Acute Coronary Syndrome 2m2u3y

Acute coronary syndrome Dinesh k lamsal :MD

Background: The initial diagnosis of acute coronarysyndrome (ACS) is based entirely on history, risk factors, and, to a lesser extent, ECG findings. The symptoms are due to myocardial ischemia, the underlying cause of which is an imbalance between supply and demand of myocardial oxygen.

Internationally: In Britain, annual incidence of angina is estimated at 1.1 cases per 1000 males and 0.5 cases per 1000 females aged 31-70 years. In Sweden, chest pain of ischemic origin is thought to affect 5% of all males aged 5057 years. In industrialized countries, annual incidence of unstable angina is approximately 6 cases per 10,000 people.

Mortality/Morbidity: • When the only treatment for angina was nitroglycerin and limitation of activity. • patients with newly diagnosed angina had a 40% incidence of MI and a 17% mortality rate within 3 months. • A recent study shows that the 30-day mortality from ACS has decreased as treatment has improved, a statistically significant 47% relative decrease in 30-day mortality among newly diagnosed ACS from 1987-2000. • This decrease in mortality is attributed to aspirin, glycoprotein (GP) IIb/IIIa blockers, and coronary revascularization via medical intervention or procedures

Incidence : • Sex: Incidence is higher in males among all patients younger than 70 years. This is due to the cardioprotective effect of estrogen in females. At 15 years postmenopause, the incidence of angina occurs with equal frequency in both sexes. Evidence exists that women more often have coronary events without typical symptoms, which might explain the frequent failure to initially diagnose ACS in women. • Age: ACS becomes progressively more common with increasing age. In persons aged 40-70 years, ACS is diagnosed more often in men than in women. In persons older than 70 years, men and women are affected equally. •

Pathophysiology: • Myocardial ischemia is most often due to atherosclerotic plaques, which reduce the blood supply to a portion of myocardium. Initially, the plaques allow sufficient blood flow to match myocardial demand. • When myocardial demand increases, the areas of narrowing may become clinically significant and precipitate angina. Angina that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest, and without recent change in frequency or severity of activity that produce symptoms, is called chronic stable angina. • Over time, the plaques may thicken and rupture, exposing a thrombogenic surface upon which platelets aggregate and thrombus forms. The patient may note a change in symptoms of cardiac ischemia with a change in severity or of duration of symptoms. This condition is referred to as unstable angina.

Contd… (1) • The excessive mortality rate of coronary heart disease is primarily due to rupture and thrombosis of the atherosclerotic plaque. • Inflammation plays a critical role in plaque destabilization and is widespread in the coronary and remote vascular beds. Systemic inflammatory, thrombotic, and hemodynamic factors are relevant to the outcome. • Evidence indicates that platelets contribute to promoting plaque inflammation as well as thrombosis. A new theory of unbalanced cytokinemediated inflammation is emerging, providing an opportunity for intervention.

Contd …..(2) • Patients with STEMI have a high likelihood of a coronary thrombus occluding the infarct artery. • Angiographic evidence of coronary thrombus formation may be seen in more than 90% of patients with STEMI but in only 1% of patients with stable angina and about 35-75% of patients with unstable angina or NSTEMI. • However, not every STEMI evolves into a Qwave MI; likewise, a patient with NSTEMI may develop Q waves

Causes: • Atherosclerotic plaque is the predominant cause. Coronary artery vasospasm is less common. • Alternative causes of angina include the following: – Ventricular hypertrophy due to hypertension, valvular disease, or cardiomyopathy – Embolic occlusion of the coronary arteries – Hypoxia, as in carbon monoxide poisoning or acute pulmonary disorders – Cocaine and amphetamines, which increase myocardial oxygen demand and may cause coronary vasospasm – Underlying coronary artery disease, which may be unmasked by severe anemia – Inflammation of epicardial arteries – Coronary artery dissection

Risk factors Male gender Diabetes mellitus (DM) Smoking history Hypertension Increased age Hypercholesterolemia

Hyperlipidemia Prior cerebrovascular accident (CVA) - These patients constitute 7.5% of patients with ACS and have high-risk features. Inherited metabolic disorders

Methamphetamine use Occupational stress Connective tissue disease

CLINICAL • History: Typically, angina described as a sensation of chest • •

• •

pressure or heaviness that is reproduced by activities or conditions that increase myocardial oxygen demand. Some present with only neck, jaw, ear, arm, or epigastric discomfort. Other symptoms, such as shortness of breath or severe weakness, may represent anginal equivalents. A new case of angina is more difficult to diagnose because symptoms are often vague and similar to those caused by other conditions (eg, indigestion, anxiety). Patients may have no pain and may only complain of episodic shortness of breath, weakness, lightheadedness, diaphoresis, or nausea and vomiting.

• Patients may complain :Palpitations tolerance

, Decreased exercise

Differential diagnosis: (on hx) Stable angina – Involves episodic pain lasting 5-15 minutes – Provoked by exertion – Relieved by rest or nitroglycerin

Unstable angina : Patients have increased risk for adverse cardiac events, such as MI or death. Three clinically distinct forms exist, as follows: • New-onset exertional angina • Angina of increasing frequency or duration or refractory to nitroglycerin • Angina at rest

Contd …. • Variant angina (Prinzmetal angina) – Occurs primarily at rest – Triggered by smoking – Thought to be due to coronary vasospasm Elderly persons and those with diabetes • may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. Elderly persons may also present with only altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever. As many as half of cases of ACS • are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. Maintain a high index of suspicion for ACS especially when evaluating women, diabetics, older patients, patients with dementia, and those with a history of heart failure.

Diff . Dx. With others dis……

• • • • • • • • • • •

Anxiety As Asthma Dcm Esophagitis Gastroenteritis Htn-ive ER Mi Percarditis Pneumothorax Pulmonary edema

Physical: • Physical examination results are frequently normal. If chest pain is ongoing, the patient usually will lie quietly in bed and may appear anxious, diaphoretic, and pale. • Hypertension may precipitate angina or reflect elevated catecholamines due to either anxiety or exogenous sympathomimetic stimulation. • Hypotension indicates ventricular dysfunction due to myocardial ischemia, infarction, or acute valvular dysfunction. • Congestive heart failure (CHF) • Jugular venous distention – Third heart sound (S3) – A new murmur may reflect papillary muscle dysfunction – Rales on pulmonary examination, suggesting left ventricular (LV) dysfunction or mitral regurgitation – Presence of a fourth heart sound (S4), a common finding in patients with poor ventricular compliance due to preexisting ischemic heart disease or hypertension

Investigation Lab Studies: Troponin- for diagnosing myocardial necrosis. It is detectable in serum 3-6 hours after an MI, and its level remains elevated for 14 days.

CK-MB - levels begin to rise within 4 hours after MI, peak at 18-24 hours, and subside over 3-4 days lactase dehydrogenase – rises within 24 hours of MI , peak within 3-6

days, and returns to the baseline within 8-12 days Cardiac markers -should be used liberally to evaluate patients with prolonged episodes of ischemic pain, with new changes on ECG, or with nondiagnostic or normal ECGs in whom the diagnosis of ACS or MI is being considered.

C b c- is indicated to determine if anemia is a precipitant b s l, renal function, and electrolytes levels, for patients with new-onset angina. Creatinine levels (For use ACE)

Imaging Studies: Chest x-ray: may demonstrate complications of ischemia, such as pulmonary edema , thoracic aneurysm or pneumonia. Echocardiogram: identifying precipitants for ischemia, such as ventricular hypertrophy and valvular disease. Radionuclide myocardial perfusion imaging

Other Tests :ECG is the most important ED diagnostic test for angina – Transient ST-segment elevations (fixed changes suggest acute MI): In patients with elevated ST segments, consider LV aneurysm, pericarditis, Prinzmetal angina, early repolarization, and WolffParkinson-White syndrome as possible diagnoses. – Dynamic T-wave changes (inversions, normalizations, or hyperacute changes): In patients with deep T-wave inversions, consider also CNS events or drug therapy with tricyclic antidepressants or phenothiazines. – ST depressions that may be junctional, downsloping, or horizontal – Diagnostic sensitivity may be increased by performing right-sided leads (V4R), posterior leads (V8, V9), and serial recordings.

TREATMENT Prehospital Care: • Obtain IV access. • ister supplemental oxygen. • Aspirin should be given in the field, 162-325 mg chewed and swallowed. • Telemetry and prehospital ECG, if available, may be helpful in selected circumstances. Certain EMS systems have investigated protocols for prehospital istration of thrombolytic therapy. This has not become a trend due to unproven benefit and due to the increase in availability of percutaneous coronary intervention (PCI) in many medical centers as an alternative to thrombolysis for STEMI. • Perform pulse oximetry. • ister sublingual or aerosolized nitroglycerin if chest pain is ongoing and is felt to be cardiac in origin.

Emergency Care

:

• Goals of ED care are rapid identification of patients with STEMI, exclusion of alternative causes of nonischemic chest pain, and stratification of patients with acute coronary ischemia into low- and highrisk groups. • Obtain IV access, ister supplemental oxygen, and provide telemetry monitoring if these procedures have not already been accomplished in the prehospital phase. In addition, obtain a 12-lead ECG as soon as possible after arrival. • Complete a history and physical examination, with focus on risk factors for coronary ischemia; onset, duration, and pattern of symptoms; and early identification of complications of myocardial ischemia (eg, new murmurs, CHF). • Perform frequent reassessment of vital signs and symptoms in response to istered therapies. • Serial ECGs and continuous ST segment monitoring may be useful. • Many EDs have an observation unit that may be an appropriate disposition for patients who meet ission criteria. • Medical therapy : Medication. • Consultations: Cardiology

MEDICATION Drugs: antiplatlets (aspirin-160-324 mg PO or chewed; suppository if patient is unable to take PO medications ) Nitrates (Nitroglycerin-400 mcg SL or spray q5min, repeated up to 3 times, If symptoms persist, ister 5-10 mcg/min IV infusion ) Analgesics (Morphine sulfate - 2-4 mg IV q5-15min; titrate to symptomatic relief or adverse effects (eg, lethargy, hypotension, respiratory depression ) Anticoagulants (Heparin -- Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin.) dose : 80 U/kg IV bolus, followed by an infusion of 18 U/kg/h Beta-adrenergic blockers (Metoprolol - 5 mg slow IV infusion q5min; to a maximum dose of 15 mg or desired heart rate) Low molecular weight heparins ( Enoxaparin-1 mg/kg istered SC q12h in conjunction with oral aspirin (100-325 mg/d) Adenosine diphosphate receptor antagonists (Clopidogrel-300 mg PO

loading dose, followed by 75 mg PO qd

)

Inpatients care • Patients with unstable angina and/or ECG changes should be itted to a telemetry bed. A certain subset of patients with stable angina may be treated as outpatients with antianginal agents, but close follow-up is necessary. • Patients with symptoms refractory to aggressive medical treatment, shock, suspected or known aortic stenosis, or new or worsening mitral regurgitation are at high risk. Management for these patients should include the following: – ission to an intensive care unit setting – Cardiology consultation

• Consideration for intra-aortic balloon pump (IABP) and early angiography to delineate anatomy • Continue antiplatelet and antianginal medications initiated in the ED. Subsequent dosing is determined by symptomatic response and tolerance of side effects. • The routine use of lidocaine as prophylaxis for ventricular arrhythmias in patients with ACS is not indicated. In MI, it has been shown to increase mortality rates. Lidocaine may be used for patients with complex ventricular ectopy or for patients with hemodynamically significant, nonsustained, or sustained ventricular tachycardia.

Complications: • • • •

Acute myocardial infarction Cardiogenic shock Ischemic mitral regurgitation Arrhythmias – Supraventricular arrhythmias (rare complication of ischemia, may actually precipitate ischemic events) – Ventricular arrhythmias; simple and complex premature ventricular contractions (PVCs), and nonsustained ventricular tachycardia (NSVT) • Atrioventricular nodal blockade – Usually transient in setting of reversible ischemia – Treatment guided by location of block and hemodynamic stability. • Ventricular rupture occurs in the interventricular septum or the LV free wall

Prognosis: • Patients with angina either go on to infarct or have their disease stabilized by medical and/or interventional therapies. Patients with angina are a heterogeneous group; therefore, prognosis varies with respect to stability of disease, demographics, comorbidity, and current intervention. • Patients with ACS with atrial fibrillation (AF) are associated with increased morbidity and mortality (Mehta, 2003). • Patients with ACS and DM, especially those with ST elevation, had increased in-hospital mortality. Among patients with ACS and DM, those receiving insulin had worse outcomes. Outcomes were similar for those on hypoglycemic medication or on diet alone (Hasdai, 2003). • In chronic stable angina, prognosis is generally excellent. Factors that have been shown to impact prognosis include the following: – Aspirin reduces progression to both nonfatal MI and cardiac death. – Beta-blockers control anginal symptoms and reduce cardiac complications in patients with hypertension. – PTCA and revascularization improve the prognosis in high-risk patients. – Poor prognostic factors include male sex, diabetes, and hypertension.

• In unstable angina, prognosis is determined by the ability to control symptoms acutely, preventing progression to AMI. Factors associated with a poorer prognosis include the following: – Evidence of myocardial necrosis, as determined by elevated troponin T – Delays in angiography in patients at high risk (Early angiography allows for triage to medical therapy, PTCA, or revascularization.)