in a crowded waiting room causes many people to hesitate before coming to the hospital. People are also afraid of the embarrassment and cost of a false alarm.

Recognize the Symptoms of a Heart Attack As explained in the previous chapter, knowing your risk factors and knowing that you might well be at risk for a heart attack is the first step in saving your life. Step 2 is knowing how to recognize the symptoms of a heart attack. Thousands of people die every year because they didn’t recognize the symptoms of cardiac arrest. People will self-treat chest discomfort for hours with antacids, thinking they are suffering from the aftereffects of the previous night’s pizza.

In reality, at times it can be extremely difficult to tell if you are having The Big One. Back in 1912, James Herrick, a cardiologist in Chicago, published an important paper based on fifty years of observing and treating heart attack patients. He divided the patients into four different groups, depending on their symptoms. He described patients in group 1 as “cases in which death is sudden, seemingly instantaneous and perhaps painless.” Those in group 2 were “cases in which the attack is anginal, the pain severe, the shock profound and death follows in a few minutes or several minutes at most.” The people in groups 1 and 2 probably represent the 30 percent of people who even today do not live long enough to get to the hospital. Group 3 comprised “non-fatal cases with mild symptoms. Slight anginal attacks without the ordinary causes (walking), perhaps some of the stitch pains in the precordia, may well be due to obstruction of small coronary twigs.” These patients were probably having what today we call a mini-heart attack. Those in group 4 were described as “the usual type.” Herrick wrote: “These were cases in which the symptoms are severe, are distinctive enough to enable them to be recognized as cardiac, and in which the accident is usually fatal, but not immediately, and perhaps not necessarily so… . The pain is described as crushing, tearing, or squeezing in nature, and is often of such great intensity that the patient prays for death to end his anguish.” In other words, a major heart attack is far from being subtle. Even if you don’t have every classic symptom, you will definitely know something is seriously wrong. Today, patients who come to the emergency room with a full-blown heart attack will describe their pain fairly typically. Most complain of a feeling of pressure or constriction as intense as “an elephant sitting on my chest!” These feelings often radiate into the throat and into the left arm. The patients are frequently drenched in sweat. Many times they are nauseated; sometimes they have been vomiting. They look pale, no matter what their skin color. They may be lightheaded from low blood pressure or dizzy as a result of an irregular heartbeat. People with mini-heart attacks and unstable angina, on the other hand, may have symptoms that are fairly atypical and at times nonspecific. The pain may come and go. It may be in the jaw or in the back. It may feel more like shortness of breath. People may feel intermittent palpitations, lightheadedness, or nausea. When these people are seen in the emergency room or in the physician’s office, they may look quite well. They may have good color and normal vital signs. All diagnostic tests may be negative.

This is why the diagnosis of a mini-heart attack or angina can be too commonly missed. Recognizing if you are at risk for a heart attack can be the difference between life and death. A dramatic example of this involves the 1972–73 New York Knicks. This team broke my heart that season by defeating my beloved Los Angeles Lakers to win the NBA championship in five games. Two of this historic team later had the same heart problem with quite different outcomes. Phil Jackson, the coach of nine NBA title-winning teams (including three with the Lakers), was a top reserve on that Knicks team. Another member of that team was Dave DeBusschere, who, in 1996, was named as one of the fifty greatest players in NBA history. He was a prototype power forward who was not only a defensive stopper but also could light it up scoring if the team needed him to do so. What most people don’t know is that DeBusschere was also a Major League baseball pitcher. He pitched for the Chicago White Sox for two seasons in the early 1960s. In 2003, Dave DeBusschere had a heart attack on a street in Lower Manhattan and died at New York University Downtown Hospital. He was 62. In late April to early May of 2003, coach Phil Jackson began experiencing tightness and pain in his chest. He sought prompt medical evaluation at a facility with expertise in diagnosing and treating these symptoms. He was found to have a 90 percent blockage of his left anterior descending artery. On May 10, 2003, he underwent an angioplasty, and, as a result, he avoided a massive heart attack. Dave DeBusschere died on May 14, 2003, only four days after Phil Jackson’s angioplasty. It is very possible they had the same blocked artery. One obtained the proper treatment, and the other did not. Tommy Lasorda is a Los Angeles Dodgers icon. He has spent more than thirtyfive years with the organization, coaching them from 1976 to 1996, and winning the World Series in 1981 and 1988. In June of 1996, he began to experience symptoms he attributed to a stomach problem—Tommy is well-known for his love of great food. While undergoing an endoscopy—a procedure where a tube with a tiny camera at its tip is inserted into the stomach looking for ulcers—he began to have crushing chest pain. An EKG was promptly performed and showed that the blood vessel to the bottom of his heart had clotted, causing the

beginning of a major heart attack. Luckily, he was in an institution that had the ability to quickly treat this problem. He underwent an emergency angioplasty, restoring blood flow to the bottom of his heart. The damage done was minimal. More than a decade later, he is still working with the club and going as strong as ever. Bill Clinton was the forty-second President of the United States (1993–2001). Aside from being President, Mr. Clinton is known for his love of jogging. The only problem with this was that he was also known for making pit stops at McDonald’s during these runs to satisfy his cravings for Big Macs. On September 3, 2004, he was itted to a New York City hospital with chest pain and shortness of breath. An angiogram showed considerable blockages of all the arteries supplying his heart. Luckily, he didn’t have a heart attack. On September 6, he underwent quadruple by surgery with good results. Today, he is doing well and is as active as ever. TV host Rosie O’Donnell had a heart attack in 2012 at the relatively young age of 50. Despite all the health-related shows she has hosted, at first she didn’t realize she was having The Big One, even though she was having the classic symptoms: arm and chest pain, paleness, and generally not feeling well. It took her until the next day to go to the hospital and be diagnosed with a heart attack caused by a coronary artery that was 99 percent blocked. She was given a stent and made a quick recovery. She’s fortunate that she survived a close brush with death. From the first day of medical school, doctors are taught that a patient’s clinical history is one of the best tools known for diagnosing diseases. Identifying a person at risk of having a heart attack should take just a few minutes. Simple questions about risk factors and the details of symptoms allow this to happen without delay. Thus, if you are a 54-year-old, pot-bellied, cigarette-smoking guy with discomfort in your chest, and you had the Grand Slam breakfast that morning, the Pastrami Burger for lunch, and KFC for dinner, and if your father died suddenly from a massive heart attack at age 55, and if you have chest pain, you are probably dealing with a significantly clogged artery to your heart. This is especially true if you are experiencing other types of symptoms as well. The new onset of feelings such as shortness of breath, dizziness, or palpitations requires an urgent and thorough evaluation.

Know Who to Call The next step in saving your own life is knowing whom to call in a medical emergency. If, indeed, you do suddenly experience the symptoms of a heart attack, you must know exactly what to do and whom to call. You must be ready to react. Crucially, you must not deny that you are actually having The Big One. You must accept that you are at risk and that it is actually happening. You must not wait for the symptoms to or treat them with an antacid. You must not think that you can drive yourself to the hospital or have your spouse or next-door neighbor take you there. You do not want to wait while your son or daughter drives across town to get you to where you need to go. This wastes valuable time. The more precious minutes you lose, the higher the risk that you will not survive. A third of people with heart attacks die before they can reach a hospital. Call 911 immediately. The reason you call for EMS right away is to minimize your time to first medical . The shorter this time is, the more likely you are to survive. The paramedics can stabilize you. They can monitor your heartbeat and immediately treat you if you develop a life-threatening arrhythmia. You need to know what emergency medical services are available in your area. While this may vary from place to place—even from town to town—it is fairly easy to get the information for your home and workplace locations. Some EMS services are through local fire departments. The city or county can provide others. Some are provided by various medical centers or are run privately. You must research what is available in your area before you have your heart attack! Find out the standard operating procedures for 911 medical calls in your area. In some places, if you call 911, the paramedics will take you directly to the closest hospital with state-of the-art care. In other places, they have to take you to the nearest hospital—which might not be the best hospital for treating a heart attack If the paramedics say they are taking you to a hospital without optimal services, you must demand that you be taken to a heart attack center, even if it is somewhat farther away. Before you can do this, however, you need to know

what hospital in your area provides these services so you can tell the paramedics where you need to go. Do not assume that they know. You also need to know if the paramedics in your area are adequately trained to recognize the signs and symptoms of a heart attack. Are they able to perform an EKG at your house or workplace and make an immediate diagnosis of a heart attack? Are they equipped to alert the emergency department of the center of excellence that a heart attack is in progress so that the cath lab and the interventional cardiologist are activated? Doing this kind of advance research isn’t that hard. Call all the nearby hospitals (ask for the community relations manager) or check their websites. Ask if they have catheterization labs and interventional cardiologists standing by. Ask how many cath procedures are done at the hospital each year. To find out about your local EMS services, start by checking with your local fire department. If they can’t answer your questions, they will probably be able to put you in touch with the people who can. Also, check online. When I googled EMS for my area, I quickly was able to find what services were available to me. When you have to call 911, you want to know ahead of time who is coming to help you, how long it will take them to get to your house, and where they will take you. This will save your life!

Know Where to Go The final step in saving your own life is knowing which hospital is best for you and making sure you are taken there directly. The hospital you are taken to by EMS has a tremendous influence on your survival. You must thoroughly investigate what is available to you in your particular area. You must find out where the closest center of excellence is to where you live and work. You need to examine what kind of resources the institution has. Are they modern and state-of-the-art? How well organized are they?

What are their response times? What relationship do they have with the local EMS? Are EKGs done at the scene? Are they able to perform emergency angioplasty in a short amount of time, ideally in less than ninety minutes? Do they only give clot-busting medication? If they do, what options do you have if this treatment fails, as it can up to 50 percent of the time? Can they then transport you to a center with angioplasty capabilities in a timely fashion? How many cardiac emergencies do they handle every year? How well do they take care of those patients? Which heart doctors take care of the most patients and how successful are they? Is emergency heart surgery available if you must have it? If you must have a heart transplant, can the hospital keep you stable until a heart becomes available? The answers to these questions are not always simple to obtain. There is no one, clear-cut place to go to find this information. Instead, you have to track this information down through a variety of sources that depend a lot on where you live. Different areas approach tracking heart attacks in different manners. Again, your local medical center is always a good place to start. Call the hospital’s main number and ask to speak to someone about the facility’s heart attack program; also check the hospital’s website, which often has a lot of good information. Ask the hospital’s representative about their relationship with the EMS in your area. Ask what they can do for you if you are having a heart attack. A valuable resource for getting information about your local hospitals is Hospital Compare, a website offered by the United States Department of Health and Human Services. You can access information about hospitals by name, proximity, or geography. It will show you how hospitals in your area compare in their treatment of heart attacks and their outcomes. Other sites, such as the American Heart Association (AHA), can provide useful

information. The AHA has a program called Mission: Lifeline, which is a community-based initiative aimed at quickly activating the appropriate chain of events critical to restoring blood flow for someone having a heart attack. Don’t forget that simply asking family , friends, and neighbors who have had heart attacks can provide a lot of information about local hospitals and doctors. The more time you spend learning about your options, the better chance you will have if and when you experience your own heart attack. You may save your life by being prepared. If an appropriate hospital isn’t available in your area, you have a serious problem. You or a loved one could die unnecessarily from a heart attack. What can you do in that case? Start a grassroots effort in your community to fix the problem. Simple steps, such as better training for local paramedics, equipping ambulances with EKG machines, and increasing awareness of the problem, can be very effective. When a community has a system where access to state-of-the-art care is widespread and available to everyone, lives are saved. If a million people die each year of a heart attack and we improve the treatment system by only 10 percent, that equals 100,000 lives saved. The life you save may even be your own!

The Latest Guidelines for Treating Heart Attacks Every ten years or so, the American College of Cardiology and the American Heart Association issue updated t guidelines for the management of STEMIs. In 2012, the latest guidelines had a change that means a lot: Communities are encouarged to create regional systems for STEMI care. The new guidelines also recommend extending to 120 minutes (from 90) the time frame for getting a STEMI patient from a hospital without a cath lab to one that does. What that means is that a small hospital without a cath lab has a bit more time to send a patient on to a regional STEMI care center, rather than giving him or her a clot-busting drug. Even though time is muscle, catheterization is safer and more effective for a blocked artery. Giving small hospitals a broader timeframe will in the end lead to more transfers to regional

STEMI centers and better outcomes. The full guidelines go on for pages and are mostly of interest to physicians who treat heart patients. If you’re at risk of heart attack or have already had one, the points below from the new guidelines might help you understand where your doctor is coming from in the treatment he or she prescribes for you. Defining STEMI. STEMI is a clinical syndrome defined by characteristic symptoms of myocardial ischemia in association with persistent electrocardiographic (ECG) ST elevation and subsequent release of biomarkers of myocardial necrosis. Creating regional STEMI systems. All communities should create and maintain a regional system of STEMI care that includes assessment and continuous quality improvement of emergency medical service (EMS) and hospital-based activities. Performance can be facilitated by participating in programs such as Mission: Lifeline and the D2B (door-to-balloon) Alliance. PCI is best. Primary percutaneous coronary intervention (PCI) is the recommended method of reperfusion when it can be performed in a timely fashion by experienced operators with an ideal first medical (FMC)-todevice time system goal of 90 minutes or less. Antiplatelet drugs should be given. A loading dose of a P2Y12 receptor inhibitor should be given as early as possible or at the time of primary PCI to patients with STEMI. Options include: clopidogrel (Plavix) 600 mg; or prasugrel (Effient) 60 mg; or ticagrelor (Brilinta) 180 mg. Antiplatelet drugs should be continued for at least a year after getting a stent. P2Y12 inhibitor therapy should be given for at least 12 months to patients with STEMI who receive a stent (bare-metal stent or drug-eluting stent) during primary PCI. Drugs to lower blood pressure should be given. Oral beta-blockers should be initiated in the first 24 hours in patients with STEMI who do not have any other contraindications. Statin therapy helps. High-intensity statin therapy should be initiated or continued in all patients with STEMI and no contraindications to its use.

Check for heart failure. Left ventricular ejection fraction should be measured in all patients with STEMI. Do cardiac rehab. Exercise-based cardiac rehabilitation/secondary prevention programs are recommended for patients with STEMI.

9. Other Causes of Chest Pain that Can Kill You

A heart attack isn’t the only cause of chest pain that can kill you. It’s still the most likely, but other very serious health problems can mimic the pain of a heart attack and be just as deadly.

Pulmonary Embolus For a variety of different reasons, blood flow returning from the body to the heart through the veins can be dangerously slowed down. This problem, called venous stasis, most commonly occurs in the lower extremities or the pelvic area. When the blood flow is slowed, blood clots can form within the veins. This is known as deep venous thrombosis (DVT) or phlebitis. It is called deep because it involves the veins deep within the lower extremities. (Superficial phlebitis occurs in veins just under the skin. This is far more common, but it is rarely dangerous. Varicose veins are twisted, swollen veins in the leg. They are unsightly and sometimes painful, but they’re rarely a problem.) The clots in DVT block the flow of blood back to the heart and can cause symptoms such as pain, warmth, and swelling. However, many times, the clots don’t cause symptoms in the legs. The real risk from the blood clots of DVT is that pieces of them have a nasty tendency to break off and then travel to different locations in the body. Embolization, as this is called, can be very dangerous. The most dangerous place for these clots to go is into the lungs—a problem known as pulmonary embolization. The clots can cut off blood flow to areas of the lungs, keeping the blood from obtaining sufficient levels of oxygen. And this can result in serious illness and many times even sudden death. This whole process—deep venous thrombosis and/or pulmonary embolus—is known as venous thromboembolism (VTE). This syndrome is extremely common, but, as discussed below, often goes undiagnosed because the clinical

diagnosis is difficult to make. About three hundred thousand people are diagnosed with VTE every year in the United States. The problem is that the number of people who actually have this problem may be far more, possibly greater than six hundred thousand. A pulmonary embolus causes between fifty thousand and a hundred thousand deaths every year in the United States.

Diagnosing VTE The clinical diagnosis of VTE is extremely hard to make, which is why it is so often missed. The symptoms are variable and include sudden shortness of breath, chest pain on deep breathing (pleuritic chest pain), cough, palpitations, rapid heart rate, anxiety, lightheadedness, and even loss of consciousness (syncope). VTE is a medical emergency. If you have any of the symptoms or any combination of them, seek medical attention right away! Unfortunately, the symptoms are very often nonspecific and can be due to many other kinds of problems. This means that many people don’t call for help in time. What’s even more concerning is that the signs and symptoms of VTE may be completely absent in 50 percent of patients. The index of suspicion must be extremely high in order to make this diagnosis. A useful test to rule out the presence of VTE is the D-dimer blood test. This test measures the presence of a breakdown product of a blood clot. If the result is normal, then the likelihood of a pulmonary embolism is low. The bad news is that when this test is positive, it can be due to a variety of different causes, only one of them being pulmonary embolus. In this situation, other diagnostic tests are needed. The quickest and most accurate way to make the diagnosis of pulmonary embolus is to perform a CT pulmonary angiogram. In this diagnostic exam, the patient is scanned using computed tomography, which rapidly takes a series of X-ray images in slices around a single axis of rotation. The many twodimensional images are then analyzed by a computer that reconstructs the images so that internal organs can be viewed with extreme clarity. Newer CT systems can even generate three-dimensional images. A CT scan takes only a

few minutes to perform, is painless, and is accurate more than 90 percent of the time. Not everyone, however, is a candidate for this examination. Because of the need for an iodine-containing contrast dye, it cannot be used in patients with kidney problems or in people with known allergies to iodine-containing agents. If someone is not a candidate for a CT pulmonary angiogram, then the next option usually is a ventilation-perfusion scan (V/Q scan). This test uses nuclear imaging similar to that used for a nuclear stress test. Isotopes are injected into a vein, and the blood flow to the lungs is imaged using a special camera and computers. A different isotope is then inhaled deeply into the lungs. Using the same camera, images are taken, showing the degree of lung ventilation. A lung area that is ventilated (meaning air is getting to it) but not perfused (meaning blood isn’t getting to it) suggests a pulmonary embolus. The lack of perfusion is probably caused by a clot blocking a vein in the area. Scans are graded as low, intermediate, or high probability for pulmonary embolus. The accuracy of the test is only about 60 percent, however, and falsenegative tests are fairly common. Still considered the gold standard, but rarely used nowadays, is pulmonary angiography. During this procedure, a catheter is advanced to the pulmonary artery, usually from the groin, and dye is injected directly into the main pulmonary artery. If present, pulmonary emboli are clearly seen. The disadvantage of this test is that it is invasive and has inherent risks, such as bleeding and dye reactions. With the increasing availability of CT scanners, the need for this procedure has been practically eliminated.

Treating VTE Treatment of venous thromboembolism centers on thinning the blood with drugs to prevent further clotting and to give the body a chance to absorb the existing clot. Thrombin is a protein in the blood, which, when present in its active form,

causes blood to clot. It does this by interacting with another protein, fibrinogen, converting it to fibrin, its active form. Fibrin is a protein fiber, which then forms a mesh that traps red blood cells. The end result is a blood clot or thrombus. Heparin is a large, glucose-containing compound that is extracted from the liver, intestines, and lungs of slaughtered animals. It has been used as a blood thinner since 1916 and works by indirectly inhibiting the action of thrombin and blocking the cascade of reactions that forms a clot. Heparin, or one of its derivatives, is usually given to the patient as soon as the diagnosis of pulmonary embolus is made. It is given intravenously or may be injected under the skin. The person’s blood is usually adequately thinned within a few hours. Most doctors believe that to completely treat pulmonary embolism and deep venous thrombosis, the blood must be adequately thinned for about six months. Heparin can only be given as an injection, however, so it is not practical for long-term treatment. Instead, we use a blood-thinning drug called warfarin (the brand name is Coumadin), which can be taken orally. It thins the blood by blocking the action of vitamin K, a crucial component of the body’s bloodclotting system. Interestingly enough, it is in the same drug class as brodifacoum, an agent used to poison rats and mice. If istered properly, warfarin is extremely effective in treating VTE. It is also, however, a very difficult drug to take. The proper dose of the medication varies greatly in different individuals. It is virtually impossible to predict what the right dose for someone will be. As a result, frequent blood testing is required to monitor how thin the blood is and then adjust the dosage of warfarin. The blood test is called prothrombin time—it measures how long it takes your blood to clot. The results are reported as your INR, or international normalized ratio. If your INR is too high, you are at risk for bleeding complications, but if it’s too low, you are at risk for clotting. The therapeutic range for warfarin is an INR between 2 to 3. Warfarin is not effective until after about five days of treatment. Heparin or its derivatives need to be given during this time. The frequent blood testing for people on warfarin is inconvenient, but so far,

there is no other effective alternative oral treatment for VTE. People taking warfarin should also avoid alcohol and need to keep an eye on their consumption of green leafy vegetables, which are high in vitamin K. They also need to take the drug at the same time every day. As tedious as the frequent blood tests and other restrictions are, people with VTE must comply with the regimen or they are deep trouble. Bleeding problems from warfarin for about one-third of all emergency room visits and emergency hospitalizations among older adults. Two new drugs, Pradaxa (dabigatran) and Xarelto (rivaroxaban), are now available as possibly safer alternatives to warfarin. These drugs are approved only for treating people with atrial fibrillation (irregular heartbeat) that is not caused by a problem with a heart valve. Xarelto is also approved for preventing blood clots after hip or knee replacement surgery. These drugs are not approved for treating VTE.

Clot Busters for Pulmonary Embolism Pulmonary embolism, at times, can be extremely sudden and severe and cause a person to become unstable, even to the point of shock. These individuals may not have enough time to be treated with heparin. Their blood clots may need to be actively dissolved. The same clot-busting medications used in treating heart attacks—streptokinase or TPA (tissue plasminogen activator)—are often used in treating massive pulmonary emboli. The use of thrombolytic therapy can be life-saving in these critical situations. The best treatment for VTE, however, is to prevent it from happening. This involves being proactive and assessing potential high-risk situations. Your risk of VTE is raised if: You sit still for a long time, for example on a long car trip or plane ride. You’ve already had a heart attack. You’re elderly.

You’re obese. You’re pregnant. You’re taking birth control pills. You’ve recently had surgery or been injured. You’ve had a hip fracture. You’ve already had a stroke. You have cancer. You have congestive heart failure or cor pulmonale (weakened heart due to lung disease). You’re immobilized or paralyzed. Combine any of these factors and your risk increases even more. You can take some practical steps to prevent a blood clot. For example, if you’re taking a long trip, either by plane, train, car, or bus, it is very important to get up and move around for a few minutes every one to two hours in order to keep your blood circulating adequately. Dehydration is also common on long trips. This can thicken the blood and make it more likely to clot. Drinking plenty of fluids while traveling is helpful in preventing this problem. If prolonged bed rest is required, such as after a surgery, an accident, or even a heart attack, the risk of forming blood clots is increased. Thinning the blood during these times with drugs helps reduce the risk of clots. Alternative methods of birth control, other than oral contraceptives, should be considered if appropriate. If oral contraceptives are the first choice, never smoke while taking them. This dramatically increases the risk of blood clots and at times can lead to death. Sometimes weird things can happen.

A patient of mine is a 38-year-old salesman who frequently travels on business between Los Angeles and New York City. On one flight, he developed pain in his right calf. It bothered him throughout the day and was somewhat worse the following morning. He attended morning meetings and headed off to JKF to catch an afternoon flight to Burbank. About four and a half hours into the flight, he developed the sudden onset of tingling and numbness into his left arm. He found himself slurring his speech and became dizzy and lightheaded. He immediately notified the attendant, who in turn made the captain aware. The captain was advised to continue into Burbank and was told that medical personnel would waiting. The patient’s symptoms began slowly improving as the flight continued, and he maintained stable vital signs. On arrival, about forty-five minutes later, paramedics quickly took him to an ambulance and transported him directly to the nearest hospital. An initial CT scan of his brain showed no evidence of a stroke. An ultrasound of his right leg showed significant deep venous thrombosis. He was then started on heparin and was itted into the hospital for close observation. In the hospital, his symptoms continued to improve throughout the day. The following morning, a repeat CT scan now showed evidence of a small stroke. An echocardiogram was then performed and showed the patient to have an abnormal opening in the wall that separates the right atrium and left atrium of the heart, a congenital condition called patent foramen ovale. Actually, this condition isn’t that uncommon and doesn’t usually cause any trouble or require treatment. In severe cases, the problem can easily be treated with a closure device that can be inserted through the groin under X-ray guidance. Usually, blood clots forming in veins travel through the venous system and into the right side of the heart. From there, they get pumped to the lungs, which is where they usually get caught in a vein, without ever ing back to the heart and into the arterial circulation. However, if a person has a patent foramen ovale, under the right circumstances, the clot can travel from the right side of the heart to the left side of the heart and from there directly into the brain, causing a stroke. This is exactly what happened to my patient. Luckily, the degree of damage was minimal, and he has made pretty much a full recovery. Some people are not nearly as lucky. They may suffer severe disability and even death.

Aortic Dissection In the fall of 1988, a 48-year-old man came to my hospital with a one-week history of intermittent chest pain. He reported that it felt like a sharp sensation that would shoot directly into his back. It wasn’t really related to exertion and was frequently occurring at rest. He had no history of heart disease. He did have a history of high blood pressure but didn’t take his medication regularly. He also had a long history of cigarette smoking. He was not known to have diabetes, but his cholesterol was high and he had a family history of heart disease. One day his pain became quite severe, to the point where it scared him. He drove himself to the emergency room. In the ER, his pain improved. An EKG showed no specific findings, and his chest X-ray showed a slightly enlarged heart and some fullness of the aorta. Because he was at extremely high risk of having significant coronary artery disease, he was itted to the CCU for close observation. After just an hour in the unit, he suddenly developed the worst chest pain he had ever experienced. A repeat EKG was quickly performed and now showed evidence of acute STEMI involving the bottom part of the heart. It appeared that the right coronary artery had totally occluded. The doctor who had itted the patient ordered clot-busting medication. In 1988, thrombolytic therapy was the standard of care for treating heart attacks. I was fresh out of my cardiology fellowship and just happened to be seeing another patient in the unit. I overheard the internist discussing thrombolytic therapy with the nurse. I told him that it was widely felt that emergency angioplasty was much more effective than thrombolytic therapy in the treatment of acute myocardial infarction (MI). I reminded the internist that we had the capability of doing this procedure at this hospital right away. As an astute internist, he was intrigued by this. He was also surprised to learn we could do this at the hospital—he was unaware that we had it available. He and the patient discussed this option, and they both agreed to proceed. The cath lab was notified, and fortunately there was a room available. The patient was promptly taken to the lab and prepared for the procedure.

A pre-shaped catheter was introduced via the right groin, up the aorta, and around the aortic arch to the take-off of the left coronary artery (LCA). The standard tip catheter, however, couldn’t reach the artery. Two more catheters with longer tips were attempted, again without success. This was definitely a red flag. Luckily, in my training I had run across this situation before. I immediately realized that this patient could have an aortic dissection, meaning he had a tear within his aorta. I immediately exchanged the left coronary catheter for what’s called a “pig-tail” catheter and did an angiogram of the aortic arch. This picture clearly showed a large tear, or dissection, that extended from the origin of the aorta at the heart all the way to just above the arteries leading to the kidneys. It had also extended to the right coronary artery; it was this that had caused the patient’s heart attack. Luckily, thrombolytic therapy wasn’t given. If it had been, the patient would have died suddenly of a ruptured aorta. The cardiovascular surgeons were summoned, and the patient went directly to the operating room for repair of his aorta. Despite the high risk of this operation, the patient did well and was able to recover fully. I still see him twice a year, and he is doing just fine.

What Is an Aortic Dissection? The aorta, also called the great artery, is the largest blood vessel in the body. It is about 3 centimeters, or 1.5 inches, in diameter. It begins at the aortic valve, the outflow tract of the left ventricle. Blood is pumped from the left ventricle through the aortic valve into the aorta. The aortic valve prevents blood from flowing back into the left ventricle. The blood is then carried by the aorta and the arteries that branch off from it to deliver oxygen to all parts of the body. The aorta, like all arteries, is composed of structural fibers that are quite elastic. This allows the aorta to stretch and contract so that it can handle the large quantities of blood it receives under high pressure. Just like another other artery in the body, the aorta is prone to develop atherosclerosis, which causes it to harden and become stiff. This can result in high blood pressure—and having high blood pressure makes the stiffening worse. In most people, some loss of flexibility in the aorta is part of the natural aging process. That’s why blood pressure tends to gradually increase over the

years. In some people, the stiffening process can be accelerated. The degree of stiffness can be extreme and the hypertension can be excessive. In this subgroup, the aorta itself can actually tear open from the pressure. In an aortic dissection, the inner layer of the blood vessel tears. Blood is forced through the tear into the middle layer of the blood vessel. That forcibly separates the inner and middle layers. Blood fills the separated area and can make it even larger, to the point where the vessel bulges outward—an aortic aneurysm. If the blood-filled area or the aneurysm ruptures through the outer layer of the aorta, the dissection is usually fatal. Aortic dissection is relatively uncommon, and it is extremely dangerous. About two thousand cases occur yearly in the United States. If not treated, a quarter of those people die in the first day. Fifty percent of them die in the first week. Surgery to repair the tear is complex and can involve replacing the entire torn area of the aorta with a synthetic graft, with or without replacement of the aortic valve. Sometimes, by surgery also must be done. Mortality from the surgery can be as high as 20 to 30 percent.

Symptoms of Aortic Dissection The symptoms of aortic dissection resemble those of a heart attack, which is why, in the case above, I began treating the patient for a coronary artery blockage. The difference is that an aortic dissection also has some symptoms of a stroke. The usual symptoms are: Sudden severe pain in the chest or upper back pain that radiates to the neck or down the back. Patients say the pain is a tearing or ripping sensation, not the crushing pain of a classic Big One. Fainting. Shortness of breath. Stroke symptoms, such as sudden difficulty speaking, vision impairment, weakness or paralysis of one side of the body. Sweating.

Weak pulse in one arm compared to the other. Most victims of aortic dissection are men in their 60s, but it can happen to anyone. The famed Olympic volleyball player Flo Hyman died suddenly in 1986 during a match in Japan. She was only 32, but she had an aortic dissection that bulged out into an aneurysm that burst. The reason for the dissection was that she had Marfan syndrome but didn’t know it. Marfan syndrome is a genetic condition that affects the connective tissue, including the tissue that hold arteries together. People with Marfan syndrome are usually very tall (she was 6 feet, 5 inches tall), with long limbs. What made Flo Hyman such a great athlete was also what killed her. More commonly, the major risk factor for aortic dissection is uncontrolled high blood pressure. This is probably responsible for about two-thirds of all cases. Another common cause in not wearing your seatbelt and being in a really bad car accident that tears the artery.

Aortic Aneurysm Sometimes, chest pain can be caused by an aortic aneurysm, a bulge in the wall of the aorta that involves all three layers of the vessel. The aneurysm makes the wall bulge out like a balloon. And like a balloon, the bulge can burst. An aortic aneurysm can be caused by an aortic dissection, but often it’s caused by an area of weak collagen, the connective tissue that holds us together. You are more at risk if you’re male and have a history of smoking, high blood pressure, and high cholesterol, but I see patients who are women (with and without risk factors) and men who don’t have any of the risk factors. Aneurysms usually develop slowly and have no symptoms. Small aneurysms are not uncommon. As long as they stay small, they’re unlikely to be a problem. If the aneurysm is bigger than about 5.5 centimeters (roughly 2 inches), however, it’s at risk of bursting open, with fatal results. The aneurysm itself can sometimes cause chest or abdominal pain, but most of the time it’s painless and you have no way of knowing it’s there. Sometimes, an aortic aneurysm is spotted when you have an X-ray or scan of the chest or abdomen for some other reason. If you’re a male between the ages of 65 and 75 and have ever been a smoker, your doctor may send you for an ultrasound scan

to check for an abdominal aortic aneurysm. (This isn’t recommended for women, even if they have a history of smoking. The benefit from the screening for women is so small that it’s not really worth doing.) If you discover you have an aortic aneurysm, you may not need any treatment if it’s small. Your doctor will probably send you for an ultrasound every six months to keep any eye on it and see if it’s getting bigger. If the aneurysm is growing or is already large enough to be worrisome, you may need to consider having it repaired. Sometimes we can use a stent, inserted using a catheter, to block off the aneurysm. Often, however, major surgery is needed. This is sometimes a difficult decision, especially for older people. I recently saw a woman in her 80s who was found to have a large aneurysm. She is not a great candidate for surgery, but surgery is not out of the question, either. If she goes ahead with surgery, she might not survive it or might have a severely diminished quality of life afterward—or she might do well for years to come. If she doesn’t have surgery, the aneurysm may burst at some point and kill her quickly. Given her age and state of health, all I could do was explain the pros and cons—I couldn’t make a recommendation. This patient finally decided that at her age, she would take her chances and not have surgery. Most people with an aortic aneurysm do not discover it until they it ruptures and causes severe pain and internal bleeding. Without emergency surgery to patch the ruptured area, death will occur rapidly, sometimes within minutes. Less than 20 percent of people with a ruptured aortic aneurysm survive it.

Causes of Chest Pain that Probably Won’t Kill You Sometimes, chest pain is so severe that you think The Big One has come, but it’s actually from something else that hurts a lot but probably won’t kill you. Don’t decide that for yourself, though. If you have severe chest pain that lasts for more than a few minutes, call 911 at once. Let the EMTs and the ER doctors figure out what the problem is.

Collapsed Lung

A collapsed lung, also called pneumothorax, happens when air gets into the pleural cavity, the space between your lungs and ribcage. The lung can’t expand fully, which causes shortness of breath and a lot of pain. If you have a collapsed lung, it’s probably because you’ve been hit in the ribs hard enough to break one or more ribs, or have been shot, stabbed, or otherwise injured in that area. At that point, it will probably be the EMTs making the decision that you need to go to the emergency room. If you’re on your own, you’ll have no doubt that it’s time to call 911. Sometimes, however, a collapsed lung can happen on its own, for no apparent reason. In fact, a bleb—a small pocket of air inside the lung—has ruptured and let the air leak into the pleural cavity. For some reason, this is most likely to happen to tall, thin men, especially if they smoke. Pneumothorax is usually treated by using a needle or chest tube to let the air drain out of the collapsed area. The pain usually goes away quickly once the air is removed.

The Case of the Mistaken Heart Attack I was once called in to do an emergency angiogram for a 59-year-old woman. For several months, she’d been having chest discomfort. She described it as a fullness under her right breast, which would radiate into her throat. The discomfort happened at various times, sometimes related to exertion, but also when she was at rest. Sometimes she’d have the pain after meals. At first, the discomfort was mild to moderate, about a 3 to 4 out of 10 on the pain scale. It occurred about two to three times a month and lasted from anywhere between a few minutes up to a half hour. She would sometimes experience some nausea. To figure out what the problem was, her internist did blood work, a chest X-ray, and an EKG, which were all within normal limits. Over the next few weeks, her symptoms became more frequent and more severe. One evening, she and her husband went out to a local seafood restaurant. She ordered her favorite dish, the New England clam chowder, which was also the specialty of the house. It was very creamy and delicious. About halfway through the bowl of chowder, she

developed the most severe pain she had ever experienced, a 9 out of 10. It was associated with extreme nausea, profound sweating, and lightheadedness. Her husband became appropriately alarmed and insisted that they go to the ER, which was only a few blocks away. Upon arrival, she was immediately seen by the ER physician, who ordered a stat EKG (stat is what doctors say when they mean immediately if not sooner). This showed ST elevation in leads II and III and AVF, the classic sign of an inferior myocardial infarction, and indicated that the right coronary artery was totally occluded. I was on STEMI call for the ER that night and was paged immediately by the ER doctor. I happened to be at the hospital seeing another patient, so I was able to go right down to the ER. On evaluation, the patient looked very uncomfortable. She told me she didn’t have any known heart disease, that she didn’t have diabetes, and had stopped smoking when she became pregnant with her first child at age 30. She took an ACE inhibitor for hypertension and was told to watch her diet because her LDL cholesterol was starting to creep up. She had been menopausal since age 51 but had not taken hormone replacement therapy. On physical exam, her blood pressure was 147/96 with a heart rate of 98. Her temperature was 99.8. Her lungs were clear. Her heart sounds were normal and she had no murmurs. An abdominal exam showed some tenderness in the right upper quadrant. The rest of the exam was within normal limits. Because of the threatening EKG changes and the severity of her symptoms, a Code STEMI was called and the cardiac catheterization lab was activated. Within thirty minutes, the patient was on the X-ray table and I was doing coronary angiography. To my surprise, the patient’s coronary arteries were wide open and totally free of atherosclerosis. A ventriculogram showed normal wall motion, with no evidence of any heart damage. By then, the lab work was ready and showed that her liver function tests were abnormal, indicating inflammation, and her bilirubin was extremely elevated, indicating bile duct obstruction. A stat ultrasound of the liver was then performed and showed an enlarged, swollen gallbladder with numerous gallstones. A surgeon was summoned, and the patient was taken straight to the operating room, where her gallbladder was removed. The patient did well and was able to be discharged home in just a few days. I often tell people this story to illustrate how even an experienced ER doctor and an experienced cardiologist can be fooled by gallbladder pain that looks like a

heart attack. And then there’s the opposite: what seems to be gallbladder pain that is actually a heart attack. I recently treated an older woman with a history of gallstones. She waited forty hours to come to the ER, thinking her chest pain and nausea were another bout of gallbladder trouble. They weren’t. By toughing out the pain for so long, she ended up with permanent damage to her heart.

Gallbladder Attack The most common cause of severe chest pain that probably won’t kill you is a gallbladder attack. Your gallbladder is a small, pear-shaped organ that’s located under your liver. Its function is to collect bile, a digestive fluid produced in the liver, and pump it through a tube called the common bile duct into your small intestine, where it helps digest dietary fat. Some people produce gallstones, hard deposits that are usually made from cholesterol, the main ingredient in bile. Gallstones can range in size from a grain of sand to a large pebble. You might have just one or two, or your gallbladder could be full of them. Many people have gallstones that never cause any symptoms. If they find out they have them, it’s often by chance when they’re having an ultrasound or some other scan of the abdominal area for another reason. It doesn’t really matter how many gallstones you have until one gets pushed out of the gallbladder and becomes stuck in the common bile duct. That’s when the pain starts, because the stone blocks the flow of bile out of the gallbladder. The severe pain is quite similar to the pain of a heart attack. It usually starts suddenly, is usually felt in the upper abdomen, and often radiates into the right shoulder. At the same time, patients break out into a sweat, feel nauseous, and may vomit. One common reason people with full-blown STEMIs wait to call 911 is because they think they’re having a gallbladder attack. And plenty of people call 911 thinking they’re having The Big One, only to discover that it was “only” a

gallbladder attack. What this tells us is that gallbladder or heart, you need emergency medical assistance. Don’t wait. Call 911.

Pancreatitis Pancreatitis is an inflammation of the pancreas, a large gland that sits in your abdomen just behind your stomach. Your pancreas produces enzymes that are needed for digestion. It also produces insulin, the hormone your body uses to carry blood sugar into your cells, where it is used for energy. Pancreatic enzymes are released through a tube called the pancreatic duct, which connects to the common bile duct. Both bile and pancreatic enzymes from there into the duodenum (the first part of the small intestine). Gallstones can inflame the common bile duct, which in turn leads to pancreatic inflammation. If this happens, the result is acute pancreatitis. Heavy alcohol use can also lead to acute pancreatitis. Aside from being extremely painful, acute pancreatitis is dangerous—the complications can be life-threatening. The main symptom of acute pancreatitis is gradual or sudden pain in the upper abdomen that often radiates into the back. Other symptoms include nausea and vomiting and a rapid pulse. Given the symptoms, people with acute pancreatitis often think they might be having a heart attack, especially when the pain comes on suddenly. Acute pancreatitis is a medical emergency, just as a heart attack is. Call 911 immediately.

10. How to Prevent a Heart Attack

Now you know exactly what you need to do to save your life if you are having a heart attack. However, if you can avoid The Big One completely, you will obviously be much better off. We are now at the point where the ultimate question arises: What do you do to prevent yourself from having a heart attack?

Investigate Your Risk To know your risk of having a heart attack, you need to take a careful look at the current state of your heart. First, assess your personal risk factors for the development of atherosclerosis, as described in chapter 5. Next, determine if you’ve had previous heart damage. Find out if your heart is getting enough blood. If it’s not, you have ischemia—lack of blood flow to an organ, in this case your heart muscle. If ischemia is present, it must be treated—with medication, stents, or surgery. If ischemia is not present but you are at risk (from high cholesterol, for instance), take steps to prevent it. If you have any significant risk factors for atherosclerosis, you must be riskstratified to find out your chances of having a heart attack. The best place to start is with your personal health care professional.

Talk to Your Doctor When you seek medical attention to determine your risk of having a heart attack,

your physician will look at a number of well-established risk factors. In an ideal world, your examination will start before you actually get to the office. Your doctor will give you a prescription (“script” in doctor talk) for blood work to be done in advance of your visit so that you can discuss the results. The standard blood tests usually include your fasting cholesterol level and blood sugar, a test called hs-CRP to check your overall level of inflammation, tests of your kidney and liver function, and a test to check for anemia. These should be done at least several days before the visit to be sure the results get to the doctor in time. At the office, your exam will start with taking your medical history. Your doctor will want to know both your personal medical history and your family history, going back to your grandparents, if possible. Because heart disease is so common, chances are you have some close relatives who have it or have died from it. Your doctor will be particularly interested in close relatives who have had heart attacks or other heart trouble at a relatively young age. By talking to you, your health care professional can assess your family history, habits, eating behavior, activity levels, and any symptoms you may be experiencing, such as chest pain or shortness of breath. Your doctor will then examine you for your vital signs, including your blood pressure, pulse, breathing rate, body temperature, weight, and height. Your pulses will be checked to see if you have clogged arteries to your arms, legs, or brain, or if you have an irregular heartbeat. Your eyes will be checked to assess damage to their blood supply from atherosclerosis. Your doctor will listen to your heart and lungs to see if there is any physical evidence of heart muscle weakness, valve problems, or respiratory problems. Your legs will be checked for edema (swelling from retained fluid). Based on the conclusions derived from the blood work, history, and physical, your physician may want to perform some diagnostic tests to learn more about the condition of your heart.

Diagnostic Tests for Heart Disease

Diagnostic tests for heart disease look mainly for two things: First, to find out you have already had heart damage. And second, to see if your heart is getting enough blood by checking for ischemia. When a particular organ is not getting enough blood, in this case the heart, you have ischemia. It is almost always due to a clogged artery that nourishes the organ. When the artery is clogged, it doesn’t get enough oxygen, which is carried by red blood cells. The lack of blood flow results in oxygen deficiency of the muscle cells. This can cause them to malfunction and, if severe, can result in their death. Many people with ischemia have symptoms. Angina, or chest pain, is a common symptom of ischemia. Some people will have pain in other areas, such as the back or even in the teeth or jaw. What is not commonly known is that many people with ischemia have no symptoms at all. This has been termed silent ischemia. Someone who has myocardial ischemia, that is, whose heart is not getting enough blood, is at very high risk of having a heart attack, whether they have symptoms or not. The more areas of the heart that are ischemic, the higher the risks of having a heart attack. Ischemia is a very serious and dangerous medical problem.

EKG Testing To assess the presence of existing heart disease, often the first test performed is an EKG, short for electrocardiogram. The presence of previous heart attacks, abnormal thickness of the heart, and irregularities of the heartbeat can sometimes be diagnosed with an EKG. The EKG has been and continues to be a valuable tool in the diagnosis of heart attacks. Its advantage as a test is that it is inexpensive, fast, painless, and readily available. However, the EKG does have its limitations. The EKG may be falsely negative. This means that the EKG may read as normal while a person is actually having significant heart problems. Even a heart attack, at times, can present with a normal EKG. It can also be falsely positive, suggesting a person is

having a heart attack when in reality he or she is fine. A study in the American Heart Journal reported that up to 40 percent of people with mini-heart attacks and unstable angina had EKGs that were considered normal! This is why, when a high-risk individual with symptoms has a normal EKG, both the patient and the doctor should not get a false sense of security. A normal EKG only tells us in this case that further investigation is needed!

Echocardiogram An echocardiogram uses ultrasound waves to produce an amazingly accurate image of the heart. Ultrasound images are made using very fast-moving sound waves, with a frequency greater than the upper limit of human hearing. Ultrasound can be used to image any of the organs of body, including a fetus inside the womb. A probe containing a specialized crystal is used to produce ultrasound. When electricity is run into the special crystal, it vibrates at a very rapid rate and creates ultrasound waves. These waves are then beamed directly into the organ being studied. The organ then reflects the sound waves back to the probe at different levels of intensities, depending on the unique composition of the tissues. The probe senses these differences and sends them to a computer, which generates images that allow direct examination of the structure and function of a particular organ. Ultrasound is painless and quick. The sound waves do no harm to the body. An echocardiogram produces a live image that can be used to actually see the heart beating. It provides a wide range of valuable information, such as heart size and function, status of the valves, and presence of fluid accumulations surrounding the heart. It can show if the heart has been damaged by a previous heart attack, and the affected segment will not contract well. A wall motion abnormality, as this is called, is easily visible on the echocardiogram. It is a sign of weakness of the heart. An echocardiogram is extremely useful in the diagnosis of an acute heart attack. If the heart is getting enough blood, all of its walls—the front, the back, and the

bottom—will contract normally. If the blood supply to a particular segment is cut off, then that segment will develop a wall motion abnormality. It won’t move as well and often will stop moving completely. I had a patient recently who was a great example of how valuable an echocardiogram can be for diagnosing a heart attack. A 49-year-old man with no history of heart disease came to my emergency room with chest pain. The pain had been happening off and on for about a month. It became sustained and severe while he was taking out the trash out late that afternoon. After about ninety minutes, he finally decided to come to the hospital. The patient had no history of high blood pressure, high cholesterol, or diabetes. He did have a family history of heart disease; a paternal uncle needed by surgery when he was in his mid-60s. The patient had been smoking about a pack of cigarettes a day since he was approximately 15 years old. When the patient was first seen by the ER physician, the pain was still present but had subsided somewhat. It went from a 7 to about a 3 on a pain scale of 1 to 10. The ER doctor ordered an immediate EKG. The EKG was felt to be nonspecific, which didn’t help with the diagnosis. At that point, I was called in to consult on the case. When the EKG doesn’t point directly to a heart attack, a crucial decision must be made. If this person is actually having a heart attack and he is only observed without receiving state-of-the-art therapy, he may go on to have significant muscle damage because he didn’t get prompt treatment. The damage could potentially lead to weakness of the heart and possibly congestive heart failure in later years. His life span could be significantly shortened if this happens. Thus, the decision that must be made at that moment could literally be the difference between life and death. Because the patient continued to have pain, even though it was less severe, and because he was at high risk for a heart attack, we decided to do an immediate echocardiogram to evaluate the heart’s wall motion. The echo showed that the front part of the heart (the anterior wall) wasn’t moving at all!

We suspected that this was a new finding, not something left over from a previous problem, because the patient was having ongoing chest pain and was at high risk of having heart disease. The next step was to take the patient immediately to the cath lab. An emergency angiogram showed a total closure of the left anterior descending artery, the vessel supplying the front of the heart. Angioplasty was performed. We were able to restore blood flow quickly and limit the amount of damage from the blocked artery. Six years later, this patient is still alive and well. Even better, he has successfully stopped smoking. Some people do listen.

CT Coronary Angiography and Calcium Score A newer approach to detecting coronary artery disease is CT coronary angiography with a calcium score, also called a coronary calcium scan. This painless test, which uses a CT scanner to take pictures of your coronary arteries, can show the presence of arterial plaque that has calcified, that is, arterial plaque that has hardened because calcium has accumulated in the lesion. We usually do this test for people who are at medium risk for heart disease because they have several risk factors, but who don’t have any symptoms (yet). If the test reveals a low calcium score—meaning there is little or no calcium in your arteries—the risk of dying of a heart attack is quite low. If the scan shows blockage, then further testing is needed to see if the heart is getting enough blood. Your scan results are looked at by a radiologist, who assigns a number that is your calcium score. The range is from 0 to more than 400. If your score is over 100, you probably have heart disease that calls for further investigation. The higher your score, the greater your risk of having a heart attack. If your score is low, however, you may still have arterial blockages, because not all blockages contain calcium. Overall, if you are at medium risk for a heart attack and your calcium score is between 100 and 400 or higher, you are more likely to have a heart attack sometime in the next three to five years than someone with a low

score.

Assessment of Ischemia Once the strength of the heart is assessed, the next step is to see if the heart is getting enough blood. We need to know if ischemia is present. There are a number of ways to assess ischemia. The most common way to make the diagnosis is to try to provoke ischemia, with either exercise or medication, and then monitor it with EKG, echocardiogram, or nuclear imaging. This sounds scary and dangerous, but it’s really very safe and not uncomfortable. There is a slight risk that the testing will cause mild chest pain, but if it does, we stop immediately. The most common way to assess ischemia is with a simple exercise stress test where you walk on a treill and are monitored by EKG. Your blood pressure and your heart rate are also closely monitored. The speed and grade on the treill are gradually increased so that you have to work harder. The goal is to attain at least 85 percent of your predicted maximal heart rate for your age. Your maximal heart rate is the highest heart rate you can achieve during maximal exercise. You can calculate it approximately by subtracting your age from 220. So, if you are 50, your maximal heart rate is approximately 170 beats per minute; 85 percent of that would be 145 beats per minute. If you normally take a beta blocker drug such as atenolol (Tenormin), metoprolol (Lopressor), nadolol (Corgard), or propranolol (Inderal LA) to treat high blood pressure, skip taking it the day of your exercise stress test. These drugs make your heart beat more slowly and with less force. You will probably not be able to reach 85 percent of your maximal heart rate if you take the drug that day, and your results won’t be accurate. Alternatively, you can do other tests for ischemia instead. If the heart does not get enough blood during the exercise, the EKG can show characteristic changes suggesting ischemia. The ST segment will usually become depressed if the heart is ischemic. So if ST segment depression is induced with exercise, whether or not the exercise causes

any other symptoms such as shortness of breath, this suggests that myocardial ischemia is present. The benefit of the exercise stress test is that it is widely available and relatively inexpensive. The problem is that the accuracy of the test is fairly poor. Depending on the population of people you are studying, it may be reliable only about 60 percent of the time. It’s also more unreliable for women than for men. This means that the results may suggest disease in someone who doesn’t actually have it—a false positive test. To increase the accuracy of the stress test, it is commonly used in conjunction with a type of echocardiogram called a stress echocardiogram. Ultrasound pictures of the heart are taken first while the patient is at rest and again after walking on a treill. If a particular segment of the heart stops moving with stress, this suggests a blocked artery to that area. The accuracy of a stress echo is quite good—it can be as high as 85 to 90 percent accurate.

Nuclear Imaging The accuracy of a stress test can also be increased with the use of nuclear scans of the heart. Again, while this sounds scary, it is perfectly safe and will not leave you glowing in the dark. An element is a substance that contains only one kind of atom. An isotope is any of two or more forms of a chemical element that have the same chemical properties but have different atomic weights because they have extra neutrons in the nucleus of each atom. Still with me? Many isotopes can be radioactive, which means they emit photons (units of light) when their energy level changes. Special cameras can detect the photons and send that information to a computer, which will then generate an image. By injecting tiny, very safe amounts of radioactive isotopes attached to a protein into the bloodstream, we can create a nuclear image of an organ. For a nuclear cardiac image, we use a protein that has a special affinity for heart tissue. The circulation carries the isotopes to you heart, where they then give off photons

that are converted into an image. Nuclear imaging of the heart is a valuable diagnostic tool for detecting clogged arteries. This is especially true for people with angina but no apparent heart attack. Two separate scans are usually compared: a resting scan and a stress scan. The stress can come from walking on the treill. If the patient can’t do the treill for some reason (severe hip arthritis, for example) we can provoke stress with medications. If a person has normal circulation, all areas of the heart will receive adequate amounts of blood and there will no defects in the photon image. If, however, there is a blockage, the part of the heart supplied by that particular artery will not get enough blood to meet its needs. Not only will the patient commonly experience chest pain (angina) from the test, but the nuclear imaging will show a defect in the area of the heart supplied by the blocked artery. If the resting scan is normal but the defect exists with stress—whether or not there is also chest pain—this indicates a significantly blocked artery and an increased risk of having a heart attack. If the defect exists at both rest and with stress, this indicates an area damaged by a previous heart attack. Nuclear imaging is also called stress perfusion imaging, because we can actually see the isotopes as they move through the circulation. It’s a valuable tool for differentiating true-positive from false-positive ST depression. The accuracy can be as high as 90 percent.

Drugs for Stress Testing Most of the time, stress tests are done while a person walks on a treill. Often, however, a person can’t walk well for a variety of different reasons. Orthopedic problems, paralysis as a result of a previous stroke, problems with equilibrium, and poor conditioning can all prevent someone from being able to exercise long enough on the treill to get a meaningful result. If 85 percent of the maximal predicted heart rate is not attained, the accuracy of the test drops dramatically. Under these circumstances, the heart can be stimulated using a variety of

medications. Doing so is safe, although it can cause mild chest pain in people with angina. We often use a drug called dobutamine, which is a derivative of epinephrine (adrenaline). When someone can’t walk on the treill, we can inject the drug into a vein to make the heart beat stronger and faster. This can provoke angina and EKG changes suggestive of the heart not getting enough blood. If the echocardiogram is used, abnormalities of wall motion can be detected. If nuclear imaging is used, lack of blood supply (perfusion defects) can be detected. Another drug we use in stress testing is adenosine. This is an extremely potent drug that causes the arteries to enlarge to their maximum diameter (vasodilatation). If one of the coronary arteries is significantly blocked, it cannot properly enlarge and blood is drawn into the healthier blood vessels. We call this coronary steal. With nuclear imaging, the defect can be detected in this region of compromised blood flow. An advantage to this test is that it is accurate even if a heart rate of 85 percent of the predicted maximum is not attained.

Cardiac Catheterization People who have normal blood flow to the heart—that is, they do not have ischemia at peak exercise or under vasodilator stress—have a less than 1 percent risk of dying of a heart attack each year. This is a very good prognostic sign. However, people who have multiple risk factors and have significant amounts of ischemia on diagnostic testing have an extremely increased risk of having a cardiac event. These individuals frequently benefit from cardiac catheterization with angiography of the blood vessels leading to the heart. The cardiac catheterization tells us if they have blockages in their coronary arteries. Because the arteries are directly visualized, the accuracy of the diagnosis of coronary artery disease is quite high, up to 98 percent. When comparing tests that are used to diagnose coronary artery disease, the gold standard today is coronary angiography. The test is performed by advancing very thin (2 to 3 millimeter) hollow tubes

called catheters through an artery in either the groin or the arm all the way, through the aorta to where the coronary arteries branch off. Dye (contrast fluid) is injected directly into the artery through the catheter. At the same time, X-ray movies are taken. The movies show if clogged arteries are present and if they are, how severe and extensive the degree of blockage is. Cardiac catheterization is a procedure with many benefits. If critically blocked arteries are identified before they abruptly close, heart attacks can be avoided and lives can be saved. There are usually three different circumstances where you may need a heart cath. One is if you have The Big One, that is, an acute myocardial infarction, and you need to be taken to the cath lab immediately to restore blood flow to the heart and limit damage. This is a medical emergency and must be done as soon as possible. : time is muscle. A second circumstance is if you have the new onset of symptoms such as chest pain, go to the hospital, and are found to have one of the Little Ones—unstable angina or a mini-heart attack. Typically, the heart cath is done the following day, after you have been stabilized with a variety of medications. Third is when you have the new onset of symptoms or you are asymptomatic but are at high risk of having a problem and you are evaluated on an outpatient basis. Your primary physician may obtain a screening test for ischemia or may refer you to a cardiologist for evaluation. In either circumstance, you may need to go to the hospital for an elective outpatient cardiac catheterization. Regardless of why you need the procedure, it is of ultimate importance that you understand it thoroughly and realize the implications of having this test. The most common heart cath procedure is coronary angiography with a ventriculogram of the left ventricle. This means that X-ray pictures are taken of the blood vessels to the heart, and dye is injected into the left ventricle to determine its pumping strength and see if the heart has been damaged. If you’re having the angiography as an outpatient (not in an emergency), the only preparation you need to do is take nothing by mouth for about six hours before the procedure. This is to minimize the slim chance of nausea and vomiting as a result of medications, the dye, or other factors. Vomiting is dangerous because it can result in aspiration and possible pneumonia.

If you take any diabetes drugs to lower your blood sugar, particularly glucophage (Metformin), tell your doctor in advance. We don’t want you to have low blood sugar while we’re doing an angiogram, so your doctor will probably tell you to skip that medication that morning or even for a day or two before. Bring them with you so you can take them after the procedure is over. Do not take any drugs for erectile dysfunction, such as sildenafil (Viagra), for at least twenty-four hours before the procedure. For the procedure, you’ll be asked to put on a hospital gown and lie on a table under a large X-ray machine in the cath lab. You’ll be given an intravenous injection of a drug to relax you, but you’ll be awake, though sleepy, throughout the procedure. An area on your left wrist or right groin will be shaved, disinfected, and numbed with a shot of local anesthetic. The catheter is then inserted into the artery in that area and slowly moved toward your heart. When it gets to the heart, X-ray pictures are taken as the catheter is moved to various parts of the heart. To get a better picture, a small amount of contrast material (dye) will be injected through the catheter into your heart or one of your coronary arteries. Pictures are taken to show the arteries as the dye moves through them. When the cardiologist has enough pictures, the catheter is withdrawn. A closure device is often used to close the hole in your artery, and firm pressure is applied to the area where the catheter was inserted to stop the bleeding. From start to finish, an angiography procedure typically takes about an hour. You can usually go home later that same day and return to your normal activities in a day or two. Cardiac catheterization can have significant but, luckily, fairly rare complications. They can’t always be predicted, so it’s important to look at your individual situation and decide if the benefits of the procedure outweigh the potential risks. The risks and benefits will be explained in detail to you and to whoever else is involved in making your health care decisions by the physician performing the procedure. Ironically, cardiac catheterization can be complicated by a heart attack during the procedure. This is usually caused by blunt trauma to the blood vessel from the catheter, causing a tear or dissection. The tear then stimulates blood clot formation, which cuts off blood flow to the affected area. Sometimes a blood clot forms within the catheter and is inadvertently injected

into the coronary circulation (embolization). This too can halt blood flow to the heart and cause a heart attack. Treatment of this devastating complication can include potent blood-thinning medications, emergency angioplasty with stent placement, or even emergency by surgery, depending on the severity of the particular situation. When you choose the medical center for your procedure, keep these complications in mind. If this unfortunate event happens to you, it is crucial that you are in an institution that can provide the appropriate emergency care. Luckily, the risk of such an event is quite rare, about one in eight thousand to ten thousand procedures. I have never had an embolization happen to one of my patients. Another potential risk of a cardiac catheterization is a stroke—sudden damage to the brain as a result of interruption of its blood supply. A stroke is basically a brain attack. It can result in paralysis, speech problems, and impaired vision. A severe stroke can result in death or a lifetime dependency on others for your care. It is a devastating complication of cardiac cath. It can be caused by interruption of blood flow from blood clots that have formed within the catheter or from dislodged plaque that then travels into the brain’s circulation. Trauma to the blood vessels supplying the brain can also be a cause of stroke. Another cause is bleeding into the brain, a risk that is greater if potent anticoagulants are required during the catheterization. Luckily, again, the risk of having a stroke during a cath is quite rare. It occurs in only about one in twelve thousand to fifteen thousand cases. It has never happened to one of my patients. Bleeding complications are probably the most common problem with cardiac catheterization. Most of the bleeding complications occur at the site of access into the circulation, usually the groin or arm. The bleeding can range anywhere from simple bruising to profound blood loss requiring blood transfusion or even intervention by a vascular surgeon to stop the bleeding or restore blood flow to the limb as a result of blood clot formation. Loss of a limb is an extremely rare but known complication.

People who have had multiple procedures in the same vessel, who are unable to lie flat and not move their leg, and/or who are on potent blood thinners for whatever reason are at higher risk for vascular bleeding. Women are at higher risk of having these complications, mostly because their vessels are smaller. Also, women tend to be older when they’re diagnosed, so they are more likely to also have other health problems, such as high blood pressure or diabetes. Fortunately, bleeding problems are becoming much less common. New technologies have been developed to close the entry site and reduce the risk of bleeding. Newer blood-thinning regimens are equally effective but carry less risk of bleeding. Because of this, the risk of a bleeding vascular complication is now about 0.2 percent, which is very low. Rarely, bleeding in other areas can occur. This includes bleeding from the gastrointestinal tract, the urinary tract, or possibly the lungs. Contrast agents, or dye, are iodine-containing chemicals injected into the artery. X-ray pictures can then be taken which directly visualize the vessel. Without the contrast agent, the blood vessels are not visible on the X-rays. Some people react to the iodine dye with nausea, vomiting, low blood pressure, or a slow heart beat. These reactions are usually minor and go away quickly. More modern agents have made these side effects rare. A more worrisome side effect of the contrast agent is anaphylaxis, an allergic reaction to the iodine. It usually causes itching and hives, but it can progress to the point of producing asthma (bronchospasm), which can become severe. The allergic reaction can also cause swelling of the face and throat, which can obstruct the airway and lead to an inability to breathe (respiratory failure). Less serious allergic reactions to iodine contrast dye are fairly uncommon, about two in one thousand patients. However, for someone with a history of a previous allergy to the dye, the incidence can be as high as ten to fifteen in a thousand. Because having the catheterization is usually a medical necessity, people who are allergic to the dye can be pretreated with antihistamines and steroids to prevent or minimize the reaction. In patients whom I have pretreated for allergy to a contrast agent, I have never seen a problem during heart cath. Anaphylaxis from the dye is even less common. I have seen it twice in my

career. It happened to be in the same guy during acute myocardial infarctions nine years apart. Both times, during emergency angioplasty, he developed anaphylactic shock with respiratory failure because of a dye reaction. Luckily, he responded to epinephrine and steroids and survived both times. It’s been seven years now since the last time, and he is still doing quite well. The contrast agent can also cause damage to the kidneys, although this is uncommon. People with preexisting kidney problems, diabetes, and dehydration are at increased risk of developing this complication. Even though all of these unfortunate events can be scary, it is important to keep in mind that the risk of this procedure, when indicated, usually far outweighs the potential risk. It is essential, however, that you and the physician performing the procedure discuss the risks and benefits in detail and that you understand these issues and are willing to proceed. In my experience, every patient, even the few who had complications, were glad they had the catheterization.

Epilogue

My obsession with heart attacks began with the death of my grandpa Joe. How could something so quickly kill a person who just a little while before was perfectly healthy? How could someone so young die? Since that time I have dedicated my life to answering this question. I think a large part of this was the realization of my own mortality. I saw what happened to my grandfather. I also saw that my dad had severely clogged arteries in his neck and in his legs. He died of a stroke, which occurred during his sixth vascular surgery to try to save his left leg. My uncle had died at age 62 in his sleep from a pulmonary embolus. Another uncle had his first heart attack when he was 49 and lived with a weak heart for 11 years before he died from congestive heart failure. My grandmother died of a massive heart attack at the age of 88. It was clear that I was at high risk of following the exact same path of my relatives. I have strong family history for dying of a heart attack. I decided to be proactive. I took a long, hard look at what else I could to do to preventing myself from dropping dead of a heart attack at too young an age. I checked my blood pressure, which I hadn’t done for quite some time, even though I am a doctor. It just shows you that denial extends to all levels. I was quite disturbed to find it was 156/92. Not just pre-hypertensive but full-blown high blood pressure, with its inherent risk of heart attack and stroke. I got a fasting lipid and my feeling of being disturbed rapidly progressed to a sensation best described as terror. My total cholesterol was in the low 300s, as were my triglycerides.

My HDL was pretty good, about 50, but my LDL, the bad one, was in the 200s. My BMI was around 27 (you’re overweight if your BMI is greater than 25) and my waist was at its all-time high at 36 inches. My exercise sessions were getting further and further apart. I saw myself as a time bomb about to explode. I got an EKG, which was really abnormal. It looked as if I had already had a major heart attack. An echocardiogram, however, showed that my heart was strong and all the walls were moving equally. , EKGs are wrong up to 35 percent of the time. My first priority after that was to see if my heart was getting enough blood. I then had a nuclear stress test, which thankfully showed that all the areas of my heart were getting enough blood. I had no ischemia. I then went on to pursue my own risk factor modification program. I went on a low-fat, low-carb, and low-calorie diet. I bought a pedometer and made sure I walked at least 10,000 steps a day. My blood pressure and my cholesterol counts remained high even though I was losing weight. Because of my high risk of an event, I began taking medication to control my BP and cholesterol. The first blood pressure medication I took got my pressure to 118/70, which was acceptable. But I developed a dry cough, which really bugged me. I switched to another drug that did as good a job but didn’t give me a cough. I decided to try a statin to control my lipids because I strongly believe they are effective at preventing a first heart attack not only by lowering LDL but also in stabilizing a plaque that is ready to rupture. It worked quite well. My LDL is now around 60 and my HDL is still in the low 50s.

So far, so good after about ten years of doing this. Every one has a similar story. We can all name countless relatives with similar histories. With heart attacks being the number-one killer in the U.S., we all are affected. We must all take a serious look at ourselves and assess what our own personal risk of dying of a heart attack is. We need to seek medical attention and be tested to see if our hearts are getting enough blood. If they aren’t, we need to be referred to a cardiologists who can determined the most appropriate therapy for ischemia If you do this, you will significantly reduce your risk of having The Big One. But as we all know, you can do everything exactly right and still, when you least expect it, you can have a heart attack. Knowing what to do in this crucial time is life-saving. With the sudden onset of any new, intense chest discomfort, difficulty breathing, sweating, or lightheadedness, don’t deny what is happening. Call 911 and get to a heart center. If you are having a heart attack, a heart center is where you will get the gold standard of care. As you have read, if you get to the door of a heart center’s emergency room with a heart attack in progress, they can get you to the cath lab, open your artery quite quickly, and preserve your heart muscle. I wrote about an example of “a door to balloon time” of only 23 minutes. This is about as good as you can get. Recently the “front door to balloon time” standard is being perfected. This measures the time from the arrival of the paramedics to the heart attack scene to an open artery. To accomplish this, many areas of the country are establishing regional STelevation myocardial infarction (STEMI) receiving center (SRC) networks. So, someone having a full-blown heart attack is quickly taken straight to an SRC

that is a center of excellence and is prepared to provide the best possible care. The patient is taken to the nearest SRC even if another hospital is closer. That’s because the SRC has the capacity to perform emergency angioplasty. If we can make the front door to balloon time be less than 90 minutes everywhere, we can save thousands of lives. Regional heart centers are beginning to develop, but right now they are few and far between. If you don’t have a STEMI network in your area now, then it is imperative that a grassroots effort be made to quickly get these programs going. We want everyone to have an equal opportunity to get the gold standard of care.

Call 911 Be this as it may, the limiting factor in saving lives is the time from the onset of symptoms to the 911 call. Too many people wait too long to get help. If you wait too long, your risk of dying becomes very high. Many attempts have been made to inform the people how to recognize when they have problem. TV, radio, magazine, and newspapers have made little difference. My goal in writing this book was to educate you on what you can do to save your life. I hope that it makes a difference in your life It is now up to you.