Advances In Canine Cardiology - Veterinary Focus - Vol. 18 (3) - 2008, Richard Harvey zp1w

Advances in Canine Cardiology Veterinary Focus - Vol. 18(3) 2008 Richard Harvey PhD, BVSc, DVD, FIBiol, MRCVS - Editor Biomarkers in the Diagnosis of Canine Heart Disease Caryn Reynolds and Mark Oyama New Echocardiographic and Doppler Techniques Valérie Chetboul Interventional Cardiovascular Procedures Suzanne Cunningham and John Rush How I Treat... Valvular Heart Disease in the Dog Adrian Boswood Royal Canin Viewpoint... Nutritional Management of Early Cardiac Disease: ACT with SPEED Daniel Baker and Denise Elliott How I Approach... Syncope in Dogs - A Syndrome, not a Disease Marianne Skrodzki and Eberhard Trautvetter Cut-out and Keep Guide... Electrocardiography in Dogs Michael Johnson Editorial Committee: Dr. Denise A. Elliott, BVSc(Hons), PhD, Dipl. ACVIM, Dipl. ACVN, Scientific Affairs, Royal Canin, USA; Dr. Philippe Marniquet, DVM, Scientific Communication Manager, Royal Canin, ; Dr. Pauline Devlin, BSc, PhD, Marketing Director, Royal Canin, UK; Dr. Franziska Conrad, DVM, Scientific Communications, Royal Canin, ; Dr. Julieta Asanovic, DVM, Dipl. FCV, UBA, Scientific Communications, Royal Canin, Argentina.

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Biomarkers in the diagnosis of canine heart disease

Caryn Reynolds, DVM Matthew J. Ryan Veterinary Hospital, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, USA Dr. Reynolds is a Cardiology Resident at the School of Veterinary Medicine within the University of Pennsylvania. She received her DVM from Colorado State University in 2006. Caryn Reynolds completed a Small Animal Medicine and Surgery internship and a Cardiology Research internship at the Ryan Veterinary Hospital within the University of Pennsylvania.

Introduction Traditionally, the evaluation of heart function has been accomplished by electrocardiography, radiography, and echocardiography. These tests are relatively time-consuming and expensive, and in the case of echocardiography, may not be available to all patients. Within the past 10 years, cardiac biomarkers, primarily cardiac troponin and natriuretic peptides, have become a mainstay for both the diagnosis and patient monitoring in human heart disease. Recently, veterinary research has provided insight into the utility of these blood-based cardiac biomarkers in canine and feline patients. A biomarker is defined as a substance elaborated by a specific tissue that can be detected in circulation. To be clinically useful, it should be released in proportion to a particular disease process, and provide information regarding

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Mark Oyama, DVM, Dipl. ACVIM (Cardiology) Matthew J. Ryan Veterinary Hospital, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, USA Dr. Oyama graduated from the University of Illinois in 1994. He completed an internship at The Animal Medical Center in NYC and then a residency in cardiology at the University of California, Davis. Mark Oyama is currently an Associate Professor at the Department of Clinical Sciences within the University of Pennsylvania.

presence, severity, and prognosis of the disease. Ideally, the biomarker would be stable and easy to detect with a widely available, rapid, and inexpensive assay. Biomarkers are commonly used in veterinary patients to evaluate the function of other organs; for example, BUN and creatinine are used to monitor kidney function, while ALT assesses hepatocellular damage. In the past, the classic enzymatic assays of cardiac disease, such as creatine kinase, lacked requisite sufficient sensitivity and specificity for useful clinical application in dogs. In contrast, cardiac troponin and natriuretic peptide testing appears to offer useful information in cases of canine heart disease. This review discusses available veterinary information regarding these tests and potential applications.

Natriuretic peptides Chronic overstimulation of the renin-angiotensinaldosterone system occurs with heart disease,


which leads to cardiac enlargement, volume overload, and congestive heart failure. The natriuretic peptides counteract this activity by stimulating natriuresis, renal blood flow, diuresis, and vasodilation as well as enhancing diastolic heart function. Circulating atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) levels are increased primarily in response to increased myocardial wall stress. ANP originates mainly from the atria while BNP comes from both the atrial and ventricular myocytes. Both are released as precursor molecules then cleaved by serum proteases to form equal amounts of the active C-terminal fragments (sometimes referred to as C-ANP and C-BNP), and an inactive N-terminal fragment (NT-proANP and NT-proBNP) (Figure 1). C-ANP and C-BNP have ultrashort half-lives, and measurement of circulating concentrations can be difficult; NT-proANP and NT-proBNP have longer half-lives and are more stable for collection and sample handling, making measurement more practical in the clinical setting. Canine-specific ELISA tests for NT-proANP and NT-proBNP have recently become available. Currently, measurement of plasma or serum natriuretic peptide concentrations is considered part of the diagnostic database for the human cardiovascular patient. In the emergency setting, NT-proBNP can be used in conjunction with physical examination, thoracic radiography, and electrocardiography to differentiate primary respiratory causes of dyspnea from congestive heart failure (1). BNP independently predicts the risk of death or heart failure in the asymptomatic patient, making it a valuable tool for risk assessment and patient screening. Measurement of BNP concentrations also helps clinicians monitor the short-term response to congestive heart failure therapy (2). In humans, renal function, gender, obesity, and age influence blood natriuretic levels, and must be considered when interpreting results. Several studies have been published recently evaluating the utility of blood natriuretic peptides, NT-proBNP in particular, testing for dogs. The major indications for use are discussed below.

Diagnosis of heart disease Boswood, et al. reported a significant difference between dogs with heart disease, dogs with


ProBNP

NT-proBNP

Inactive More stable Longer half-life

C-BNP

Biologically active Less stable Shorter half-life Figure 1.

NT-proBNP is formed when proBNP is cleaved by serum endopeptidases to form C-BNP. NT-proBNP is biologically inactive, but has greater stability than C-BNP, and because NT-proBNP is formed in a 1:1 proportion with C-BNP, measurement of NT-proBNP reflects the amount of biologically active C-BNP that is produced in situations of underlying heart disease.

heart failure, and dogs with primary respiratory disease. Based on a cut-off value of 210 pmol/L, NT-proBNP had a positive predictive value of 94% and a negative predictive value of 77% for predicting dogs with heart disease or heart failure (3). This means that dogs with a positive test were 94% likely to have heart disease or failure while dogs with a negative test were 77% likely to not have heart disease or heart failure. In another study by Oyama, et al. (4) of 119 dogs with mitral valve disease, 18 dogs with dilated cardiomyopathy, and 40 healthy control dogs, serum NT-proBNP discriminated dogs with cardiac disease from healthy dogs with a positive predictive value of 97% and a negative predictive value of 61% when using a cut-off value of 445 pmol/L. In addition, it was reported that NT-proBNP was correlated to heart rate, respiratory rate, echocardiographic heart size, and renal function. Moreover, NTproBNP could be used to determine which dogs had clinically significant radiographic heart enlargement vs. those that did not, using a cut-off value of 680 pmol/L (positive predictive value, 81%; negative predictive value, 86%). The results of these studies suggest that NT-proBNP measurement can be utilized in conjunction with other diagnostic tools, including physical examination, radiography and echocardiography

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to help diagnose heart disease in dogs. The commercial laboratory currently performing NT-proBNP assay maintains that heart disease is unlikely in patients with serum or plasma NT-proBNP is ≤566 pmol/L. Prospective studies are currently being conducted to determine whether NT-proBNP can be used for serial monitoring of dogs with asymptomatic mitral valve disease to assess the risk of any individual dogs for developing actual congestive heart failure secondary to its disease.

Etiology of respiratory signs Fine, et al. (5) evaluated 46 dogs with cough or respiratory distress and determined that dogs with congestive heart failure had significantly higher median NT-proBNP concentrations than those with respiratory disease (heart failure, median, 2554 pmol/L, interquartile [25%-75%] range, 1652-3476; respiratory, median, 357 pmol/L, interquartile range, [193-566]. These results highly the possibility that NT-proBNP can help determine the underlying cause of respiratory signs in dogs. Indeed, in a study of 116 dogs presenting to referral hospitals for moderate to severe respirator y signs (i.e., cough, wheeze, dyspnea, etc), serum NT-proBNP >1200 pmol/L had a positive predictive value of 85.5% and a negative predictive value of 81.6% for distinguishing dogs with congestive heart failure from those with signs due to primary respiratory disease (6). These results are similar to scientific abstracts presented by Fine, et al. and Wess, et al., which show good sensitivity for the diagnosis of congestive heart failure in dogs with respiratory disease (5,7). Determining the cause of respiratory signs in older, small-breed dogs in which mitral valve disease and chronic primary respiratory diseases often occur concurrently can be challenging. A finding of NT-proBNP >1200 pmol/L in these cases can be particularly helpful if historical, physical examination, or radiographic findings are either not available or are equivocal (8). A rapid in-hospital point-of-care test, as is available in human emergency hospitals, would be valuable in veterinary patients that do not tolerate radiography due to the severity of their respiratory distress until stabilized by initial treatment. In cases of severe pulmonary disease and concurrent



pulmonary hypertension NT-proBNP can be falsely elevated and this has the potential to confound interpretation of the test results.

Screening for occult disease Currently, diagnosis of occult DCM in dogs typically requires echocardiography and Holter monitor, whic h are relatively expensive, inconvenient (with respect to the need for the dog to wear the Holter monitor for 24hrs), and not available to all dog owners. In a study of 118 Doberman Pinschers, Boxers, and Great Danes, NT-proANP, C-BNP, and cardiac troponin were significantly different between the 21 dogs diagnosed with occult cardiomyopathy vs. the healthy dogs. Of the three biomarkers, BNP had the best sensitivity and specificity (95.2% and 61.9%, respectively) for detection of occult disease (9). Larger studies are currently being conducted to evaluate the utility of NT-proBNP and NT-proANP as screening tests for occult DCM. A biomarker that detects early cardiomyopathy in asymptomatic patients would have substantial clinical utility. Based on the results of these studies, cut-off values, sensitivity, specificity, and positive and negative predictive values will help determine how to use this test in a clinical setting for predisposed dogs, such as Dobermans, Boxers, and Great Danes.

Considerations for interpretation of result As NT-proBNP testing becomes more widely available, there are some factors to consider regarding interpretation of the results. In a study comparing normal dogs to dogs with renal azotemia (and structurally normal hearts), the renal dysfunction group had a serum mean NT-BNP level of 1069 pmol/L (range 179-2071), which was significantly elevated compared to the normal group (mean 282 pmol/L, range 179578 pmol/L) (10). Thus, renal dysfunction may falsely elevate canine NT-proBNP concentrations, as is the case in humans. Little is known about the day-to-day variation in NT-proBNP concentrations. Theoretically, diet, water intake, and exercise could influence the NT-proBNP concentration in both healthy and diseased dogs. In a study of weekly variation of



BIOMARKERS IN THE DIAGNOSIS OF CANINE HEART DISEASE

NT-proBNP in healthy dogs, the variability in serum and plasma NT-proBNP was as high as 51% in some dogs. The degree of variation caused some dogs to occasionally test above the current upper reference limit of 566 pmol/L. Thus, overtly healthy dogs, with only mild elevation of a single NT-proBNP test, may benefit from serial testing (11). While NT-proBNP and NT-proANP are more stable than their C-terminal counterpart, strict adherence to the sample handling, storage, and shipping directions as provided by the assay manufacturer should be followed. Plasma or serum samples should be separated quickly and frozen as significant degradation of NT-proBNP occurs within 3 to 5 hours if samples are allowed to reach temperatures above 4° C (12). In summary, based on the currently available research, blood natriuretic peptides can be used in conjunction with other diagnostic tools, including physical examination, radiography, and echocardiography to help diagnose heart disease and determine the underlying cause of respiratory signs in dogs. The NT-proBNP assay may also have utility in detecting occult cardiomyopathy in asymptomatic dogs. The current recommendations indicate that heart disease is unlikely in dogs if the NT-proBNP level is <566 pmol/L. In patients with respiratory signs, an NT-proBNP greater >1200 pmol/L is likely associated with congestive heart failure. Most of the current literature involves NT-proBNP testing, and the clinical utility of NT-proANP is slightly less clear; further studies are warranted to determine the best way to use this test in conjunction with NT-proBNP or other cardiac biomarkers, such as cardiac troponin.

Cardiac troponin The troponin complex is composed of 3 subunits (cTnI, cTnT, and cTnC) that help regulate excitationcontraction coupling in the cardiac myocyte. cTnI is the inhibitory component that prevents interaction between actin and myosin until cTnC binds to calcium ions. Injury to the sarcomere causes detachment of cTnI from actin and subsequent disruption of the cellular membrane allows leakage of cTnI into the general circulation. Therefore, a high level of cTnI detected in serum or plasma is considered to be a highly sensitive and specific

indicator of myocardial cell damage and necrosis. The close homology of cTnI among mammals allows accurate measurement in dogs and cats using immunoassays developed for humans. In human medicine, cardiac troponins are an integral diagnostic criteria of acute coronary syndromes. Elevated cTnI can be detected within 3-4 hours following the onset of myocardial injury and remain increased for 4-7 days after the initial myocardial infarction. Chronically, heart failure patients retain modest elevations in circulating cTnI, which can be used to monitor progression of disease and provides prognostic information. Elevated cTnI is associated with adverse long-term outcome and is an independent predictor of mortality (13,14). It is likely that cTnI measurement in veterinary patients offers similar prognostic information, despite the fact that myocardial infarction is relatively less common in dogs.

Detection of myocardial damage Cardiac troponin I immunoassays have been validated in dogs (15,16). cTnI is a marker of myocardial necrosis and is not specific to the underlying cause of the myocardial damage; this means that primary heart disease or systemic disease that secondarily affects the heart can cause cTnI elevations. In human medicine, endstage renal failure, sepsis, and trauma are reported causes of elevated values. In dogs, pyometra, gastric dilatation-volvulus (GDV), pericardial effusion, trauma, and sepsis can cause dramatic increases in cTnI. Myocarditis can cause 100-fold increases in cTnI, as occurs in dogs afflicted with babesiosis and Chagas’ disease. Cardiac troponin can be used in conjunction with other diagnostics to provide prognostic information in cases of sepsis and GDV. In patients with acute arrhythmias or systolic dysfunction, extreme elevation in cTnI is consistent with myocarditis and can be a tool to monitor response to therapy. In a small pilot study, Linklater, et al. (17) showed a decreased survival time in dogs with mitral valve disease who had elevated cTnI and presented to the emergency hospital for congestive heart failure. Further studies are indicated to better classify the prognostic ability of cTnI in congenital and acquired heart disease.




BIOMARKERS IN THE DIAGNOSIS OF CANINE HEART DISEASE

Diagnosis of heart disease Oyama, et al. evaluated cTnI in 269 dogs with and without heart disease. They reported significant elevation in cTnI in dogs with cardiomyopathy (median 0.14 ng/mL), mitral valve disease (0.11 ng/mL), and subaortic stenosis (0.08 ng/mL), compared to healthy dogs (0.03 ng/mL). A decreased median survival time was found in dogs with cardiomyopathy and cTnI greater than 0.20 ng/mL (18). In Boxers with arrhythmogenic right ventricular cardiomyopathy, cardiac troponin can be elevated (19). In another study of Dobermans, Boxers, and Great Danes with occult dilated cardiomyopathy, cTnI was significantly increased when compared with healthy dogs (19); however, although cTnI is elevated in many asymptomatic dogs, the lack of specificity of this test makes it unlikely to be useful as a standalone screening test. In this instance, strategies

that combine various biomarker assays, such as testing for both cTnI and NT-proBNP may provide a better diagnostic tool for asymptomatic patients. Further studies are needed to assess the sensitivity, specificity, and predictive value of this combination.

Conclusion Cardiac biomarkers are an exciting new tool for the diagnosis of heart disease in dogs. NT-proBNP tests can be used to help diagnose heart disease and distinguish cause of respiratory signs in dogs. Cardiac troponin tests reflect the severity of t he underlying myocardial damage, and are likely to be correlated with prognosis. As research continues and these tests become more widely used in clinical practice, other applications such as risk assessment, monitoring therapy, and prognostic ability will likely be further elucidated.

REFERENCES 1. Swedberg K, Cleland J, Dargie H, et al. Guidelines for the diagnosis and treatment of chronic heart failure: executive summary (update 2005): The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology. Eur Heart J 2005; 26: 1115-1140. 2. Maisel A, Bhalla V, Braunwald E. Cardiac biomarkers: a contemporary status report. Nat Clin Pract Cardiovasc Med 2006; 3(1): 24-34. 3. Boswood A, Dukes-McEwan J, Loureiro J, et al. The diagnostic accuracy of different natriuretic peptides in the investigation of canine cardiac disease. J Small Anim Pract 2008: 49(1): 26-32. 4. Oyama M, Fox P, Rush J, et al. Clinical utility of serum N-terminal pro-Btype natriuretic peptide concentration for identifying cardiac disease in dogs and assessing disease severity. J Am Vet Med Assoc 2008; 232(10): 1496-1503. 5. Fine D, Declue A, Reinero C. Evaluation of circulating amino terminalpro-B-type natriuretic peptide concentration in dogs with respiratory distress attributable to congestive heart failure or primary pulmonary disease. J Am Vet Med Assoc 2008; 232(11): 1674-1679. 6. Oyama M, Rush J, Rozanski E, et al. NT-pro-BNP assay distinguishes cardiac vs primary respiratory causes of respiratory signs in dogs (abstr) in Proceedings. 26th Annu Forum Am Coll Vet Intern Med 2008.

10. Schmidt M, Reynolds C, Estrada A, et al. Effect of renal dysfunction on Nterminal pro-B-type natriuretic peptide: a canine biomarker for heart disease (abstr) in Proceedings. 26th Annu Forum Am Coll Vet Intern Med 2008. 11. Kellihan H, Oyama M, Reynolds C, et al. Weekly variability of plasma and serum NT-pro-BNP measurements in normal dogs (abstr) in Proceedings. 26th Annu Forum Am Coll Vet Intern Med 2008. 12. Farace G, Beardow A, Carpenter C, et al. Effect of shipping temperature on canine N-terminal prohormone atrial natriuretic peptide and N-terminal prohormone brain natriuretic peptide (abstr) in Proceedings. 26th Annu Forum Am Coll Vet Intern Med 2008. 13. Healey J, Davies R, Smith S, et al. Prognostic use of cardiac troponin T and troponin I in patients with heart failure. Can J Cardiol 2003; 19(4): 383-386. 14. Peacock W, DeMarco M, Fonarow M, et al. Cardiac trtoponin and outcome in acute heart failure. N Engl J Med 2008; 358: 2117-2126. 15. Schober K, Kirbach B, Oechtering G. Noninvasive assessment of myocardial cell injury in dogs with suspected cardiac contusion. J Vet Cardiol 1999; 1:17-25. 16. Sleeper M, Clifford C, Laster L. Cardiac troponin I in the normal dog and cat. J Vet Intern Med 2001; 15(5): 501-503.

7. Wess G, Timper N, Hirschberger J. The utility of NT-pro-BNP to differentiate cardiac and respiratory causes of coughing or dyspnea in dogs (abstr) in Proceedings. 25th Annu Forum Am Coll Vet Intern Med 2007.

17. Linklater A, Lichtenberger M, Thamm D, et al. Serum concentrations of cardiac troponin I and cardiac troponin T in dogs with class IV congestive heart failure due to mitral valve disease. J Vet Emerg Crit Care 2007; 17(3): 243-249.

8. Fine D, DeClue A, Reinero C. Brain natriuretic peptide for discrimination of respiratory distress due to congestive heart failure or primary respiratory disease (abstr) in Proceedings. 25th Annu Forum Am Coll Vet Intern Med 2007.

18. Oyama M, Sisson D. Cardiac troponin-I concentration in dogs with cardiac diease. J Vet Intern Med 2004; 18: 831-839.

9. Oyama M, Sisson D, Solter P. Prospective screening for occult cardiomyopathy in dogs by measurement of plasma atrial natriuretic peptide, B-type natriuretic peptide, and cardiac troponin-I concentrations. Am J Vet Res 2007; 68(1): 42-47.


19. Baumwart R, Orvalho J, Meurs K. Evaluation of serum cardiac troponin I concentration in Boxers with arrhythmogenic right ventricular cardiomyopathy. Am J Vet Res 2007; 69(5): 524-528.



New echocardiographic and Doppler techniques

Valérie Chetboul, DVM, PhD, Dipl. ECVIM-CA (Cardiology) The Cardiology Unit of the National Veterinary School of Alfort, Dr. Chetboul graduated in Veterinary Medicine from the National Veterinary School of Alfort in 1984. She completed a postgraduate course in university teaching at the same school and is currently working as a Professor in Small Animal Internal Medicine and Cardiology. Valérie Chetboul also belongs to a Cardiology Research Unit (National Institute of Health and Medical Research) attached to the Paris XII University where she is responsible for the non-invasive cardiovascular imaging in small and large animals. She was awarded her PhD in Gene therapy in the cardiology field in 2000 from the Paris XII University and became a Diplomate of the European College of Veterinary Internal Medicine (Cardiology section) in 1999. Dr. Chetboul was editorin-chief of the Journal of Veterinary Cardiology (2002-2006) and is currently co-editor of the Cardiovascular Imaging section of the Journal.

KEY POINTS ± Tissue Doppler imaging (TDI) offers a non-invasive

and sensitive Doppler analysis of regional myocardial motion thanks to the quantification of myocardial velocities in real time ± The main advantage of the two-dimensional color TDI mode over the pulsed-wave TDI mode and the color TDI M-mode is its ability to simultaneously quantify myocardial velocities in several segments within 1, 2 or 3 myocardial walls ± Strain and strain rate imaging are two TDI-derived techniques allowing quantitative assessment of regional myocardial deformation and rate of deformation, respectively ± Two-dimensional speckle tracking echocardiography is a newly-developed ultrasound technique providing a non-Doppler assessment of regional myocardial motion, including velocity, strain and strain rate, displacement, and also amplitude of systolic rotation

Introduction Quantitative assessment of myocardial function is of great importance in the diagnosis, treatment, and management of heart diseases and also in the understanding of their physiopathology. Standard echocardiography is commonly performed on both humans and small animals to non-invasively assess myocardial function, and several bidimensional (2D) and M-mode measurements such as systolic left ventricular diameter and index volume or fractional shortening (%FS) are often used as indices of myocardial performance. Tissue Doppler imaging (TDI) and its derived modalities, strain (St) and strain rate (SR) imaging, are newly-developed ultrasound techniques permitting quantitative assessment of myocardial function by calculating myocardial velocities in real time (1,2) and by measuring myocardial segmental deformation (contraction or stretching) and rate of deformation (3,4), respectively. Two-dimensional speckle tracking




various myocardial parameters including velocity, St and SR, displacement, and also amplitude of systolic rotation (5-7).

Tissue Doppler imaging Physical basics of TDI are similar to those of conventional Doppler imaging, except the fact that TDI is based on the ability of ultrasound instruments to eliminate Doppler information coming from blood flow and to keep those from the myocardial wall (1). In order to display the low velocity/high amplitude Doppler signals of the myocardium and to suppress the high velocity/low amplitude Doppler signals of blood flow, specific adjustments of Doppler setting are required such as the suppression of high- filters and decrease in gain setting (1).

TDI modes Figure 1. The three TDI modes: the pulsed-wave mode (1A), the color M-mode (1B) and the two-dimensional (2D) color mode (1C). 1A: The pulsed-wave TDI mode provides information on myocardial movements through a single sample volume, which is placed within the myocardial wall thickness. When the myocardium moves towards the transducer, myocardial velocities are positive (above the baseline). Conversely, when the myocardium moves away from the transducer, myocardial velocities are negative (under the baseline). 1B: This color M-mode TDI tracing of the left ventricular free wall (radial motion) shows on the same image both systolic and diastolic velocities within the entire wall thickness. Myocardial velocities towards the transducer are encoded in red, and those away from the transducer in blue. Using a specific software, the mean myocardial velocity (defined as the average of velocity values measured along each M-mode scan line throughout the myocardial wall thickness) may then be calculated throughout the whole cardiac cycle. 1C: Using the 2D color mode, myocardial velocities are superimposed on 2D mode images (here right parasternal transventricular short axis view). Velocities towards the transducer are colored in red whereas those away from the transducer are colored in blue. Using a specific software myocardial velocities may then be analyzed within one or several segments (see Figure 2). LV: left ventricle.

echocardiography (2D STE) is an even more recent ultrasound modality based on 2D grayscale echocardiographic images. This non-invasive technique provides a new opportunity for the non-Doppler assessment of regional myocardial motion, thanks to the measurement of


Three TDI modes are available (1). The pulsedwave TDI mode provides information on myocardial movements through a single sample gate, which is placed within the myocardial wall thickness to analyze its radial or longitudinal motion (Figure 1A). With the color M-mode (Figure 1B), myocardial velocities are analyzed along a selected single scan line, which is placed in the same manner as for conventional transventricular M-mode to analyze the radial motion of the interventricular septum (IVS) or the left ventricular free wall (LVFW). Using 2D color TDI mode (Figure 1C), real time color Doppler is superimposed on the gray-scale of 2D mode images and the Doppler receive gain is adjusted to maintain optimal coloring of the myocardium. One of the main advantages of 2D color TDI mode over the two others is its ability to simultaneously quantify myocardial velocities in several segments within 1, 2 or 3 walls, thereby allowing assessment of intra- and interventricular myocardial synchrony (Figures 2 and 3, (8)).

Left and right normal TDI myocardial velocity profiles: the normal non-uniform aspect Radial and longitudinal LVFW velocities may be quantified with correct to good repeatability and reproducibility in small animals using the right parasternal short axis view and the left apical 4-chamber view, respectively (9,10). After a short isovolumic contraction phase (9-14), all radial and



NEW ECHOCARDIOGRAPHIC AND DOPPLER TECHNIQUES

Figure 2. Example of normal radial velocity profiles recorded within 2 segments of the left ventricular free wall using the two-dimensional color TDI mode in a healthy dog (right parasternal transventricular short axis view). This simultaneous recording of myocardial velocities in a sub-endocardial (yellow) and sub-epicardial (green) segment indicates that the sub-endocardium is moving more rapidly than the sub-epicardium in systole and also in diastole, thus defining a marked myocardial velocity gradient throughout the whole cardiac cycle. As with the pulsed-wave TDI mode, myocardial velocities are positive when the myocardium moves towards the transducer whereas they are negative when it moves away from the transducer. Color display of velocity is superimposed on the right parasternal transventricular short axis view (left upper ). A: peak myocardial velocity during late diastole. AVC: aortic valve closure. AVO: aortic valve opening. E: peak myocardial velocity during early diastole. IVC: isovolumic contraction phase. IVR: isovolumic relaxation phase. LV: left ventricle. S: peak myocardial velocity during systole.

longitudinal velocity profiles include one positive systolic wave (S), and after a short isovolumic relaxation phase, two diastolic negative waves (E and A, respectively in early and late diastole, Figures 2 and 4). Fusion of the two negative diastolic waves E and A into one negative diastolic wave EA is often observed in the cat due to a rapid heart rate (9). Normal radial LVFW motion is characterized by non-uniformity (13,14), with myocardial layers moving more rapidly in the sub-endocardium than in the sub-epicardium, thus creating an intra-myocardial radial velocity gradient throughout the cardiac cycle (MVG, Figure 2). Normal longitudinal myocardial motion is also characterized by non-uniformity (9-14), with myocardial velocities decreasing from the base to the apex, thus producing a longitudinal MVG (Figure 4). A physiologic heterogeneity in the longitudinal myocardial motion has also been demonstrated in the normal cat between the IVS and the LVFW, with higher early diastolic velocities, acceleration,

and deceleration in the former than in the latter (15). Similarly (16), longitudinal right ventricular myocardial (RVM) velocities have been shown to be higher at the base than the apex, and also higher than LVFW velocities of the corresponding segment (basal or apical). This additional heterogeneity may be explained by the difference in loading conditions between the two ventricles, and probably also by the differing regional myocardial fiber architecture.

Factors of variations The main factors of variation of TDI variables are breed, heart rate, and anesthesia. For example, in one study (13) involving a large population of healthy dogs (n=100), a breed effect was demonstrated for longitudinal S wave measured at the base. In the dog (13), a positive correlation has been shown between heart rate and longitudinal S wave at the base. A similar relationship between heart rate and systolic velocities has been reported in the cat (14), involving radial subendocardial and sub-epicardial S waves, as well as




Figure 3. Example of interventricular dyssynchrony assessed by the two-dimensional color TDI mode in a dog with dilated cardiomyopathy. The longitudinal velocity profiles obtained from 3 basal segments of the left ventricular free wall (LVFW, red), the interventricular septum (IVS, green), and the right myocardial wall (RVMW, yellow) show a delayed peak systolic LVFW velocity (arrows) compared with the 2 others. Color display of velocity is superimposed on the left apical 4-chamber view (left upper ). S: peak myocardial velocity during systole. LA: left atrium. LV: left ventricle. RA: right atrium. RV: right ventricle.

Figure 4. Example of normal longitudinal velocity profiles recorded within 2 segments of the left ventricular free wall using the two-dimensional color TDI mode in a healthy dog (left apical 4-chamber view). This simultaneous recording of myocardial velocities in a basal (yellow) and apical (green) segment indicates that the base is moving more rapidly than the apex in systole and also in diastole, thus defining a myocardial velocity gradient throughout the whole cardiac cycle. Color display of velocity is superimposed on the left apical 4-chamber view (left upper ). A: peak myocardial velocity during late diastole. AVC: aortic valve closure. AVO: aortic valve opening. E: peak myocardial velocity during early diastole. IVC: isovolumic contraction phase. IVR: isovolumic relaxation phase. LA: left atrium. LV: left ventricle. S: peak myocardial velocity during systole.





Figure 5. Example of abnormal radial velocity profiles recorded within 2 segments of the left ventricular free wall using the two-dimensional color TDI mode in a young Golden Retriever dog with muscular dystrophy (right parasternal transventricular short axis view). The sub-endocardial (yellow) and sub-epicardial (green) velocity profiles are nearly superimposed in systole, thus indicating a very low systolic myocardial velocity gradient (double arrows, for comparison see normal radial velocity profiles in Figure 2). This TDI systolic dysfunction was not detected using conventional echocardiography (fractional shortening of 38%, i.e., within the normal ranges). Color display of velocity is superimposed on the right parasternal transventricular short axis view (left upper ). A: peak myocardial velocity during late diastole. AVC: aortic valve closure. AVO: aortic valve opening. E: peak myocardial velocity during early diastole. IVC: isovolumic contraction phase. IVR: isovolumic relaxation phase. LV: left ventricle. RV: right ventricle. S: peak myocardial velocity during systole.

longitudinal annular and basal S waves. One study performed on healthy dogs (10) showed that anesthesia significantly decreases both radial and longitudinal myocardial velocities, up to 60% compared to values measured in awake animals.

Current applications of the TDI technique TDI offers a non-invasive, sensitive, and quantitative analysis of regional myocardial motion. One of the major applications of the TDI technique is the detection of slight myocardial alterations that are equivocal or even not apparent using conventional ultrasound techniques. Using a dog model of dilated cardiomyopathy (DCM), our group demonstrated (17) that TDI is more sensitive than conventional echocardiography in detecting preclinical regional myocardial abnormalities before occurrence of left ventricular dilation and overt systolic dysfunction (Figure 5). Similarly, in a feline model of hypertrophic cardio-

myopathy, TDI has been shown to consistently detect LVFW dysfunction despite the absence of myocardial hypertrophy in affected males and in carrier females (18). TDI may also be used to accurately investigate myocardial dysfunction associated with heart diseases, thus providing new insights in the understanding of their pathophysiology. For example, diastolic dysfunction has traditionally been thought to be the only abnormality in cats with HCM. One study using the 2D color TDI mode showed that systolic dysfunction is an additional component of myocardial alteration (19). Such a systolic dysfunction is characterized by a decrease in longitudinal systolic velocities and gradients (despite normal or increased fractional shortening) and the high prevalence of post-systolic contraction waves (Figure 6). A recent study performed by another group using the pulsed-wave TDI mode confirmed these




Figure 6. Example of abnormal longitudinal velocity profiles recorded within 2 segments of the left ventricular free wall using the two-dimensional color TDI mode in a cat with hypertrophic cardiomyopathy (left apical 4-chamber view). Note that E is lower than A in the basal segment (yellow curve), thus confirming a diastolic dysfunction. Moreover, the apical velocity curve (green curve) shows post-systolic contraction waves (green arrows), which were confirmed using strain imaging. A: peak myocardial velocity during late diastole. E: peak myocardial velocity during early diastole. S: peak myocardial velocity during systole.

results, demonstrating a systolic impairment along the longitudinal axis of the LVFW in cats with HCM (15). Another important TDI application is the assessment of a treatment effect on myocardial function. For example, our group has recently used the TDI technique to demonstrate the beneficial regional systolic myocardial effect of non-cultured skeletal muscle cell transplantation in an animal model of non-ischemic DCM (20).

Strain and strain rate imaging St and SR imaging are two TDI-based techniques that complete the TDI analysis by measuring myocardial segmental deformation and rate of deformation, respectively. Both Doppler techniques have been shown to be repeatable and reproducible methods for assessing systolic radial and longitudinal LVFW function, and also systolic longi-


Figure 7. Example of normal regional radial strain (7A) and strain rate (7B) profiles recorded within the left ventricular free wall in a healthy dog (right parasternal transventricular short axis view). The radial strain profile (expressed in %) is positive and maximal in end-systole (arrows), and then decreases during diastole, thus confirming a regional systolic expansion (i.e., thickening) and a diastolic compression (i.e., shortening), respectively (7A). The strain rate profile (expressed in s-1) is positive during systole (SRS) indicating a regional thickening and then features 2 negative diastolic peaks during early filling and atrial contraction (SRE and SRA) corresponding to a biphasic thinning phase. Color display of strain and strain rate are superimposed on the right parasternal transventricular short axis views (left upper s of Figures 7A and 7B, respectively). Strain length = 12 mm. Region of interest size = 3/3 mm. AVC: aortic valve closure. AVO: aortic valve opening. LV: left ventricle.

tudinal function of the IVS and the RVM in the awake dog (4). Myocardial St represents the deformation of a myocardial segment over time (3,4) and is expressed as the % of change from its original dimension (Figure 7A). Myocardial SR is the temporal derivative of St (3,4) and is measured in s-1 (Figure 7B). SR describes the rate of myocardial deformation, that is, how quickly




Figure 8. Example of an abnormal regional longitudinal strain profile recorded within the right ventricular myocardial wall in a dog with pulmonary arterial stenosis (left apical 4-chamber view). The longitudinal strain profile is negative, thus confirming a regional compression (i.e., myocardial shortening) during systole. However, the maximal negative strain value is measured after T wave on the ECG tracing, i.e., in diastole instead of systole. These post-systolic contraction waves (PSC) confirm a marked right myocardial systolic dysfunction. This systolic dysfunction is also characterized by a peak systolic strain (arrows) lower than the published reference ranges (4). Color display of velocity is superimposed on the left ventricular 4-chamber view (left upper ). Strain length = 12 mm. Region of interest size = 6/3 mm. AVC: aortic valve closure. AVO: aortic valve opening. RA: right atrium. RV: right ventricle.

a myocardial segment shortens or lengthens. Therefore, compared to TDI, St and SR imaging offer true measures of local myocardial deformation, thereby separating active from ive myocardial motion (3,4). Conversely, myocardial velocities assessed by TDI do not discriminate between actively contracting myocardium and ive motion due to heart translation and tethering effects. Regional systolic St and SR have already been shown to be powerful and sensitive non-invasive indices of myocardial contractility (Figure 8), and these indices have also been suggested to be sensitive and effective measures of myocardial synchrony (3,8). However, St and SR imaging present several major limitations resulting in a high risk of misinterpretation. These include angle dependency (as for the TDI technique), a low signal to noise ratio (particularly for SR imaging), and many types of artifacts due to stationary reverberations, dropout zones, and low lateral resolution. These artifacts may create false regional myocardial

akinesia or dyskinesia. St and SR curves should therefore always be interpreted carefully by a trained observer while taking into both the alignment with the ultrasound beam and the location of the sample area throughout the cardiac cycle. Myocardial segments with obvious artifacts should always be excluded from post-processing analysis.

Two-dimensional speckle tracking echocardiography 2D STE is the most recent ultrasound technique developed in cardiology to assess regional myocardial function concomitantly in several segments (5-7). The 2D STE principle is based on the formation of speckle patterns due to reflection, scattering, and interferences between tissue and ultrasound beams in routine grayscale 2D echocardiographic images (5-7). These speckles appear as small, bright elements homogeneously distributed within the myocardium on 2D mode images. They represent natural acoustic tissue markers that can be tracked from frame to frame throughout the cardiac cycle. Thus 2D STE allows




Figure 9. Example of normal left ventricular (LV) rotation profiles recorded within 6 apical myocardial segments using two-dimensional speckle tracking echocardiography in a healthy dog (right parasternal apical short axis view). The software algorithm has automatically defined 6 equidistant myocardial segments within the interventricular septum and the LV free wall. Figure 9 shows on the right the 6 corresponding LV apical rotation versus time curves, and the orange dotted line the averaged LV rotation versus time curve of the 6 segments. As seen from the apex, the 6 myocardial segments go through a homogenous systolic wringing motion with an initial clockwise rotation (negative rotation) followed by a dominant counterclockwise rotation (positive rotation). This may also be observed on 2D color-coded views (left) showing a clockwise (red) and then counterclockwise (blue) rotation in early and end-systole (ES), respectively.

a non-Doppler assessment of regional myocardial motion (velocity, rotation, St, and SR) by filtering out these random speckles, and then performing autocorrelations to evaluate the motion of stable structures. One of the major advantages of 2D STE compared to the Doppler-based techniques, such as TDI or TDI-derived techniques (St and SR imaging), is its independence of both cardiac translation and insonation angle. When the latter are used, an incorrect alignment between the ultrasound beam and the myocardial wall motion may lead to substantial errors (underestimation of velocity, St, and SR), which is not the case with 2D STE. Another advantage of 2D STE is that it offers direct measures of myocardial displacement, whereas with Doppler-based techniques, all measurements are done in reference to an external point, e.g., the transducer. Our group has shown that 2D STE is a repeatable and reproducible method for assessing radial LV


St and SR in the awake dog. Moreover, these non-Doppler measurements correlate well with those obtained by the TDI-based techniques, at least in normal myocardial segments (6). However, which of these techniques is actually the best (particularly the most sensitive for the detection of myocardial dysfunction) still remains unknown. Another study (7) demonstrated that 2D STE provides also a repeatable and reproducible noninvasive assessment of the systolic LV wringing motion in the awake dog (Figure 9). Peak LV basal and apical systolic rotations and systolic global LV torsion, defined as apical rotation relative to the base, have been shown to be altered in dogs with hypokinesia (7). Similar alterations of the LV systolic wringing motion also have been identified in humans with various heart diseases (DCM and myocardial infarction) and could contribute to a certain extent to the reduction in stroke volume in these pathologic settings.




Similarly to the other three ultrasound methods, 2D STE presents several technical limitations, including the failure to obtain reliable STE measurements mostly because of reverberation artifacts and drop-outs, and also because of the use of shortaxis images (6). Regarding the latter, longitudinal myocardial motion may cause speckles to move in or out of the image plane, thereby decreasing the reliability and the possibility of the speckle tracking process.

Conclusion The recent development of Doppler imaging techniques, such as TDI, St and SR imaging, offers a new opportunity for the non-invasive assessment of regional myocardial function in small animals.

The non-Doppler technique, 2D STE, may provide a complement or alternative to the TDI and TDIbased techniques to quantify myocardial synchrony and also to assess the complex pattern of regional myocardial motion including the LV wringing motion. The combined use of these imaging indices, whose repeatability and reproducibility are adequate for routine clinical use, provides additional information beyond that obtained from conventional echocardiography. Further studies are now required in large populations of diseased patients to determine the comparative clinical relevance of these new imaging variables, and their potential additive value with regards to prognosis and therapeutic implications.

REFERENCES 1. Chetboul V. Tissue Doppler Imaging: a promising technique for quantifying regional myocardial function. J Vet Cardiol 2002; 4: 7-12. 2. Uematsu M, Miyatake K, Tanaka N, et al. Myocardial velocity gradient as a new indicator of regional left ventricular contraction: detection by a two-dimensional tissue Doppler imaging technique. J Am Coll Cardiol 1995; 26: 217-223. 3. D’hooge J, Heimdal A, Jamal F, et al. Regional strain and strain rate measurements by cardiac ultrasound: principles, implementation and limitations. Eur J Echocardiography 2000; 1: 154-170. 4. Chetboul V, Carlos Sampedrano C, Gouni V, et al. Ultrasonographic assessment of regional radial and longitudinal systolic function in healthy awake dogs. J Vet Intern Med 2006; 20: 885-893. 5. Helle-Valle T, Crosby J, Edvardsen T, et al. New noninvasive method for assessment of left ventricular rotation: speckle tracking echocardiography. Circulation 2005; 112: 3149-3156. 6. Chetboul V, Serres F, Gouni V, et al. Radial strain and strain rate by two-dimensional speckle tracking echocardiography and the tissue velocity based technique in the dog. J Vet Cardiol 2007; 9: 69-81. 7. Chetboul V, Serres F, Gouni V, et al. Non-invasive assessment of systolic left ventricular torsion by 2-dimensional speckle tracking imaging in the awake dog: repeatability, reproducibility, and comparison with tissue Doppler imaging variables. J Vet Intern Med 2008; 20: 885-893. 8. Estrada A, Chetboul V. Tissue Doppler evaluation of ventricular synchrony. J Vet Cardiol 2006; 8: 129-137. 9. Chetboul V, Athanassiadis N, Carlos Sampedrano C, et al. Quantification, repeatability, and reproducibility of feline radial and longitudinal left ventricular velocities by tissue Doppler imaging. Am J Vet Res 2004; 65: 566-572. 10. Chetboul V, Athanassiadis N, Carlos Sampedrano C, et al. Assessment of repeatability, reproducibility, and effect of anesthesia on determination of radial and longitudinal left ventricular velocities via tissue Doppler imaging in dogs. Am J Vet Res 2004; 65: 909-915.

12. Gavaghan BJ, Kittleson MD, Fisher KJ, et al. Quantification of left ventricular diastolic wall motion by Doppler tissue imaging in healthy cats and cats with cardiomyopathy. Am J Vet Res 1999; 60: 1478-1486. 13. Chetboul V, Carlos Sampedrano C, Concordet D, et al. Use of quantitative two-dimensional color tissue Doppler imaging for assessment of left ventricular radial and longitudinal myocardial velocities in dogs. Am J Vet Res 2005; 66: 953-961. 14. Chetboul V, Carlos Sampedrano C, Tissier R, et al. Quantitative assessment of velocities of the annulus of the left atrioventricular valve and left ventricular free wall in healthy cats by use of two-dimensional color tissue Doppler imaging. Am J Vet Res 2006; 67: 250-258. 15. Koffas H, Dukes-McEwan J, Corcoran BM, et al. Pulsed tissue Doppler imaging in normal cats and cats with hypertrophic cardiomyopathy. J Vet Intern Med 2006; 20: 65-77. 16. Chetboul V, Carlos Sampedrano C, Gouni V, et al. Quantitative assessment of regional right ventricular myocardial velocities in awake dogs using Doppler tissue imaging: repeatability, reproducibility, effect of body weight and breed, and comparison with left ventricular myocardial velocities. J Vet Intern Med 2005; 19: 837-44. 17. Chetboul V, Escriou C, Tessier D, et al. Tissue Doppler imaging detects early asymptomatic myocardial abnormalities in a dog model of Duchenne's cardiomyopathy. Eur Heart J 2004; 25: 1934-1939. 18. Chetboul V, Blot S, Carlos Sampedrano C, et al. Tissue Doppler imaging for detection of radial and longitudinal myocardial dysfunction in a family of cats affected by dystrophin-deficient hypertrophic muscular dystrophy. J Vet Intern Med 2006; 20: 640-647. 19. Carlos Sampedrano C, Chetboul V, Gouni V, et al. Systolic and diastolic myocardial dysfunction in cats with hypertrophic cardiomyopathy or systemic hypertension. J Vet Intern Med 2006; 20: 1106-1115. 20. Borenstein N, Chetboul V, Bruneval P, et al. Non-cultured cell transplantation in an ovine model of non-ischemic heart failure. Eur J Cardiothorac Surg 2007; 31: 444-451.

11. Koffas H, Dukes-McEwan J, Corcoran BM, et al. Peak mean myocardial velocities and velocity gradients measured by color M-mode tissue Doppler imaging in healthy cats. J Vet Intern Med 2003; 17: 510-524.




Interventional cardiovascular procedures Suzanne Cunningham, DVM, Dipl. ACVIM (Cardiology)

John Rush, DVM, MS, Dipl. ACVIM (Cardiology), Dipl. ACVECC

Department of Clinical Sciences, Tufts Cummings School of Veterinary Medicine, North Grafton, USA

Department of Clinical Sciences, Tufts Cummings, School of Veterinary Medicine, North Grafton, USA

Dr. Cunningham is a Clinical Professor of Cardiology at Tufts Cummings School of Veterinary Medicine in North Grafton, MA. She received her DVM from Cornell University in 2003 and completed a Small Animal Medicine internship, and residency in Cardiology at Tufts Cummings School of Veterinary Medicine. Suzanne Cunningham recently became a Diplomate of the American College of Veterinary Internal Medicine in Cardiology. Her current research interests include interventional cardiology and investigation of novel therapies for cardiomyopathy and congestive heart failure.

Dr. Rush is Professor at the Tufts Cummings School of Veterinary Medicine in North Grafton, MA. He is a Diplomate of the American College of Veterinary Internal Medicine in Cardiology and also a Diplomate of the American College of Veterinary Emergency and Critical Care. He obtained his DVM and Master’s Degree from the Ohio State University, completed an internship at the Animal Medical Center in New York, and did a residency at the University of Wisconsin-Madison. Dr. Rush has a number of publications in the fields of cardiology and emergency and critical care medicine.

Introduction The advent of minimally invasive, catheter-based interventions has revolutionized the treatment of cardiovascular disease in people and transcatheter interventions are becoming more commonplace in veterinary medicine. Transcatheter procedures allow for the correction of several congenital and acquired cardiac defects without the attendant morbidity and mortality associated with surgery. Since the first balloon valvuloplasty was performed in a Bulldog in 1980, the scope of interventional procedures has expanded to include myriad novel techniques. Interventional procedures are now commonly used for the successful treatment of patent ductus arteriosus, pulmonic stenosis, atrioventricular valve stenoses, vascular stenoses, atrial and ventricular septal defects, heartworm disease, and life-threatening bradyarrhythmias, conditions that were once treatable only with considerable surgical morbidity and mortality. The focus of


this paper is to introduce the most common interventional procedures available for the treatment of congenital and acquired cardiovascular diseases in companion animals.

Patent ductus arteriosus Patent ductus arteriosus (PDA) is one of the most common congenital heart defects in the dog, but is uncommon in the cat. Failure of ductus closure results in left-to-right shunting with resultant pulmonary overcirculation, cardiac enlargement, pulmonary vascular injury, and congestive heart failure (CHF) that typically develops by one year of age. Typical diagnostic findings in left-to-right shunting PDA include a continuous cardiac murmur at the left heart base and hyper-dynamic arterial pulses. Thoracic radiographs demonstrate pulmonary overcirculation. Echocardiographic findings typically reveal a volume overload to the left heart and continuous turbulent blood flow



Figure 1. Stainless steel embolization coils of varying sizes. Thrombus formation is stimulated by the synthetic Dacron fibers embedded within the coils.

in the main pulmonary artery originating from the junction of the ductus arteriosus. Due to the high likelihood of progression to CHF, closure of the PDA is recommended in virtually all cases. Transcatheter PDA occlusion provides a minimally invasive alternative to open surgical ligation, circumventing the need for thoracotomy and its attendant surgical morbidity. While successful in experienced hands, surgical PDA ligation via thoracotomy carries the risk of catastrophic hemorrhage due to tearing of the ductus and surgical mortality has been reported to range from 4 to 10%. Transcatheter PDA occlusion may be achieved by coil embolization or deployment of various self-expanding devices designed for human patients (1) or dogs (2).

Figure 2. Lateral selective angiograms in a young female Papillon with a patent ductus arteriosus (PDA). In the left hand contrast is injected in the descending aorta and blood flow is documented through the PDA and into the main pulmonary artery. The angiogram in the right hand was obtained following deployment of a coil in the PDA and confirms complete occlusion of ductal flow.

Coil occlusion entails the transcatheter delivery of embolization coils into the ductal lumen (Figure 1). The coils are made of metal (e.g., stainless steela) and are manufactured to retain a helical structure after deployment from the catheter. Enmeshed within the coils are synthetic Dacron fibers, which stimulate thrombus formation. The PDA is most commonly accessed from the ascending aorta using femoral arterial access. Selective angiography allows delineation of ductal anatomy and measurement of the minimal ductal diameter to determine the feasibility of coil occlusion and allow selection of appropriately sized coils. When deployed within the target vessel, the resulting thrombus formation results in occlusion of ductal flow (Figure 2). Successful coil deployment is typically achieved in 85-90% of coil embolization attempts, with complete occlusion of ductal flow occurring in at least 60% of patients assessed one year after occlusion (3). Dogs with persistent flow through the PDA following coil occlusion generally have hemodynamically insignificant residual shunt volumes and infrequently require a second procedure to achieve complete occlusion (3). Risks inherent in coil embolization include hemorrhage, great vessel perforation, infection, hemolysis and most commonly, embolization of coils to the pulmonary or systemic circulation. Pulmonary embolization of 1-2 small to medium sized coils is generally well-tolerated and retrieval of coils in the pulmonary circulation is generally unnecessary and ill-advised. Successful coil embolization of PDA from a retrograde transvenous approach has also been described in the cat (4). Coil embolization is more difficult to achieve in dogs with large PDA and those that lack a




Figure 3.

Figure 4.

A self-expanding multi-layered nitinol mesh device used for occlusion of patent ductus arteriosus (PDA) is shown fully deployed from the delivery catheter. During actual deployment, the delivery catheter is advanced through the aorta and PDA and positioned in the main pulmonary artery. The flat distal disc is first deployed into the pulmonary artery, and then the delivery catheter is gently retracted into the PDA to engage the distal disc with the pulmonary ostium of the PDA. The proximal disc is then deployed within the ductal lumen and the device is then released from the delivery cable.

Post-operative right lateral thoracic radiograph of an adult female Springer Spaniel with cardiac enlargement and patent ductus arteriosus (PDA). A double-disc nitinol mesh canine ductal occlusion device has been deployed within the PDA. This dog had complete elimination of PDA flow and resolution of congestive heart failure following device placement.

narrowing at the junction of the ductus and the pulmonary artery. Coil occlusion of PDA measuring >0.5 cm in minimal ductal diameter has been discouraged by some veterinary cardiologists. Various self-expanding devices allowing transcatheter occlusion of large PDA have been devised for use in human patients and a canine-specific deviceb has recently become commercially available (Figure 3). Initial experience with this device has been very promising, with successful occlusion of large PDA and immediate complete occlusion rates reported at 94% (2) (Figure 4), compared to immediate occlusion rates of 34% with coil embolization techniques (3).

Pulmonic stenosis Pulmonic stenosis, another common congenital cardiac defect in the dog, may occur at subvalvular, valvular or supravalvular locations. Valvular stenosis, characterized by dysplastic pulmonary valve leaf lets that are thickened, fused and immobile, is the most common manifestation of the disease and is also the most amenable to balloon valvuloplasty. Dogs with pulmonic stenosis typically exhibit a loud systolic ejection murmur at the left heart base and variable degrees of right ventricular (RV) hypertrophy. Disease severity is gauged by the Doppler echo-derived pressure gradient across the pulmonic valve, in combination with the degree of RV hypertrophy, right atrial


enlargement, tricuspid valve regurgitation, and the presence or absence of either cardiac arrhythmias or clinical signs. Dogs with gradients across the pulmonic valve of <50 mmHg are typically considered to have mild disease and may remain asymptomatic without intervention. However, dogs with severe disease (Doppler gradient >100 mmHg) are likely to manifest signs of right-sided CHF, arrhythmias, syncope or sudden death, warranting preemptive treatment with surgery or valvuloplasty. Balloon valvuloplasty is the current treatment of choice in these dogs to prevent or ameliorate clinical signs. Pulmonic balloon valvuloplasty entails inflation of a balloon dilation catheter engaged within the pulmonary annulus at the level of stenosis (Figure 5). The balloon size is dictated by the diameter of the pulmonary annulus and aorta and the balloon width chosen is typically 1.2 to 1.4 times the diameter of the pulmonary annulus, or the approximate diameter of the normal aortic annulus (5). In smaller dogs it may be difficult to an introducer or dilation catheter of sufficient diameter through the jugular or femoral vein and a double balloon procedure may be elected whereby two smaller balloon catheters from both the jugular and femoral locations are inflated simultaneously to allow for a greater effective balloon diameter (5). The best candidates for valvuloplasty are those dogs with dysplastic pulmonary valve leaflets and a normal pulmonary annulus size. Dogs with a fibrous



INTERVENTIONAL CARDIOVASCULAR PROCEDURES

Subaortic stenosis

Figure 5. Lateral fluoroscopic images during pulmonic balloon valvuloplasty of a 7-month-old female Boxer with valvular pulmonic stenosis. A transesophageal echo (TEE) probe is evident within the esophagus and the round structure in the lower left hand corner of the image is a dime used to standardize cardiac measurements. A guidewire can be seen traversing the right atrium and right ventricle and entering the main pulmonary artery. The balloon dilation catheter is positioned across the region of the stenotic pulmonic valve in both figures. In the left hand the indentation noted in the partially inflated balloon is created by the stenotic pulmonary valve leaflets. In the right hand the balloon is fully inflated and the indentation in the balloon is no longer apparent. Valvular stenosis was successfully relieved with a 65% reduction in transvalvular pressure gradient following 3 sequential balloon inflations.

subvalvular ring and those with concurrent hypoplasia of the pulmonary annulus (characterized by an aorta-to-pulmonary artery ratio of >1.2) may have a more uncertain outcome (6). Bulldogs, Boxers and other breeds (e.g. Beagle, Bichon Frisé) may have pulmonic stenosis complicated by the presence of an abnormal coronary artery (the R2A coronary anomaly), in which a single right coronary artery gives rise to a branch that encircles the RV outflow tract, and balloon valvuloplasty of this lesion may result in fatal hemorrhage secondary to avulsion of the circumpulmonary coronary artery (7). Up to 20% of dogs with pulmonic stenosis may have a concurrent atrial septal defect or patent foramen ovale, which can result in hypoxemia due to increased right-to-left shunting during balloon valvuloplasty. In order to identify these potential complicating lesions, cardiac and coronary anatomy should be carefully scrutinized by echocardiography and/or selective angiography prior to balloon valvuloplasty. The overall reported success rate of the procedure exceeds 90%, resulting in a 46% immediate mean reduction in pressure gradient and sustained clinical improvement in 80% of previously symptomatic dogs (8).

Aortic stenosis most often results from subvalvular obstruction secondary to a ridge of fibrous tissue in the left ventricular outflow tract. Valvular aortic stenosis is uncommon in the dog. Typical clinical findings include a loud systolic ejection quality murmur heard well at the left and right heart base, weak arterial pulses, and a prominent left ventricular (LV) apical impulse. The stenotic lesion results in a pressure overload to the LV and characteristic echocardiographic findings of concentric LV hypertrophy often associated with hyperechoic regions of the papillary muscles and subendocardium, a reflection of tissue hypoxia, ischemia, and resultant fibrosis. This myocardial injury and hypoxia may also result in electrocardiographic abnormalities such as LV enlargement patterns, ST segment depression and ventricular arrhythmias. The severity of subaortic stenosis (SAS) is also categorized, in part, according to the measured echocardiographic Doppler gradient across the aortic valve. Severely affected dogs with transvalvular aortic pressure gradients exceeding 80 to 100 mmHg may develop cardiac arrhythmias, bacterial endocarditis of the aortic valve, syncope, left-sided CHF or sudden death. The natural history of subaortic stenosis includes sudden death in at least 1 out of 5 severely affected dogs, and the average survival time of dogs with severe SAS has been reported to range from 19 months to 56 months (9). Balloon valvuloplasty is less successful in the treatment of aortic stenosis compared to pulmonic stenosis. Although the procedure may yield an immediate reduction in the aortic outflow gradient, one retrospective analysis of severely affected dogs showed no difference in survival times between dogs treated with valvuloplasty compared to those managed medically with atenolol, a beta-blocker (9). Reasons for the failure of valvuloplasty to consistently benefit dogs with severe SAS are poorly understood, but a report of dogs with SAS undergoing open surgical resection of the subaortic fibrous ring also failed to show any benefit of this procedure on survival times (10). To date, there have been no studies to establish whether earlier intervention at several months of age, or combined valvuloplasty and beta-blocker treatment would improve clinical outcomes. Thus, while many cardiologists routinely ister



Figure 6. Right parasternal long axis transthoracic echocardiographic view from a dog with an atrial septal defect (ASD). An atrial septal occluder device has been positioned across the interatrial septum and can be noted as the bright hyperechoic double disc structure between the right atrium (RA) and left atrium (LA). LV = left ventricle, RV = right ventricle. Picture courtesy of Texas A&M University.


ventricular enlargement, pulmonary hypertension, increased right atrial filling pressures, and the eventual development of right-sided CHF. Surgical correction of ASD requires cardiopulmonary by and is associated with significant risk and expense. Successful transcatheter closure of secundum ASDs has been reported in the dog using a self-expanding double-disk septal occluder devicec (11,12) (Figure 6). Transthoracic and transesophageal echocardiographic assessment of ASD anatomy are crucial in determining the size and location of the defect and ensuring that there is a sufficient rim of interatrial septal tissue to the device while avoiding interference with surrounding cardiac structures. Animals with Eisenmenger’s physiology, characterized by severe pulmonary hypertension and a large right-to-left-shunting atrial or ventricular septal defect, are not candidates for surgical or transcatheter closure of the defect.

Ventricular septal defects atenolol to affected dogs, it has also been our practice to selectively choose certain dogs for aortic balloon valvuloplasty. Those dogs with a component of valvular aortic stenosis, and those with a thin fibrous subaortic ring and limited muscular hypertrophy of the interventricular septum are offered balloon valvuloplasty, and we are much more likely to be enthusiastic about the procedure in young dogs, before marked remodeling and fibrosis of the left ventricle have developed. In our experience, it is easier to engage the subaortic ring if 2 smaller balloons are used rather than trying to relieve the obstruction with a single balloon. Balloon dilation of the aortic valve is associated with greater risk and often results in more serious arrhythmia than that encountered during pulmonic balloon valvuloplasty.

Atrial septal defects Atrial septal defects (ASD) are relatively uncommon defects, though a genetic predisposition has been noted in the Boxer, Doberman Pinscher, Samoyed and Standard Poodle. Typical physical examination findings accompanying ASD may include a systolic ejection murmur of functional pulmonic stenosis and fixed splitting of the second heart sound. Though small ASD may be hemodynamically insignificant, large left-toright shunting defects may result in right-sided volume overload with attendant right atrial and


Ventricular septal defects (VSD) are amongst the most common congenital defects in the cat, and a predisposition for VSD has been described in the English Springer Spaniel, Keeshound and English Bulldog. Ventricular septal defects are associated with a loud systolic heart murmur, often most prominent on the right chest wall at the right cranial sternal border. The degree of cardiomegaly and pulmonary overcirculation accompanying VSD depends upon the size of the defect and the relative compliance of the right and left ventricles. Small restrictive VSD are often hemodynamically unimportant and may be well-tolerated for the life of the animal. However large defects may result in considerable left-to-right shunting with leftsided volume overload and chamber enlargement, pulmonary vascular damage, and left-sided CHF. Surgical palliation of large VSD may include correction of the defect under cardiopulmonary by or circumferential banding of the main pulmonary artery to reduce the volume of left-toright shunting. The surgical risk to the patient and the post-operative discomfort of thoracotomy may be reduced if the repair can be accomplished with a percutaneous approach. Transcatheter occlusion of suitable defects is the treatment of choice for human patients with VSD and has been described in the dog. Catheter-based occlusion of small VSD in the dog has been reported




Tricuspid stenosis

Figure 7. Right lateral thoracic radiograph of a dog 1 year following percutaneous device occlusion of a muscular VSD. The VSD occlusion device can be seen deployed across the interventricular septum. Picture courtesy of Dr. Marco Margiocco.

using detachable embolization coils (13). Large nonrestrictive VSD located an adequate distance from the aortic valve in the muscular septum may be candidates for VSD occlusion with a double-disk septal occluderd (14) (Figure 7). Transesophageal echocardiography is necessary to determine the feasibility of VSD occlusion with a percutaneous device. Unfortunately, VSD located high in the membranous septum are both more common in dogs and cats and more difficult to treat, since the open device may interfere with either aortic or tricuspid valve function. A membranous VSD occluder has recently been designed for use in human patients, and this device may prove to be applicable to a larger number of veterinary patients. Ventricular septal defect occlusion with the currently available VSD occlusion device sizes is not feasible in the cat.

Tricuspid stenosis is an uncommon congenital defect characterized by a diastolic pressure gradient between the right atrium and ventricle, right atrial enlargement, atrial arrhythmias and eventual rightsided congestive heart failure. Tricuspid valve stenosis typically accompanies tricuspid dysplasia, a heritable disorder in the Labrador Retriever. In the absence of concurrent valvular insufficiency, affected dogs often have soft or absent cardiac murmurs and the disease may go unnoticed until clinical signs develop. Percutaneous balloon valvuloplasty of the tricuspid valve with a single or double balloon procedure (Figure 8) may be accomplished by jugular or femoral venous access and valvuloplasty may result in a significant reduction in the pressure gradient across the valve, with attendant improvements in hemodynamics and clinical signs (15).

Mitral stenosis Mitral valve dysplasia and stenosis (MS) is an uncommon congenital defect wit h breed predilections in the Newfoundland and Bull Terrier. Affected dogs typically exhibit signs of exercise intolerance, syncope and congestive heart failure and most dogs with MS do not survive beyond 23 years of age (16). Percutaneous mitral valvuloplasty is the treatment of choice for human patients with symptomatic MS. This procedure is more difficult to accomplish than other valvuloplasties due to the need for trans-septal puncture to access the left atrium, and has only been reported once in the dog (17). Valvular and supravalvular mitral stenosis have also been described in the cat but mitral valvuloplasty has not been described in this species. Figure 8. Lateral fluoroscopic images of a young Labrador Retriever with tricuspid dysplasia and valvular tricuspid stenosis. Balloon valvuloplasty was performed on the stenotic tricuspid valve utilizing a double balloon technique. Two guidewires are evident within the cranial vena cava, right atrium, right ventricle and ing into the pulmonary artery. Two balloon dilation catheters have been ed over the guidewires and are seen positioned across the tricuspid orifice. In the left hand , a waist created by the stenotic tricuspid valve leaflets is seen across the midportion of the simultaneously inflated balloons. In the right hand the balloons are fully inflated and resolution of the balloon waist demonstrates effective dilation of the stenosis.




Cor triatriatum Cor triatriatum dexter and cor triatriatum sinister are characterized by a perforate or imperforate fibrous membrane partitioning the respective right or left atrium into a proximal and distal atrial chamber. Clinical manifestations depend on the location of the membrane and the size of the communication between the proximal and distal chambers. The resultant increase in filling pressure in the proximal chamber results in signs of CHF. Cor triatriatum dexter may be palliated by percutaneous balloon dilation of the anomalous membrane to reduce the pressure gradient between the proximal and distal chambers of the right atrium (18). Balloon dilation of cor triatriatum sinister is also feasible with transseptal puncture to access the left atrium, but has not been described in companion animals.

Figure 9. Selective venogram of a young castrated male domestic short haired cat with Budd-Chiari syndrome and massive ascites secondary to an obstructive membrane within the caudal vena cava at the level of the diaphragm. In the left hand the catheter has been advanced from the femoral vein and positioned in the caudal vena cava just caudal to the diaphragm. Contrast is seen to fill the dilated cava and only a small stream of contrast can be seen ing through the membrane and into the cava cranial to the diaphragm (c). In the right hand a balloon has been advanced across the membrane and is inflated. Ascites resolved following balloon dilation of the stenosis in this cat.

Congenital and acquired caval stenosis

Supraventricular tachycardia associated with accessory pathways

Vena caval stenosis or stricture formation may occur as a congenital defect or may be acquired secondary to endothelial injury from cardiovascular devices or central venous catheters. The functional consequences of caval stenosis depend on the location and severity of the stenosis, and percutaneous treatment of symptomatic stenoses may be achieved with balloon angioplasty or intravascular stenting.

Accessory atrioventricular (AV) conduction pathways, or by tracts, are abnormal electrical communications across the fibrous skeleton that normally serves to electrically isolate the atria and ventricles. The accessory pathway may function as one limb of a rapid, narrow complex tachyarrhythmia circuit termed orthodromic atrioventricular reciprocating tachycardia (OAVRT). Vagal maneuvers and adenosine, both effective in human patients with OAVRT, are generally ineffective in terminating OAVRT in the dog and the response of reciprocating tachycardias to antiarrhythmic drug therapy is inconsistent, with affected dogs often becoming refractory to previously effective antiarrhythmic strategies. Unrelenting tachycardia results in reduced cardiac output and will eventually result in the development of tachycardiomyopathy and congestive heart failure if left untreated.

Congenital stenosis of the caudal vena cava and Budd-Chiari syndrome caused by an intraluminal fibrous membrane has been described in the cat (19). Affected cats often develop severe ascites due to impedance of venous return from the caudal vena cava. In one report, treatment of an affected cat with balloon dilation and endovascular stent placement failed to resolve the cat’s ascites and was associated with a poor outcome (19). However, the authors have performed successful balloon dilation of an obstructive intraluminal membrane in the caudal vena cava of one cat that presented with severe refractory ascites, resulting in complete resolution of clinical signs that had persisted for greater than 15 months (Figure 9). We have also performed successful balloon venoplasty in two dogs with cranial vena cava syndrome and pleural effusion due to acquired stenosis and thrombosis of the cranial vena cava secondary to transvenous pacemaker leads.


Radiofrequency catheter ablation utilizes an alternating electrical current to induce thermal damage to the accessory pathway and is the standard of care for human patients with macroreentrant tachycardias. The procedure is also highly effective for eliminating accessory pathway conduction in the dog (20) however it is only performed in a limited number of specialized centers due to the need for highly specialized




Figure 10. Right lateral thoracic radiograph of an elderly female Cocker Spaniel with high-grade second-degree AV block following permanent transvenous pacemaker implantation. The pacing lead can be seen ing through the cranial vena cava and right atrium into the right ventricular apex where it is actively fixated into the right ventricular myocardium.

equipment and expertise. Electroablation entails the placement of several multipolar electrode catheters into the right atrium, followed by electrical mapping to determine the exact location of the accessory pathway. Radiofrequency energy is then delivered to the accessory pathway through the catheter tip electrode, resulting in thermalinduced damage to the pathway and ablation of impulse conduction. Electroablation is also used for the treatment of atrial fibrillation and atrial flutter in human patients and has potential for greater application for treatment of these arrhythmias in the dog.

Bradyarrhythmias and cardiac pacing High degree second-degree and third-degree atrioventricular (AV) block are associated with signs of exercise intolerance, syncope, cardiac enlargement, and a high incidence of sudden cardiac death (21). Pacemaker therapy is the only treatment effective in alleviating clinical signs and prolonging survival in affected dogs, and pacemaker implantation is the current standard of care for patients with high grade AV block, atrial standstill, and sick sinus syndrome. Since the advent of epicardial pacing in the dog in 1967, transvenous pacing has become widespread and has largely replaced the surgical placement of epicardial leads in dogs (Figure 10).

Permanent transvenous cardiac pacing can be achieved using a wide variety of pacing modalities, including the use of one or more pacemaker leadwires. Single-chamber permanent transvenous pacing is used most frequently in the dog and is achieved by ing the leadwire through a vein, usually the jugular vein, and advancing the lead through the right atrium and into the right ventricle. Most pacemaker lead systems now allow for active fixation of an endocardial lead in the right ventricular myocardium, reducing the chance for leadwire dislodgement. The pulse generator is implanted beneath the skin, and the pacing mode and rate, amplitude and pulse width of the pacing stimulus, and a variety of more advanced features can be subsequently adjusted via an external programmer. Many pacemakers have a sensor that detects vibration and allows for rate modulation with increased activity. Although a variety of complications can occur following pacemaker implantation, such as lead fracture or dislodgement, infection, battery failure or development of congestive signs in patients with intercurrent structural cardiac disease, the vast majority of dogs (over 90%) do well and never have recurrence of clinical signs related to the cardiac bradyarrhythmia (22). The average survival of dogs following pacemaker implantation is at least 2 years and many dogs live in excess of 3 to 5 years after pacemaker implantation (21,22). Dual chamber physiologic pacing allows for preservation of atrioventricular synchrony and is utilized extensively in human patients, although it is associated with increasing pacemaker programming complexity. Acute beneficial hemodynamic and neurohormonal changes have been demonstrated with physiologic pacing modalities in the dog (23) but the long-term benefits of dual chamber pacing in veterinary patients remain uncertain. Implantable cardioverter defibrillators (ICD) are devices used extensively in human patients to prevent sudden cardiac death secondary to life-threatening tachyarrhythmias such as ventricular tachycardia and fibrillation. Sudden arrhythmic cardiac death is encountered frequently in some dog breeds (e.g., Boxer, Doberman Pinscher) and ICD technology has great potential application in these patients, however the current ICD devices designed for humans are not welladapted to use in the dog (24).





Additional interventional procedures and future directions Many other minimally invasive therapies are currently employed for the treatment of acquired cardiovascular disease in small animals. These include transjugular heartworm removal for patients with advanced heartworm disease, catheter placement for local thrombolytic therapy, thrombectomy for the treatment of arterial and venous thromboembolism, endomyocardial biopsy techniques, and pulmonary artery catheterization for measurement of cardiac output, pulmonary artery and pulmonary capillary wedge pressures. Mitral regurgitation secondary to endocardiosis is the most common cardiac disease of dogs and the most important cause of CHF. Despite recent advances in medical therapy, the average survival

of dogs with CHF is still less than 1-year after diagnosis. Various percutaneous techniques are under investigation for the treatment of mitral regurgitation in human patients, many of them employing animal models. A successful percutaneous therapy for mitral regurgitation would have a tremendous impact for the treatment of endocardiosis in the dog. Interventional cardiology is a developing field that has yet to reach its full potential in veterinary medicine. Catheter-based procedures have resulted in successful alternatives to reduce surgical morbidity and mortality in small animal patients. As the technology advances we will continue to develop novel strategies for the minimally invasive treatment of congenital and acquired cardiovascular disease in companion animals.

Footnotes: a

Cook Stainless Steel Embolization Coils, Cook Medical Inc, Bloomington, IN b Amplatz Canine Duct Occluder (ACDO), Infiniti Medical, Malibu, CA c Amplatzer Septal Occluder, AGA Medical Corp, Golden Valley, MN d Amplatzer Muscular VSD occluder, AGA Medical Corp, Golden Valley, MN

REFERENCES 1. Smith PJ, Martin MW. Transcatheter embolisation of patent ductus arteriosus using an Amplatzer vascular plug in six dogs. J Small Anim Pract 2007; 48: 80–86.

13. Fujii Y, Fukuda T, Machida N, et al. Transcatheter closure of congenital ventricular septal defects in 3 dogs with a detachable coil. J Vet Intern Med 2004; 18: 911–914.

2. Nguyenba TP, Tobias AH. Minimally invasive per-catheter patent ductus arteriosus occlusion in dogs using a prototype duct occluder. J Vet Intern Med 2008; 22: 129-134.

14. Margiocco ML, Bulmer BJ, Sisson DD. Percutaneous occlusion of a muscular ventricular septal defect with an Amplatzer® Muscular VSD occluder. J Vet Cardiol 2008; 10: 61-66.

3. Campbell FE, Thomas WP, Miller SJ, et al. Immediate and late outcomes of transarterial coil occlusion of patent ductus arteriosus in dogs. J Vet Intern Med 2006; 20: 83–96.

15. Kunze , Abbott JA, Hamilton SM, et al. Balloon valvuloplasty for palliative treatment of tricuspid stenosis with right-to-left atrial-level shunting in a dog. J Am Vet Assoc 2002; 220: 491-496.

4. Schneider M, Hildebrandt N. Transvenous embolization of the patent ductus arteriosus with detachable coils in 2 cats. J Vet Intern Med 2003; 17: 349-353.

16. Lehmkuhl LB,Ware WA, Bonagura JD. Mitral stenosis in 15 dogs. J Vet Intern Med 1994; 8: 2-17.

5. Estrada A, Moïse NS, Renaud-Farrell S. When, how and why to perform a double ballooning technique for dogs with valvular pulmonic stenosis. J Vet Cardiol 2005; 7: 41–51.

17. Oyama MA, Weidman JA, Cole SG. Calculation of pressure half-time. J Vet Cardiol 2008; 10: 57-60.

6. Bussadori C, DeMadron E, Santilli RA, et al. Balloon valvuloplasty in 30 dogs with pulmonic stenosis: Effect of valve morphology and annular size on initial and 1-year outcome. J Vet Intern Med 2001; 15: 553-558.

18. Johnson MS, Martin M, De Giovanni JV, et al. Management of cor triatriatum dexter by balloon dilatation in three dogs. J Small Anim Pract 2004; 45: 16-20.

7. Buchanan JW. Pathogenesis of single right coronary artery and pulmonic stenosis in English Bulldogs. J Vet Intern Med 2001; 15: 101-104.

19. Holt D, Saunders HM, Aronson L. Caudal vena cava obstruction and ascites in a cat treated by balloon dilation and endovascular stent placement. Vet Surg 1999; 28: 489-495.

8. Stafford-Johnson M, Martin M. Results of balloon valvuloplasty in 40 dogs with pulmonic stenosis. J Small Anim Pract 2004; 45: 148-153.

20. Wright KN, Knilans TK, Irvin HM. When, why, and how to perform cardiac radiofrequency catheter ablation. J Vet Cardiol 2006; 8: 95-107.

9. Meurs KM, Lehmkuhl LB, Bonagura JD. Survival times in dogs with severe subvalvular aortic stenosis treated with balloon valvuloplasty or Atenolol. J Am Vet Assoc 2005; 227: 420-424.

21. Wess G, Thomas WP, Berger DM. Applications, complications, and outcomes of transvenous pacemaker implantation in 105 dogs (1997-2002). J Vet Intern Med 2006; 20: 877-884.

10. Monnet E, Orton EC, Gaynor JS. Open resection for subvalvular aortic stenosis in dogs. J Am Vet Med Assoc 1996; 209: 1255-1261.

22. Johnson MS, Martin MWS, Henley W. Results of pacemaker implantation in 104 dogs. J Small Anim Pract 2007; 48: 4-11.

11. Sanders RA, Hogan DF, Green III HW, et al. Transcatheter closure of an atrial septal defect in a dog. J Am Vet Assoc 2005; 227: 430-434.

23. Bulmer BJ, Sisson DD, Oyama MA, et al. Physiologic VDD versus nonphysiologic VVI pacing in canine 3rd-degree atrioventricular block. J Vet Intern Med 2006; 20: 257-271.

12. Gordon SG, Miller MW. Percutaneous ASD repair in dogs. In: Proceedings American College of Veterinary Internal Medicine Forum, Seattle, WA, 2007.


24. Nelson OL, Lahmers S, Schneider T, et al. The use of an implantable cardioverter defibrillator in a boxer dog to control clinical signs of arrhythmogenic right ventricular cardiomyopathy. J Vet Intern Med 2006; 20: 1232-1237.



HOW I TREAT...

Valvular heart disease in the dog dog, particularly Cavalier King Charles Spaniels, appear to have a higher prevalence of disease and an earlier onset of both disease and clinical signs.

Adrian Boswood, MA, VetMB, DVC, Dipl. ECVIM (Cardiology), MRCVS Department of Veterinary Clinical Sciences, The Royal Veterinary College, London, UK Dr. Boswood graduated from The University of Cambridge in 1989. In 1990, following a period in general practice, he ed the Royal Veterinary College as an intern and remained at the Royal Veterinary College ever since where he is now a Senior Lecturer. Adrian Boswood’s main clinical interest is in medical cardiology and his research interests are in cardiac biomarkers and valvular heart disease of dogs.

A

cquired valvular heart disease in the dog is the most common cause of heart disease and heart failure in the canine population (1). Valvular heart disease in the dog is usually a chronic degenerative condition which is known by various including endocardiosis and myxomatous mitral valve disease. The disease most commonly affects the mitral valve and results in the development of mitral regurgitation. This mitral regurgitation leads to an increased volume of blood being pumped by the left ventricle due to the proportion of each ventricular ejection that goes back into the left atrium. Chronically this results in increased left ventricular and left atrial size and, in some affected animals, results in the development of clinical signs of heart failure. It typically affects older small breed dogs although certain breeds of

In patients that are regularly examined by veterinarians the characteristic left-sided systolic murmur of mitral insufficiency is usually the first clinical abnormality identified. The development of a murmur often precedes the development of clinical signs by many years. In the SVEP study (2) Cavalier King Charles Spaniels with a heart murmur and no cardiac enlargement had a median period of well over three years before developing signs of heart failure. In a recent paper Borgarelli, et al. (3) showed that in a more mixed population of asymptomatic dogs with mitral regurgitation fewer than 50% of the dogs died as a consequence of their disease during the period of follow-up. Thus in some cases mitral valve disease can be a relatively benign slowly progressive condition that does not progress sufficiently to lead to the development of clinical signs. In others the disease may progress to the point where clinical signs of heart failure result. The challenge for the clinician faced with patients with this disease is to establish a diagnosis of the disease, recognize at which stage of this progressive disease the patient in question currently resides and to appropriately and optimally treat those patients that require treatment. A diagnosis of mitral regurgitation can be suspected in any dog with a left apical systolic murmur, particularly if it is a small breed dog. There are some large breed dogs that are affected by primary mitral valve disease but this is a rarer form of the disease. Large breed dogs with primary valvular disease may have a slightly different course of disease compared to small breed dogs (4).




HOW I TREAT...

Figure 1. A lateral thoracic radiograph from a dog with advanced mitral valve disease. There is marked cardiomegaly with craniocaudal widening of the cardiac silhouette and dorsal displacement of the trachea. The lung fields are diffusely opacified by the presence of an alveolar pattern indicating the presence of pulmonary edema, in this case secondary to left-sided congestive heart failure. This is a severe example of the radiographic changes that can be associated with advanced mitral valve disease.

Confirmation of the diagnosis of primary valvular disease requires two-dimensional and Doppler echocardiography but the clinical presentation is so typical, and the disease so common, that this is not a test that is necessary to perform in every case. Thoracic radiographs are particularly useful for determination of the stage of disease by demonstrating the presence or absence of cardiomegaly and the presence or absence of left-sided congestive heart failure (Figure 1). Left apical systolic murmurs may also be caused by congenital heart disease and mitral regurgitation secondary to other causes including dilated cardiomyopathy and bacterial endocarditis. These conditions are however less commonly encountered and tend to occur in different types of dog. For the purposes of this article, I will discuss only the chronic management of patients with heart failure and not describe the acute management of patients with sudden onset of severe heart failure. The UK trade names and doses of all the drugs mentioned appear in Table 1. I will divide patients into four stages and discuss the treatment options that are appropriate at each stage in the light of what I consider to be current best evidence.


These stages are as follows: • Early disease: the patient without clinical signs and without significant cardiomegaly. • Moderately progressed disease: A patient without overt clinical signs but with evidence of cardiomegaly implying the necessity to adapt to the increased volume of blood being encountered by both the left atrium and ventricle. • Heart failure: A patient that has developed signs of congestive heart failure as a consequence of their mitral valve disease. Typically the first signs of heart failure will be left-sided failure and will include pulmonary congestion and edema. • Refractory heart failure: A patient that has redeveloped clinical signs despite receiving therapy for heart failure.

Treatment of the patient with mitral regurgitation according to the stage of disease Early disease There is little evidence to suggest the benefit of any therapy in the early stages of mitral valve disease. Two published studies have evaluated the efficacy of treatment with angiotensin converting enzyme inhibitors (ACEI) in this population (2,5). These studies produced conflicting results. The study by Kvart, et al. was a double-blind placebo controlled prospective study performed only in Cavalier King Charles Spaniels (2). This study suggested that there was no benefit of istration of ACEI in dogs prior to the onset of clinical signs irrespective of whether there was any cardiomegaly. The more recent study by Pouchelon, et al. (5) is a retrospective study conducted in a small but more heterogeneous population of dogs (Editor’s note: 141 dogs). The conclusion of the paper was that Benazepril istered in dogs with early disease may be of benefit in dogs of breeds other than Cavalier King Charles Spaniels. The fact that this was a retrospective, unblinded study with a low event rate (a low number of animals in the study reached the endpoints of cardiac death or onset of heart failure) and with different median followup periods for the treated and untreated groups mean that the conclusions should be interpreted with some caution. I would regard their conclusions as generating a useful hypothesis that should be tested in future in a placebo controlled, double-blind study and I am not yet convinced of the value of early therapy in this group.



VALVULAR HEART DISEASE IN THE DOG

Table 1. Proprietary names and doses of drugs Generic drug name Enalapril Benazepril

Dose and frequency (These doses may differ from those given in the data sheet) 0.5 mg/kg s.i.d.-b.i.d. 0.25-0.5 mg/kg s.i.d.-b.i.d.

Pimobendan

0.2-0.6 mg/kg/day divided into two doses

Frusemide Furosemide

1-2 mg/kg b.i.d. initially increasing to a maximum of 4 mg/kg t.i.d.

Spironolactone Digoxin

1-3 mg/kg b.i.d. 0.22 mg/m2 b.i.d. check trough (8 hour post pill) serum digoxin levels after 5-7 days to ensure therapeutic and not excessive concentrations have been achieved

Amlodipine

0.05-0.1 mg/kg s.i.d.-b.i.d.

Hydralazine

0.5-3.0 mg/kg b.i.d.-t.i.d. (start with low dose and titrate to effect with blood pressure monitoring)

Sildenafil

Abbreviations used: s.i.d. once daily, b.i.d. twice daily, t.i.d. three times daily, q.i.d. four times daily, mg milligram, kg kilogram, m2 meter squared.

0.5-3.0 mg/kg s.i.d.-t.i.d.

Theophylline

20 mg/kg s.i.d.

Etamiphylline Camsylate

10–33 mg/kg t.i.d. (according to data sheet)

Terbutaline

1.25-5 mg/dog b.i.d.-t.i.d.

Butorphanol

0.5 mg/kg b.i.d.-q.i.d.

Codeine

Proprietary names and doses of drugs described in the text. The doses may differ from those given in the data sheets. No responsibility is accepted for adverse reactions to the drugs given at the dosages recommended and veterinarians are recommended to cross reference to other sources (e.g. BSAVA Small Animal Formulary) prior to istration.

0.5-2 mg/kg b.i.d.

My approach to this population of dogs is not to intervene pharmacologically but to advise and educate the client. If the animal is overweight then weight control is important. Continuing to regularly exercise the patient is in my opinion probably of benefit. There is no convincing evidence to suggest a benefit of sodium restriction at this stage of the disease. Clients should be advised about the signs that might indicate the development of heart failure and the necessity for treatment; such as exercise intolerance, increased respiratory rate and effort, cough, lethargy and unexplained weight loss. Regular re-examination of these patients may help pick up early signs of clinical deterioration and will also reassure the client that one is not simply ignoring the presence of a clinically significant disease. Client reassurance is important at the early stage of the disease because over-stressing the likelihood of development of problems in the near future may cause unnecessary worry. Many dogs remain at the

early stage of mitral valve disease for many years and some will succumb to non-cardiac disease before they have ever had the opportunity to demonstrate signs of heart failure.

Moderately progressed disease Two studies have evaluated the effects of ACEI in dogs with cardiomegaly prior to the onset of signs of heart failure these are the SVEP study (2) and the VETPROOF study (6). Both of these studies evaluated the effect of treatment prior to the onset of clinical signs in dogs with mitral valve disease. Some of the dogs in the SVEP study had cardiomegaly and left atrial enlargement was one of the inclusion criteria for the VETPROOF study – therefore all the dogs in this study had some degree of cardiac enlargement. Again these studies appear to generate conflicting conclusions. The SVEP study showed no benefit of ACEI therapy with respect to delaying the onset of heart failure in Cavalier King Charles Spaniels. The VETPROOF




HOW I TREAT...

study did not show a significant effect of Enalapril on the primary endpoint of the study which was time to onset of congestive heart failure. Looking at a secondary combined endpoint of all cause mortality and onset of heart failure they appeared to show a significant difference after excluding those dogs that succumbed in the first 60 days of the study. This was not a pre-planned analysis but generates a fascinating hypothesis that there may be a non-cardiac beneficial effect on survival. The combination of results from these two studies is not enough to currently convince me of the benefit of therapy even in dogs with cardiomegaly at the time of diagnosis. It is worth pointing out that only ACEI have been evaluated as potentially beneficial treatment prior to the onset of clinical signs in large well conducted studies. There are of course other candidates for early treatment that have not been evaluated as rigorously and all that one can say with respect to other therapy is “we don’t know”. It may be in the future that some therapy is proved to be beneficial at this stage in the disease but at the moment if we are to practice “evidence-based medicine” there is insufficient evidence of a convincing benefit of therapy for me to advocate its use. A recent, as yet unpublished study, has claimed a benefit of Spironolactone prior to the onset of signs of heart failure however the absence of full disclosure of the results of this study through publication precludes further evaluation of this claim and it has not as yet changed my practice of not treating these patients. Again my management of patients and their owners at this stage of the disease consists of education and monitoring. It is important that signs of heart failure are recognized as and when they occur so that treatment can be introduced when it is known to be effective. Clients can be instructed in how to take a respiratory rate at home and should also be advised to look out for subtle signs of intolerance of exercise. Having said this it is still the case that many dogs with mitral regurgitation and cardiomegaly live for years before developing signs of heart failure so overstressing the likelihood of development of signs may lead to anxiety on the part of clients and plenty of “false alarms”.


Onset of heart failure The onset of congestive heart failure is best documented with thoracic radiographs. When a patient has developed signs of congestive heart failure secondary to mitral valve regurgitation there is convincing evidence of benefit of therapy both in of improvement of quality of life and, with some treatments, prolongation of life. Several controlled studies have been conducted from which valid conclusions on which to base our therapy can be drawn. There are multiple studies that have demonstrated the benefits of ACEI in the treatment of dogs with mitral valve disease. The LIVE study (7) and the BENCH study (8) were two of the earlier studies published. These showed that compared to placebo ACEI prolonged survival of dogs in heart failure when added to standard therapy of diuretics plus in some cases digoxin and other drugs. These studies both enrolled populations of dogs including those with mitral regurgitation. A sub-analysis of the LIVE study (7) showed benefit specifically in the group with mitral regurgitation. Thus ACEI are better than placebo in the treatment of dogs in heart failure secondary to mitral valve disease. More recently Pimobendan has been shown to be efficacious. Mitral valve disease studies have demonstrated improvements in quality of life and time to events such as hospitalization are improved with Pimobendan (9). The VetSCOPE study suggested that the beneficial effects of Pimobendan may exceed those of ACEI (10) although substantial debate remained after the conclusion of this study. The recently reported QUEST study (11), a positive controlled, singleblind, prospective study comparing Benazepril to Pimobendan concluded that the benefits of Pimobendan exceeded those of Benazepril (and by inference probably other ACEI) with a 91% prolongation of the time to reach a composite endpoint of death, euthanasia for cardiac reasons or treatment failure (Figure 2). This study suggests that if either an ACEI or Pimobendan is to be used in isolation, in conjunction with diuresis and other treatments, then Pimobendan is the preferred agent. What it does not enable us to conclude is whether not the combination of an ACEI and Pimobendan will be better still. There is also recent, as yet unpublished, evidence of a benefit of Spironolactone in dogs with mitral regurgitation and signs of heart failure.




100 90

Log-Rank Test, P=0.0099

70 60 50 40 30 20

Dogs remaining in study (%)

80

Pimobendan group 267 days, IQR 122-523 days

Benazepril group 140 days, IQR 67-311 days

10 0 0

100

200

300

400

500

600

700

800

900

1000

1100

Time (Days) Figure 2. Kaplan Meier survival analysis from the QUEST study. The median time to reaching the primary endpoint was 267 days in the Pimobendan group compared to 140 days in the Benazepril group suggesting a 91% prolongation of time to cardiac death, euthanasia for cardiac reasons or treatment failure in the group receiving Pimobendan.

The way I treat patients at this stage depends to some extent on client preference and the feasibility of istering multiple medications in these patients. The optimum treatment could consist of up to four medications. What is not in doubt is the necessity for the istration of Frusemide to patients with congestive heart failure. Therefore the two, three and four drug regimes would be: • Frusemide plus Pimobendan • Frusemide plus Pimobendan plus ACEI; or • Frusemide plus Pimobendan plus ACEI plus Spironolactone. Where minimum therapy is dictated for either financial reasons or risks of poor compliance then the two drug regime will suffice. Optimal therapy may involve istration of either the three or four drug regime although evidence of additional benefit of these therapies when added to the two drug regime is currently lacking. However, the opinion is widely held among cardiologists that there are additional benefits.

Refractory heart failure Once a patient is receiving optimal therapy following the onset of signs of heart failure there is often a period of several months when the patient is fairly stable and compensates for their heart failure (provided they continue to receive their treatment). Unfortunately, for most dogs there reaches a point where their clinical signs return despite receiving treatment and modification of treatment is necessary. Modification should consist of optimization of doses of drugs already being received plus the addition of further treatment. In this late stage of disease there is a lack of evidence of efficacy of any particular therapy and a plethora of individual opinion. If a patient is only receiving two or three of the drugs outlined in the different regimes above I would add the others to ensure that all four of Frusemide, Pimobendan, an ACEI and Spironolactone are being received by the patient. In addition to this combination there is the option to add further diuretics, further vasodilators and/or Digoxin to the treatment; the latter particularly where patients have atrial fibrillation.




HOW I TREAT...

I undertake the following modifications to treatment: • Increase the Frusemide dose and frequency up to a maximum of 4 mg/kg three times daily. • Maximize the Spironolactone dose up to 2-3 mg/kg twice daily. • Double the frequency of the ACEI istration (going from once daily to twice daily). After this one can consider addition of further diuretics, particularly thiazide diuretics as these act elsewhere within the nephron (sequential nephron blockade) and further vasodilators including Amlodipine and Hydralazine. If patients develop signs of right-sided congestive heart failure these may be secondary to the development of pulmonary hypertension. Some authors have advocated the use of Sildenafil in these circumstances (12). There are many risks associated with the istration of multiple drugs to patients with advanced valvular heart disease; the most frequently seen complications include compromised renal function and electrolyte disturbances (13). I would recommend checking a biochemistry profile in patients with mitral regurgitation prior to introduction of treatment and 7-10 days after any significant modification to therapy. In the later stages of disease it is almost inevitable that some degree of azotemia will develop. Provided this is modest then therapy can be continued but in some circumstances the creation of concurrent renal dysfunction can be a limiting factor in the ability to ister further therapy. Ultimately the majority of patients that develop signs of heart failure secondary to mitral regurgitation will succumb to their disease (75% of dogs in the QUEST study reached the primary endpoint (11)), despite further attempts at therapy. In many cases it is necessary to consider euthanasia and the decision to undertake this should be informed by the quality of life enjoyed by the patient on treatment and client preferences.

Additional problems There are two problems relating to the above classification. One is the artificial sense of certainty it creates about dogs fitting into one of the categories rather than hovering on the boundaries. The second problem relates to the clinical sign of


intractable coughing that occurs in many dogs with valvular heart disease. Any type of categorization of disease artificially divides a continuous spectrum of patients into a series of apparently distinct categories. There is often a problem with dogs lying on the boundaries between categories. There is an artificial level of certainty associated with a patient either having or not having signs of heart failure. In some patients it is difficult to judge, for instance in patients with moderate to marked intolerance of exercise, or patients with evidence of a mild interstitial lung pattern radiographically: are these patients in heart failure or not? It may be that in the future the use of biomarkers may help us to distinguish dogs that are more or less likely to be showing signs of heart failure and NTproBNP appears promising in this respect (14,15). See also first paper in this issue by M. Oyama and C. Reynolds. Sometimes however it is necessary to consider, where clinical signs and radiography or echocardiography suggest the disease is advanced, the introduction of empirical therapy to see if signs will improve. This strategy can sometimes be fraught with uncertainty because concurrent disease could be responsible for the signs that might either improve in response to the same therapy or simply resolve with time. Thus an apparent response to therapy is a tenuous reason to condemn a dog to lifelong therapy. It is very unlikely that a dog with a relatively quiet heart murmur that does not have evidence of cardiac enlargement will be showing any clinical signs as a consequence of their disease. Coughing is one very specific clinical sign in dogs with mitral valve disease that may be a consequence of the disease but not necessarily a sign of heart failure. It is widely believed that the cough in dogs with mitral valve disease, which frequently precedes signs of heart failure, is due to the physical size of the enlarged left atrium leading to compression of the left mainstem bronchus. In this circumstance treatment aimed at controlling signs of congestive heart failure may not lead to a resolution of the signs of coughing because they do not necessarily reduce the size of the left atrium. Various strategies have been suggested in these patients in an effort to improve signs. These can all be tried in these patients but,




despite the use of many or all of these, the cough frequently proves unresponsive to treatment. Strategies for treatment include: • Bronchodilation: Theophylline, Etamiphylline and Terbutaline could be considered. • Management changes: Weight loss, avoidance of smoky dusty environments, use of a harness rather than a collar to prevent further irritation to the airways. • Introduction of low doses of vasodilators or diuretics: the rationale behind this approach is to try to physically reduce left atrial size. • Cough suppressants: Butorphanol or Codeine can be used intermittently to suppress the cough when it is particularly problematic. • Anti-inflammatory medication: some authors advocate the use of intermittent low dose corticosteroids or steroids by inhaler in these circumstances.

Future directions One recent exciting development that may have significant ramifications for the identification and management of heart disease in dogs with mitral

valve disease (and other cardiac diseases) is the development of assays for cardiac biomarkers (See article on page 2). The measurement of NTproBNP seems particularly promising. Several recent studies have outlined the value of this marker in the identification of patients with heart disease and heart failure (14,15). In human patients assessment of biomarkers can assist in both the identification of patients with more advanced disease and decisions with regard to their therapy. There are also prognostic implications of elevated levels of NTproBNP in human patients; preliminary data from dogs would also suggest that there is a strong predictive association between NTproBNP concentration and outcome. It is conceivable that in future we may be able to initiate therapy with more confidence in patients with mitral valve disease that have elevated concentrations of NTproBNP. The potential for specifically targeting a reduction of natriuretic peptide concentrations in humans is already being explored (16,17) and this is an avenue worthy of further evaluation in dogs.

REFERENCES 1. Buchanan JW. Prevalence of Cardiovascular Disorders. In: Fox PR, Sisson D, Moise NS, eds. Textbook of Canine and Feline Cardiology. Philadelphia: Saunders, W.B.; 1999: 457-470.

9. Smith PJ, French AT, Van Israel N, et al. Efficacy and safety of pimobendan in canine heart failure caused by myxomatous mitral valve disease. J Small Anim Pract 2005; 46: 121-130.

2. Kvart C, Haggstrom J, Pedersen HD, et al. Efficacy of enalapril for prevention of congestive heart failure in dogs with myxomatous valve disease and asymptomatic mitral regurgitation. J Vet Intern Med 2002; 16: 80-88.

10. Lombard CW, Jons O, Bussadori CM. Clinical efficacy of pimobendan versus benazepril for the treatment of acquired atrioventricular valvular disease in dogs. J Am Anim Hosp Assoc 2006; 42: 249-261.

3. Borgarelli M, Savarino P, Crosara S, et al. Survival characteristics and prognostic variables of dogs with mitral regurgitation attributable to myxomatous valve disease. J Vet Intern Med 2008; 22: 120-128.

11. Häggström J, Boswood A, O'Grady M, et al. Effect of pimobendan versus benazepril hydrochloride on survival times in dogs with congestive heart failure due to naturally occurring myxomatous mitral valve disease: Results of the QUEST study. J Vet Intern Med 2008 Jul 11 (in press).

4. Borgarelli M, Zini E, D'Agnolo G, et al. Comparison of primary mitral valve disease in German Shepherd dogs and in small breeds. J Vet Cardiol 2004; 6: 27-34.

12. Bach JF, Rozanski EA, MacGregor J, et al. Retrospective evaluation of sildenafil citrate as a therapy for pulmonary hypertension in dogs. J Vet Intern Med 2006; 20: 1132-1135.

5. Pouchelon JL, Jamet N, Gouni V, et al. Effect of benazepril on survival and cardiac events in dogs with asymptomatic mitral valve disease: A retrospective study of 141 cases. J Vet Intern Med 2008; 22: 905-914.

13. Boswood A, Murphy A. The effect of heart disease, heart failure and diuresis on selected laboratory and electrocardiographic parameters in dogs. J Vet Cardiol 2006; 8: 1-9.

6. Atkins CE, Keene BW, Brown WA, et al. Results of the veterinary enalapril trial to prove reduction in onset of heart failure in dogs chronically treated with enalapril alone for compensated, naturally occurring mitral valve insufficiency. J Am Vet Med Assoc 2007; 231: 1061-1069.

14. Boswood A, Dukes-McEwan J, Loureiro J, et al. The diagnostic accuracy of different natriuretic peptides in the investigation of canine cardiac disease. J Small Anim Pract 2008; 49: 26-32.

7. Ettinger SJ, Benitz AM, Ericsson GF, et al. Effects of enalapril maleate on survival of dogs with naturally acquired heart failure. The Long-Term Investigation of Veterinary Enalapril (LIVE) Study Group. J Am Vet Med Assoc 1998; 213: 1573-1577. 8. BENCH, Pouchelon JL, Martignoni L, et al. The effects of benazepril on survival times and clinical signs of dogs with congestive heart failure: Results of a multicenter, prospective, randomized, double-blinded, placebo-controlled, long-term clinical trial. J Vet Cardiol 1999; 1: 7-18.

15. Oyama MA, Fox PR, Rush JE, et al. Clinical utility of serum N-terminal pro-B-type natriuretic peptide concentration for identifying cardiac disease in dogs and assessing disease severity. J Am Vet Med Assoc 2008; 232: 1496-1503. 16. Troughton RW, Frampton CM, Yandle TG, et al. Treatment of heart failure guided by plasma aminoterminal brain natriuretic peptide (N-BNP) concentrations. The Lancet 2000; 355: 1126-1130. 17. Lainchbury JG, Troughton RW, Frampton CM, et al. NTproBNP-guided drug treatment for chronic heart failure: design and methods in the "BATTLESCARRED" trial. Eur J Heart Fail 2006; 8: 532-538.




ROYAL CANIN VIEWPOINT

Nutritional management of early cardiac disease: ACT with SPEED

Daniel Baker, DVM Scientific Communications, Royal Canin USA Dr. Baker graduated from the University of Massachusetts-Amherst with a Bachelor of Science degree in biology with Honors in 1999. As an undergraduate he was one of the eighteen from around the world who took part in the East/West marine biology program at Northeastern University, allowing students to compare and contrast marine flora and fauna in three distinct parts of the world. Daniel received his DVM degree from Ross University in 2003 having completed his clinical year at the University of Minnesota. Following graduation he worked as a small animal clinician for 4 years. During this time he focused mainly in the area of emergency and critical based medicine. Daniel is currently a member of the Scientific Communications team for Royal Canin USA.

A

ccurate and timely diagnosis of early stage (Class 1 & 2, Table 1) cardiac disease historically has been difficult. Most patients show no outward evidence of being sick. Owners themselves usually do not report clinical signs related to a cardiac abnormality until later stages occur. Typical treatment of early stage cardiac disease has largely focused on benign neglect with subsequent monitoring of the patients cardiac rate, rhythm, size and associated clinical signs at six to twelve month intervals. The question that must be asked is a topic of much debate within the veterinary community. “If a patient shows no outward clinical signs


Denise Elliott, BVSc (Hons), PhD, Dipl. ACVIM, Dipl. ACVN Scientific Affairs, Royal Canin USA Dr. Elliott received her degree in Veterinary medicine with honors from the University of Melbourne in 1991. After completing an internship in Small Animal Medicine and Surgery at the University of Pennsylvania, Denise completed a residency in Small Animal Internal Medicine and Clinical Nutrition at the University of California-Davis. Denise became a Diplomate of the American College of Internal Veterinary Medicine in 1996 and the American College of Veterinary Nutrition in 2001. She received her PhD in Nutrition from the University of California-Davis in 2001, for her work on multifrequency bioelectrical impedance analysis in healthy cats and dogs. Denise is currently the Director of Scientific Affairs for Royal Canin USA.

associated with a disease, such as early cardiac disease, what if anything should be done clinically to aid in the improvement of the animal’s health”? Through the collaboration with some of the worlds leading cardiologists and nutritionists in conjunction with the innovative research performed at Royal Canin and the WALTHAM Centre for Pet Nutrition, we now realize the beneficial effects of implementing early nutritional in patients faced with cardiac abnormalities. Nutrition by itself can have profound beneficial effects at minimizing metabolic disturbances, while at the same time improving the patients over all quality of life.


Table 1. Classification of heart disease Grade

Clinical description

Class I

No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea.

Class II

Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.

Class III

Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.

Class IV

Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

Cardiac disease is now the second leading cause of death in dogs. Chronic valvular disease (CVD) s for approximately 75% of these cases while dilated cardiomyopathy (DCM) is responsible for 10-15% of cases observed. Over the past decade more advanced diagnostic tools such as: electrocardiography (ECG), Holter monitoring and echocardiography are now available to the general practitioner. This allows for early diagnosis and subsequent intervention of early cardiac disease. Nutrition’s primary role in the prevention and treatment of cardiac disease is multimodal. Through the use of key nutrients, dietar y intervention seeks to provide optimal amounts of energy, minimize oxidative stress, reduce inflammation, balance electrolytes and ultimately to improve cardiac performance. Through the use of the ACT with SPEED acronym we can better understand each key nutrients role in slowing the progression of heart disease.

ACT A

rginine, an essential amino acid, is the precursor for endogenously synthesized nitric oxide. Nitric oxide is well known for its role as an endotheliumderived relaxation factor, which in turn is responsible for maintaining normal vascular tone (1). Endothelial dysfunction has been linked, in humans and dogs, with congestive heart failure


(CHF) (2). Arginine supplementation appears to improve cardiac output in patients with cardiac disease by positively inf luencing preload and afterload (CO = HR x contractility x preload/ afterload).

Carnitine, a quaternary amine, is composed of two essential amino acids, lysine and methionine. It is commonly found concentrated in both skeletal and cardiac muscle. L-carnitine (the biologically active form) is critical for oxidation of fatty acids within mitochondria. It serves as a transport shuttle of fatty acids from outside the mitochondria into the inner membrane and in turn is a key component in the regulation of the citric acid cycle (3). L-carnitine is also responsible for transporting metabolic waste products out of the mitochondria that might other wise become cardiotoxic. L-carnitine is normally provided to the animal in sufficient amounts through intestinal absorption or following hepatic and renal synthesis. In certain breeds (Boxers, Doberman Pinschers and American Cocker Spaniels) there have been reported myocardial carnitine deficiencies (4,5). In a great many of these cases plasma carnitine levels were within normal limits. These findings suggest a membrane transport defect may be present preventing L-carnitine from entering into the myocardial cells from the plasma. Providing optimal amounts of carnitine in the diet may improve overall myocardial function.

T

aurine, a non-essential amino acid in the dog, is well known for its powerful antioxidant effects throughout the body. Taurine also is a key nutrient in the treatment of certain cardiomyopathies (6-8). Recent evidence also suggests that feeding certain lamb-based diets and severely protein restricted diets, may lead to marked taurine deficiencies with associated clinical signs (9-10). Breed associated deficiencies (e.g. American Cocker Spaniel, Portuguese Water dog) have manifested themselves in the form of dilated cardiomyopathy. Clinical improvement has resulted in several cases where the proper taurine levels were present within the diet (5-11). Taurine has also proven to have positive iontropic effects in animals with experimentally induced heart failure (12). This suggests taurine supplementation may prove beneficial in patients with cardiac disease without true taurine deficiencies.




ROYAL CANIN VIEWPOINT

With

SPEED Sodium restriction has long been thought of as the nutritional mainstay of treating cardiac disease. While sodium restriction has its place adjunctively along side additional nutritional modalities, it is the degree of sodium restriction based on the severity of cardiac disease present that must be taken into . Indeed, sodium restriction that is too severe early on in the disease process may lend itself to an exaggerated response by the renin-angiotensin aldosterone system (13-18). This can exacerbate clinical signs and the progression of the disease itself. The advent of angiotensin converting enzyme (ACE) inhibitors has further decreased the need for severe sodium restriction in most patients (19). Based on our current understanding of sodium’s relationship to cardiac physiology during certain stages of cardiac disease, tailoring the degree of sodium restriction is of the utmost importance.

Protein restriction has erroneously worked its way into the management of cardiac disease. Many of today’s diets are formulated on the antiquated thought process that protein restriction lends itself to reduced metabolic stress on the kidneys and liver (20). No known peer reviewed publications exist proving this hypothesis. What’s worse is that protein restricted diets favor the development of cardiac cachexia. This in turn will lead to the perception by the owner of a poor

Table 2. Cachexia scoring system Cachexia score

Description

0

Good muscle tone with no evidence of muscle wasting

1

Early, mild muscle wasting, especially in the hindquarters and lumbar region

2

Moderate muscle wasting apparent in all muscle groups

3

Marked muscle wasting as evidenced by atrophy of all muscle groups

4

Severe muscle wasting

*Modified from Freeman (29).


quality of life and likely hasten euthanasia. Cardiac diets should contain optimal amounts of highly digestible proteins that allow for the preservation of lean body mass.

Energy requirements in patients with cardiac disease should be considered with both the patients’ body condition score (BCS) and degree of cardiac cachexia (Table 2) in mind. The goal should be to manage caloric intake to prevent both obesity and emaciation while preserving lean body mass. Special focus needs to be placed on patients with poor BCS and/or cachexia already prevalent. Poor doing is often associated with anorexia in patients with cardiac disease. A recent study revealed the daily caloric intake in dogs with dilated cardiomyopathy was 72-84% of their expected daily energy requirements (21). Nutrient profiles therefore need be formulated with nutrients that are highly digestible and readily bioavailable.

Eicosapentaenoic acid (EPA) &

D

ocosahexaenoic acid (DHA) are essential long chain fatty acids derived from marine sources that provide profound anti-inflammatory effects throughout the body but especially within the heart. Studies have revealed that dogs with congestive heart failure have decreased concentrations of plasma EPA/DHA in comparison with healthy dogs (21). Their combined effects target the reduction of pro-inflammatory mediators actions on the cardiac infrastructure (21). Supplementation with marine derived omega-3 fatty acids have also been shown to improve cardiac cachexia scores in dogs with cardiac disease. A recent study revealed that EPA/DHA from fish oils given over a six-week period may decrease the severity and frequency of arrhythmias in Boxers who suffer from Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) (22). Several other key nutrients related to the heart should be taken into consideration. For example, vitamin E has positive effects on inhibiting lipid peroxidation of the cellular membranes of cardiac cells. Vitamin E can be looked at as a biomarker of oxidative stress. In patients with heart disease, low



NUTRITIONAL MANAGEMENT OF EARLY CARDIAC DISEASE: ACT WITH SPEED

Vitamin E concentrations have been negatively correlated with the severity of the disease (23). Vitamin B deficiencies have been reported in cats with cardiomyopathy (24). Hypomagnesemia may potentiate cardiac arrhythmias, decrease myocardial contractility and contribute to muscle weakness (25,26). This is often observed in the Cavalier King Charles Spaniel (27). Potassium, traditionally hyper-supplemented in historic cardiac diet formulations to compensate for the urine wasting secondary to diuretic therapy, is no longer necessary. With the advent of ACE inhibitor therapy that increases the renal absorption of potassium, modern cardiac diets should contain normal levels of potassium (28).

In summary, we must first identify early stage cardiac disease in our patients. Then we need to educate pet owner’s that early cardiac disease left untreated may have drastic life long complications. Many of these consequences stem from a subclinical disease process not necessarily manifesting itself as outward clinical signs. As clinicians, we now have the opportunity to offer our clients early dietary therapeutic intervention in conjunction with close monitoring of their pet’s disease state. Together we can give owners and their beloved pets, the nutritional tools necessary to aid in the management of heart disease and to improve the chance of living longer, healthier lives.

REFERENCES 1. Palmer RM, Ferrige AG, Moncada S. Nitric oxide release s for the biological activity of endothelium-derived relaxing factor. Nature 1987; 327: 524-526. 2. Wang J, Yi GH, Knecht M, et al. Physical training alters the pathogenesis of pacing-induced heart failure through endothelium-mediated mechanisms in awake dogs. Circulation 1997; 96: 2683-2692. 3. Rebouche CJ, Paulson DJ. Carnitine metabolism and functions in humans. Annu Rev Nutr 1986; 6: 41-66. 4. Keene BW. L-carnitine deficiency in canine dilated cardiomyopathy In: R. W. Kirk and J. D. Bonagura, eds. Current veterinary therapy XI. Philadelphia: W. B. Saunders Co, 1992; 780-783. 5. Kittleson MD, Keene B, Pion PD, et al. Results of the multicenter spaniel trial (MUST): taurine- and carnitine-responsive dilated cardiomyopathy in American Cocker Spaniels with decreased plasma taurine concentration. J Vet Intern Med 1997; 11: 204-211. 6. Kramer GA, Kittleson MD, Fox PR, et al. Plasma taurine concentrations in normal dogs and in dogs with heart disease. J Vet Intern Med 1995; 9: 253-258. 7. Alroy J, Rush JE, Freeman LM, et al. Inherited infantile dilated cardiomyopathy in dogs: genetic, clinical, biochemical and morphologic findings. J of Med Genet 2000; 95: 57-66. 8. Freeman LM, Rush JE, Brown DJ, et al. Relationship between circulating and dietary taurine concentrations in dogs with dilated cardiomyopathy. Vet Ther 2001; 2: 370-378. 9. Torres CL, Fascetti AJ, Rogers QR. Taurine and sulphur amino acid status in dogs fed dry commercial poultry-by-product meal or lamb meal diets. J Vet Int Med 2000; 14: 364. 10. Sanderson SL, Gross KL, Ogburn PN, et al. Effects of dietary fat and L-carnitine on plasma and whole blood taurine concentrations and cardiac function in healthy dogs fed protein-restricted diets. Am J Vet Res 2001; 62: 1616-1623.

15. Webester KT, Brilla CG. Pathological hypertrophy and cardiac interstitium. Firbrosis and renin-angiotensin system. Circulation 1991; 83:1849-1865. 16. Tan LB, Jalil JE, Pick R, et al. Cardiac myocycte necrosis induced by angiotension II. Circ Res 1991; 69: 1185-1195. 17. Pedersen HD, Koch J, Jensen AL, et al. Effects of a low sodium diet with a high potassium content on plasma endothelin-1, atrial natriuretic peptide and arginine vasopressin in normal dogs. J Vet Med 1994; 41: 713-716. 18. Pedersen HD, Koch J, Jensen AL, et al. Some effects of a low sodium diet high in potassium on the renin-angiotensin system and plasma electrolyte concentrations in normal dogs. Acta Vet Scand 1994; 35: 133-140. 19. Kock J, Pedersen HD, Jensen AL, et al. Short term effects of acute inhibition of the angiotensin-converting enzyme on the renin-angiotension system and plasma atrial natriuretic peptide in healthy dogs fed a low-sodium diet versus a normal-sodium diet. J Vet Med 1994; 41: 121-127. 20. Pensinger RR. Nutritional management of heart disease In: R. W. Kirk, ed. Current veterinary therapy III. Philadelphia: W. B. Saunders, 1968; 229-232. 21. Freeman LM, Rush JE, Kehayias JJ, et al. Nutritional alterations and the effect of fish oil supplementation in dogs with heart failure. J Vet Intern Med 1998; 12: 440-448. 22. Smith CE, Freeman LM, Rush JE, Cunningham SM, Biourge V. Omega-3 fatty acids in Boxer dogs with arrhythmogenic right ventricular cardiomyopathy. J Vet Intern Med 2007; 21: 265-273. 23. Freeman LM, Brown DJ, Rush JE. Assessment of degree of oxidative stress and antioxidant concentrations in dogs with idiopathic dilated cardiomyopathy. J Am Vet Med Assoc 1999; 215: 644-646. 24. McMichael MA, Freeman LM, Selhub J, et al. Plasma homocysteine, B vitamins, and amino acid concentrations in cats with cardiomyopathy and arterial thromboembolism. J Vet Intern Med 2000; 14: 507-512. 25. O'Keefe D, Sisson DD. Serum electrolytes in dogs with congestive heart failure. J Vet Intern Med 1993; 7: 118.

11. Gavaghan B, Kittleson MD. Dilated cardiomyopathy in an American Cocker Spaniel with taurine deficiency. Aust Vet J 1997; 75: 862-868.

26. Cobb M, Michell AR. Plasma electrolyte concentrations in dogs receiving diuretic therapy for cardiac failure. J Small Anim Pract 1991; 33: 526-529.

12. Elizarova EP, Orlova TR, Medvedeva NV. Effects on heart membranes after taurine treatment in rabbits with congestive heart failure. Arzneimittelforschung 1993; 43: 308-312.

27. Pedersen H, Mow T. Hypomagnesemia and mitral valve prolapse in Cavalier King Charles Spaniels. Zentralbl Veterinarmed 1998; 45: 607-614.

13. Koch J, Pedersen HD, Jensen AL, et al. Activation of the renin-angiotensin system in dogs with asymptomatic and symptomatic dilated cardiomyopathy. Res Vet Sci 1995; 59: 172-175.

28. Roudebush P, Allen TA, Kuehn NF, et al. The effect of combined therapy with captopril, furosemide, and a sodium-restricted diet on serum electrolyte concentrations and renal function in normal dogs and dogs with congestive heart failure. J Vet Intern Med 1994; 8: 337-342.

14. Pedersen HD, Koch J, Poulsen K, et al. Activation of the renin-angiotensin system in dogs with asymptomatic and mildly symptomatic mitral valvular insufficiency. J Vet Intern Med 1995; 9: 328-331.

29. Freeman LM. Nutritional Modulation of cardiac disease. WALTHAM Focus Special Edition Advances in Clinical Nutrition, 2000; 36-42.




HOW I APPROACH...

Syncope in dogs - a syndrome, not a disease

Marianne Skrodzki, DVM Berlin, Dr. Skrodzki studied law and veterinary medicine in Berlin and was awarded the “habilitation” and private lectureship with venia docendi for her research work on small animal diseases. She has run her own Small Animal Cardiology practice in Berlin since 2002. Marianne Skrodzki has been a guest lecturer at the University of Riga, St. Petersburg, Moscow and Tirana, with study visits to the University of Philadelphia, Utrecht and Edinburgh. Her main interests are the diagnosis and therapy of hereditary and acquired cardiac diseases in small animals. Marianne Skrodzki is internationally active, e.g. in the WSAVA and the Canine Heart Failure International Expert Forum (CHIEF).

Introduction The brain, as the controlling organ for many of the body's functions, has first priority for blood supply. Compared to other organ systems, which suffer early loss of function, the brain receives adequate blood supply with an average arterial pressure of 60-70 mmHg. A drop in blood pressure to approximately 40 mmHg brings about a reduction in brain oxygen uptake, CO2 production and glucose utilization. Below this pressure, brain function gradually comes to a standstill. As a result of regional or global brain malperfusion attacks of dizziness can occur, as can spontaneous,


Eberhard Trautvetter, DVM Berlin, Dr. Trautvetter has worked in the field of Small Animal Cardiology since 1967. Following a research trip to Pennsylvania University in 1972, he was appointed University Professor at the Freien Universität in Berlin. In 1984 he took over as Head of the Small Animal Clinic. Since his retirement in 2000, Eberhard Trautvetter has worked in a practice in Berlin and supervised graduate students studying for a doctorate in and abroad. His main scientific interest is in pedigree analysis and genetic cardiac diseases in pedigree dogs and cats; he received worldwide distinctions for his research successes, such as the Centennial Award of Merit of the University of Pennsylvania and the Honorary Medal of the CNVSPA (French Association of Veterinary Specialists in Small Animals).

reversible, brief loss of consciousness, which is medically defined as syncope (fainting). An interruption in the brain's blood supply of 810 seconds or more leads to loss of consciousness and in serious cases even to the patient's death. Syncope is not a disease, but a symptom that can occur in many conditions and diseases (Table 1). Cardiac-related syncope is caused by arrhythmia or obstruction of the ventricular outflow tracts, congenital defects with cyanosis, as well as by heart diseases, which lead to a decrease in cardiac output with global or regional malperfusion. Since loss of consciousness is accompanied by decreased skeletal



Table 1. Breakdown of seizures based on cause Cardiac origin

Extracardiac origin

Arrhythmogenic Asystole Bradycardia Tachycardia

Pulmonary Pulmonary hypertension Cough syncope Diseases causing hypoxemia

Organic heart disease Obstruction of ventricular outflow tract - Aortic, pulmonary stenosis - Hypertrophic obstructive cardiomyopathy - Heartworm disease

Neurological/neurovascular Epilepsy Ischemia Central bleeding Cerebral vasoconstriction Encephalitis (e.g. distemper) Portosystemic shunt

Tetralogy of Fallot (cyanosis) Drop in cardiac output - Valvular insufficiency - Dilated cardiomyopathy Cardiac tamponade Myxoma Drug-induced

Metabolic/Endocrine Hypoglycemia Hypocalcemia Hypoadrenocorticism Drug-induced Other Anemia Tumors

muscle tone, patients will fall over or collapse. Finally, cerebral hypoperfusion can also lead to seizures in the recovery position. Consequently, spasms, spontaneous sound utterances, as well as uncontrolled excretion and urination may be observed. Various types of seizure can merge or occur at the same time. Extracardiac causes, which lead to sudden changes in body posture and movement, but which do not strictly fulfill the definition of syncope, mainly include hypoglycemia, hypocalcemia, portosystemic shunt, diseases of the central nervous system and breathing insufficiencies with severe hypoxia (Table 1), aside from epilepsy primarily of central origin.

Case history In many cases, it is difficult to explain a seizure event by differential diagnosis. Nevertheless, given a specific case history, the cause of syncope can be identified in many patients. Therefore, the next question to ask is whether it is indeed a case of syncope, and not just a dizzy turn, or epilepsy. It is of considerable importance to know whether the patient has a proven heart condition, or whether a cardiac murmur is known to exist, without any further diagnoses or therapy having been hitherto undertaken.

Faced with a seizure event for which they are unprepared, dog owners, for the most part lay-persons, will be frightened to the extent that an objective description of the event is scarcely to be expected, if at all. Details are especially unclear regarding the duration of the fit. Also, if asked whether the animal had fallen unconscious, most owners will answer in the negative, saying: “My dog looked at me” and often misinterpret the situation. One should not, therefore, accept the details of the seizure event as gospel, instead they should be critically challenged. A suggestive line of questioning is, however, to be strictly avoided.

Of particular interest is the time at which the seizure event occurs. Generally speaking, epileptic fits occur spontaneously, or during rest or sleep. However, cardiac syncope is often caused by characteristic triggers, such as mental or physical exertion. “Cough syncope” is exclusively observed during or immediately after coughing, whereas most other seizures of extracardiac origin are not dependent upon the situation. Characteristic of epilepsy are continuous tonicclonic movements lasting more than 20 seconds, as well as a longer-lasting post ictal twilight state, the latter in contrast to syncope accompanied by cramp. The onset of cramp likewise points to epilepsy. After a syncopal episode, patients regain their bearings within seconds. After longer-lasting seizures of one or two minutes, most animals also remain dazed or confused for only a few seconds. Longer-lasting disorientation is more indicative of an epileptic fit. Exhaustion and fatigue also occur after syncope, but are more frequent and more pronounced after epileptic fits. A less decisive factor is whether, during the loss of consciousness, “spasms” are noted. Spontaneous movements not only occur in cases of convulsive seizure, but can also occur in syncope. Uncontrolled excretion and/or urination are more or less equally frequent in generalized tonic-clonic and syncopal seizures. The color of the mucous membranes or tongue, as well as type and rate of breathing during a seizure, provide important information for




HOW I APPROACH...

diagnostic discrimination, for example anemia from pulmonary disease. Family case history is helpful for an evaluation of the genetic risk of seizure causes. It is worth knowing whether any animals related to the patient died from sudden cardiac death, or whether congenital heart disease or epilepsy are known to occur commonly. In the case of repeat seizures, it is important to seek information concerning the frequency, pattern of seizure and duration of previous episodes. If the patient is known to suffer from heart disease and already undergoing therapy, the drug case history is of crucial importance. Drugs can cause a syncopal seizure, either due to an undesirable vasodilatory effect, or bradycardiac or tachycardiac effects. Aside from vasodilatory hypertensive agents (ACE inhibitors, calcium antagonists and dihydralazine) cardiac glycosides and most antiarrhythmic drugs and diuretics can be responsible for syncope.

Diagnostic evaluation Patients with syncope and primary cardiac disease show a considerably higher mortality than dogs with extracardiac syncope and syncope of an unclear cause. After an examination of the case history, the diagnosis focuses on a basic general examination, auscultation of heart and lungs, an electrocardiogram, blood pressure monitoring and a general neurological examination. During the physical examination, close attention will be paid to not only determining capillary return and the color of the mucous membranes, but also, and more especially, pulse rate and quality and symmetry of pulse waves in both rear extremities. Particular attention during auscultation is to be paid to the heart beat and also pathologically altered heart sounds. For example, a louder second heart sound can be heard in cases of pulmonary hypertonia. A more extensive auscultation will also reveal paroxysmal bradycardia or arrhythmia. A pulse deficit noted


during a simultaneous assessment of pulse and heart rate can point to a clinically relevant arrhythmia. A longer electrocardiogram recording at rest is vital for a basic diagnosis. During electrocardiography, while awake and with the help of an assistant, the animal is held on its right side. Care must be taken to be able to conclude heart disease on the basis of characteristic indices. An electrocardiogram at rest may reveal nothing, even in patients with severe heart disease. In some dogs signs of myocardial malperfusion or disturbed heart rhythms are visible only during physical exertion, another ECG should therefore be taken during, or shortly after, the patient's exertion in doubtful cases or in cases of syncope of unclear origin. Here it is simply a question of recognizing heart rhythm disturbances and determining heartbeat frequency. Accordingly, it does not matter how the dog is lying. However, an analysis of ECG amplitude should not be undertaken. Generally speaking, a conventional ECG should take a few minutes maximum and will more or less represent a “snapshot”. Rare events, such as major heart rhythm disturbances or merely sporadic arrhythmia can often only be determined following prolonged ECG. In prolonged ECG or Holter ECG, the ECG recording is taken continuously over 24 hours and the data stored. However, the recording of a “snapshot” after 24 hours can, in itself, still be too short. In seizure diagnosis, laboratory analysis simply provides additional information. Nevertheless, a complete blood count (anemia), determination of blood sugar (hypoglycemia) and electrolytes (hyperkalemia, hypocalcemia) should be conducted. In all animals presenting with syncopal seizures, an echocardiographic examination is also advisable for the identification or exclusion of a heart defect. In suspected heart disease or respiratory disease, the thoracic radiograph is part of a standard examination. Special neurological examinations can prove necessary for differential diagnostic purposes, supplemented, where applicable, by a CT or MRT scan.



SYNCOPE IN DOGS - A SYNDROME, NOT A DISEASE

Table 2. Rhythm disturbances with manifestation of syncope Asystole

Tachycardia

Bradycardia Sinusbradycardia

Atrial fibrillation

High-grade AV block

Supraventricular tachycardia

Sick Sinus syndrome

Ventricular tachycardia Ventricular flutter Ventricular fibrillation Wolf-Parkinson-White syndrome

Cardiogenic syncope Cerebral perfusion is governed by systemic blood pressure, in other words by cardiac output and peripheral vascular resistance. For this reason, a decrease in cardiac output due to various heart diseases on its own or as a result of rhythm disturbances and a drop in peripheral vascular resistance, for example through reflex-mediated vasodilation, will promote syncope.

Adams-Stokes syndrome All types of heart rhythm disturbance that lead to central hypoxia can trigger cardiac seizures. Such attacks were described for the first time last century by two physicians from Dublin (Robert Adams and William Stokes), hence the term AdamsStokes seizure. These include asystole, pronounced bradycardia and supraventricular and/or ventricular tachycardia and ventricular fibrillation. Miscellaneous forms also occur (Table 2). While it is possible in dogs with a healthy heart to compensate for a rhythm disturbance to a broad extent by adapting stroke volume, for most dogs with heart disease presenting with arrhythmia it is impossible. Syncope consequently ensues. Typical of syncope is the sudden onset irrespective of position. With the occurrence of rhythmogenic syncope, patients mostly become pale and may show tonic-clonic convulsions. The only decisive factors in the seizure pattern are the severity and duration of the heart rhythm disturbance or the degree of impaired cerebral blood flow. The clinical manifestations of seizure activity during paroxysmal brady- or tachyarrhythmia can vary

with minimal cerebral blood flow. Momentary staggering or gradual collapse in the animal occur particularly in the presence of constant arrhythmia, such as atrial fibrillation or total AV block, but mostly just in the event of physical exertion or excitement. Generally speaking, rhythmogenic syncope should be viewed as an abortive form or precursor of sudden cardiac death.

Asystole Asystole is medically described as a complete lack of electrical and mechanical activity in the heart, which is recognized as a flatline on an ECG. Blood pressure drops suddenly. Asystole of a few seconds generally only causes dizzy spells. However, the abrupt, complete interruption of cerebral blood flow can also lead to the patient's sudden collapse. Cardiac arrest lasting ten seconds brings about collapse, muscle spasms and paleness of the mucous membranes. Dogs with longer-lasting asystole suffer seizure, are cyanotic and often exhibit uncontrolled excretion or urination due to sphincter weakness. The pulse can no longer be felt, although the absence of a detectable pulse in itself is not a sure sign of asystole, since ventricular fibrillation (pulseless tachycardia) can also display the same symptom. Detectable heart sounds are absent in asystole. In cases of asystole lasting more than three minutes most patients die. Cardiac asystole can occur, for example, from cardiomyopathies, heart tumors or myocarditis. It is not uncommon for asystole to be preceded by ventricular fibrillation, which, for its part, can be triggered by any cardiovascular disease. Non-cardiac origins include, among other things, metabolic changes, such as severe acidosis in diabetes mellitus, hyper- or hypokalemia, and drug intoxication.

Atrioventricular block Deceleration, intermittent interruptions or longlasting block of conduction between the atria and ventricles are referred to as atrioventricular block (AV block). While grade I or grade II type I AV blocks remain free of symptoms and are merely indicative of the risk of a higher-grade block, grade II type II AV block, as a result of bradycardia with regular or irregular dropping of ventricular complexes, can lead to a presyncopal attack, and more rarely to seizure. It is also possible for grade III AV block to develop.




HOW I APPROACH...

Figure 1. Total AV block in a dog presenting with AV insufficiency as a result of chronic degenerative mitral valve disease; note the regular presence of atrial contractions, total block of conduction, atria and ventricles contract separately and independently, escape rhythm with broad, bizarre QRS complexes, atrial rate 120/min; Paper feed: 25 mm/s, calibration 0.5 cm = 1 mV.

In the case of grade III AV block, which is also referred to as complete or total AV block, due to the total block of conduction between the atria and ventricles, the result is a complete dissociation of atrial and ventricular excitation (Figure 1). The atria and the ventricles beat separately and independently and the atrial rate is very much higher than the ventricular rate. The rate of the ventricular escape rhythm generally measures less than 40 beats/min. Accordingly, it is important to immediately consider the possibility of total AV block where the pulse rate is under 40/min. The clinical picture ranges from asymptomatic bradycardia with a sufficiently fast escape rhythm (very rare!) through dizziness to collapse. A very low ventricular rate of, say, 25 beats/min is no longer sufficient to attain a normal minute volume, which often clinically manifests itself as an Adams Stokes seizure. The frequency of seizures varies greatly and can range from the occasional syncopal event to several seizures a day. Since there is always the danger of the absence of ventricular automatism as well, the patients in question are in constant danger of losing their lives, regardless of the frequency of the seizure. Heart muscle diseases and congenital or acquired heart valve disease and other diseases involving the electrical conduction system (ventricular septal defect, myocarditis, degenerative diseases) come into consideration as causes of highgrade AV block. Breed-specific changes, as that occurring in the bundle of His in Dobermans, occur rarely. Furthermore, various conductioninhibiting drugs (e.g. beta-receptor blockers, digitalis, calcium antagonists), and also the influence of the autonomous nerve system and hyperkalemia are causally responsible for total AV block.


Figure 2. Dog presenting with dilated cardiomyopathy; atrial fibrillation with irregular atrial fibrillation waves (F waves) and irregular RR intervals; heart rate 240/min: Paper feed 25 mm/s, calibration 1 cm = 1 mV.

Sick Sinus syndrome Sick Sinus syndrome, also known as "Sinus node dysfunction", is the generic term for various bradycardiac heart rhythm disturbances, and also for the pathological transition from bradycardia to tachycardia. The essential causes are symptoms of fatigue, or sinus node dysfunction following strain on the left atrium, or degenerative changes in the atrial conduction pathways. The isolated or combined occurrence of sinus bradycardia, sinus arrest, SA block, atrial or AV nodal escape rhythm, extrasystoles with tachycardiac episodes, paroxysmal atrial fibrillation, atrial flutter, as well as tachy-bradycardiac syndrome with changing atrial rhythm lead to ataxia or syncope as a result of a decrease in cerebral blood supply. Typical signs are absence of, or insufficient heart rate increase during exertion.

Atrial fibrillation In atrial fibrillation, the sinus node ceases to be effective as a normal pacemaker (Figure 2). The electrical impulses to start a heart contraction originate in various areas of the atria. On an ECG, no regular atrial activity is discernible. Fibrillation waves may be distinguished by their




Table 3. Common causes of arrhythmia Cardiac Cardiomyopathy Neoplasia Acquired valve diseases Congenital diseases Genetic (German Shepherd) Myocarditis

Extracardiac Stomach torsion, volvulus Neoplasia (e.g. mammary tumor, pheochromocytoma) Septicemia Fever Trauma, pain Pulmonary diseases Hypoxia Anemia Uremia Acidosis Electrolyte imbalances Drugs

shape, amplitude and direction. Conduction to the ventricle is irregular. Hemodynamically speaking, atrial fibrillation means atrial stand still, since the pump function of the atrium fails. In a rapid sequence of strokes, the diastolic duration is sometimes so short that ventricular filling is inadequate and the stroke volume is unable to trigger a pulse wave, which is clinically discernible as a pulse deficit. Atrial fibrillation in itself is not life-threatening, but can lead to insufficiency even in a primarily healthy myocardium. In patients with myocardial damage or cardiac insufficiency, tachycardiac atrial fibrillation can speed up the advancing disease process within a very short time. The faster the heart activity, the stronger the hemodynamic, and therefore also clinical, effects, since the share of the blood volume propelled by the atrial contraction is not contributing to the ventricular stroke volume. If the heart's performance, already undermined by the basic disease, is further reduced due to tachycardiac atrial fibrillation, syncope can occur as a result of peripheral or cerebral hypoxia. Mostly of secondary occurrence, atrial fibrillation appears in dogs with dilated cardiomyopathy, mitral valvular disease or persistent Ductus arteriosus, as a result of pronounced atrial dilation. Idiopathic atrial fibrillation is relatively rare.

Ventricular tachycardia Ventricular tachycardia originates in the right or left Tawara branches of the conduction system, or in the myocardium and always has a serious cardiac

o r extracardiac cause (Table 3). In German Shepherds, ventricular tachycardia is genetically found in the form of a primary arrhythmia. Highly frequent ventricular tachycardia leads very quickly, especially in primary cardiac disease, to failure of the pump function with Adams-Stokes seizures, cardiogenic shock and possibly also sudden cardiac death. Breeds especially at risk are Boxers and Doberman Pinchers. In both breeds, sudden cardiac death can occur as a result of ventricular tachycardia as the first and only “symptom” of dilated cardiomyopathy. On an ECG, ventricular tachycardia is recorded as at least three rapidly successive abnormalities, in other words deformed ventricular complexes (Figure 3). Ventricular tachycardia generally arises through a re-entry mechanism. In normal heart activity, an action potential is generated in the sinus node, directed through the atria and AV nodes into the ventricular myocardium and subsides in the heart's apex area, because the surrounding myocardium is not yet in an excitable state (refractory phase). Atrial excitation can be retrograde and therefore independent of ventricular action. Interspersed P waves of normal shape and direction are occasionally visible in the ventricular rhythm. Ventricular flutter and ventricular fibrillation are life-threatening rhythm disturbances. While in ventricular flutter at rest, the cardiac output volume is sufficient for a limited time, the increase in volume during the patient's exertion can lead to an Adams-Stokes seizure, as a momentary event. Without therapeutic treatment it is not uncommon for ventricular flutter to develop into ventricular fibrillation. With ventricular fibrillation the heart's activity remains hemodynamically ineffective. Cardiac output drops so quickly that it can result in irreversible brain and heart damage in only a few minutes. While ventricular flutter is depicted in an ECG as wave-shaped QRS complexes of more or less similar shape, size and frequency, in ventricular fibrillation QRS complexes are seen to vary greatly.

Wolff-Parkinson-White syndrome (WPW syndrome) In a healthy heart, excitation can only spread from the atria to the ventricles through the




HOW I APPROACH...

AV node. Wolff-Parkinson-White syndrome involves arrhythmia in which there is usually a second and sometimes, although rarely, several electrical conduction pathways between the atria and the ventricles. A part of the ventricle is activated prematurely by means of circulating electrical excitation through accessory conduction pathways between the atria and the ventricles, e.g. the so-called bundle of Kent. Therefore the sinus node impulse is not transmitted to the ventricles through the AV node and the bundle of His. On an ECG, an elevation is often visible just before the R wave seen superimposed on the Q wave. This is referred to as the delta wave. Paroxysmal tachycardia, with normal or wide and bizarre QRS complexes, occurs due to the circulating excitation (re-entry mechanism). The P waves are inconspicuous and often not even recognizable. The PQ duration is shortened. ST changes are possible. WPW syndrome occurs congenitally in isolated form, but is also to be observed in AV valve dysplasia, mitral insufficiency as a result of chronic degenerative valve disease and in hypertrophic cardiomyopathy.

Figure 3. Dog presenting with gastric dilation volvulus: rhythm control. Line 1: tachycardiac rhythm, heart rate 220/min with normal QRS complexes, P waves present but partly obscured by preceding T waves. Line 2: supraventricular tachycardia with 2 premature ventricular extrasystoles; Line 3: ventricular tachycardia with deformed QRS complexes, heart rate 300/min, P waves not discernible: Paper feed 25 mm/s, calibration 0.5 cm=1 mV.

Treatment of arrhythmic syncope In the first instance, it is always important in the treatment of arrhythmic syncope to consider and recognize the cause of the heart rhythm disturbances, since a causal treatment always constitutes the best therapy. It is not uncommon for the therapeutic treatment of the underlying disease to make the additional istration of an antiarrhythmic drug unnecessary. This goes for all patients with arrhythmic seizures, regardless of whether the origin is cardiac or extra-cardiac. If the animal is already being given an antiarrhythmic drug or a cardiac glycoside, possible side-effects of the drug are to be causally clarified (Table 4) and the on-going therapy may need to be changed immediately, before further therapeutic measures are taken. Owing to their pro-arrhythmic and negative inotropic characteristics and other far-reaching side effects, antiarrhythmic drugs are not without danger. They should therefore be prescribed with caution and only after totally eliminating existing congestive heart failure. Bradycardiac heart rhythm disturbances with syncopal episodes can be altered with drugs,


temporarily at best. Intravenous atropine injection should only be considered for acute treatment (Table 4). In symptomatic patients with bradycardiac arrhythmia or, for example, in Sick Sinus syndrome, causal therapy is not possible, therefore the implantation of a pacemaker is the method of choice for continually raising the pacing rate. If syncopal seizures occur in patients with ventricular stand still or total AV block as a result of pronounced hyperkalemia, the serum potassium in the blood must be lowered as quickly as possible. In such cases, for example, the intravenous istration of a 10% solution of calcium gluconate (0.1-0.3 ml/kg by slow i.v. injection) is recommended. The treatment of the underlying disease, e.g. acute kidney failure, chronic kidney disease, or hypoadrenocorticism must follow. Should syncope occur as a result of asystole, an immediate resuscitation with artificial respiration and cardiac massage would be required. Asystole can, however, not be treated through defibrillation, since an irregular heart activity must still be present for it to work.




CASE REPORT A three-year-old Boxer (weighing 25 kg) was brought into the practice after one hour's intensive play with other dogs. At the start of the seizure the dog appeared dazed and his hindquarters gradually slumped. He eventually fell on his side. His extremities were limp and respiration was slow. After approximately 30 seconds to one minute, breathing became frequent again. The dog got up, became responsive again and walked slowly over to his owner. In the otherwise hitherto symptomless dog, stamina and physical resistance in the previous three months had been somewhat limited, which his owner had put down to the high temperatures outside. Previously, on two different days, while giving his owner an enthusiastic welcome at the front door, both of the dog's rear extremities briefly gave way. It was only after in-depth reflection that the owner realized the significance of these episodes. Until then he had not set any great store by the event, since he felt that the dog had just moved awkwardly. Although the dog originated from Poland and had no known family case history, a heart noise was known to exist. However, further examinations had not yet been conducted. He was not receiving any medication. The general clinical examination concluded no particular findings, merely that the arterial pulse in both rear extremities was symmetrical and only irregular at times (pulsus irregularis) with a small pulse pressure amplitude (pulsus parvus). Thoracic auscultation identified a grade IV/VI ejection systolic murmur in the region of the aorta with the Pmax in the 4th intercostal space left side with transmission into the carotid arteries. The murmur was also audible cranially in the right half of the thorax. The dominant sinus rhythm was punctuated paroxysmally by short series of extrasystoles. During the paroxysm, a pulse deficit was partly palpable. Respiratory auscultation was within normal limits. On the ECG, with the heart rate at 180 beats/min, short and longer bursts of ventricular extrasystoles were recorded (Figure 1). During this first ECG recording, the animal was observant and showed undisturbed behavior. Subsequently, the dog was forced to climb the stairs. In doing so, he very soon had difficulty in breathing and suddenly collapsed on his side. According to the owner, this seizure pattern resembled the one previously experienced in the woods. The ECG conducted within a few seconds with the dog in seizure indictated the presence of a ventricular tachycardia as illustrated in Figure 2. The echocardiography showed the concentric left ventricular hypertrophy with normal systolic function and a dilated left atrium. The Doppler sonography examination measured a maximum speed of transvalvular blood flow of 4.8 m/sec, which corresponds to severe aortic stenosis with a maximum gradient of

Figure 1.

Figure 2.

3-year-old male Boxer presenting with subvalvular aortic stenosis. ECG tracing I, II, III, left first third of image left-ventricular extrasystole, middle of image sinus rhythm with three ventricular complexes of nomotropic origin followed by right-ventricular extrasystole, beginning with a supraventricular extrasystole: Paper feed 25 mm/s, calibration 0.5 cm= 1 mV.

ECG of the same Boxer as in Figure 1; ventricular tachycardia (210 beats/min) after brief exertion with collapse/syncope in the gradual rest phase; sinus rhythm established after a further 2 minutes.




HOW I APPROACH...

around 92 mmHg. Thickening of the mitral valve was evident together with middle-grade mitral insufficiency detected by Doppler sonography. The right half of the heart, as well as the tricuspidal and pulmonary valves were, however, macroscopic and not visible by Doppler sonography. Radiographs showed the enlarged silhouette of the heart. Compared to the arteries the V. lobaris in the area of the upper lobes of the lung appeared somewhat widened. Pulmonary edema was not discernible. The results of the blood test (hemogram, electrolytes, blood glucose, liver enzyme, creatinine and urea) were within normal biological variations. In order to reduce the load on the myocardium and regulate the rhythm, the 25 kg dog was prescribed Propranolol at a dosage of 0.8 mg/kg 3 times a day, and 40 mg Furosemide twice daily, to eliminate venous congestion. Despite recommendations to avoid strenuous exercise, the owner allowed the dog to run along beside his bike only two days after the initial examination and in outside temperatures of around 26° C. Shortly after the start of the bike ride, the dog collapsed and had another seizure as previously described. The dog died on the street within a few minutes. The postmortem examination confirmed the diagnosis of severe subvalvular aortic stenosis.

An indication for immediate intravenous istration of an antiarrhythmic drug is symptomatic tachyarrhythmia in patients who are acutely threatened by sudden cardiac death. In dogs with ventricular tachyarrhythmia Lidocane is primarily used intravenously via bolus or continuous intravenous drip. The istration of Mexiletin is also possible, wherein it is imperative that the pronounced negative inotropic effect of this substance be taken into consideration. As a possible parenteral treatment of patients with syncope resulting from tachycardiac arrhythmia, targeted use of an antiarrhythmic drug, after having excluded or eliminated congestive heart failure, can considerably improve quality of life and prognosis and reduce the risk of a recurrent seizure (Table 4). Cardiac glycosides are mainly used in cases of supraventricular tachycardia or atrial fibrillation or flutter to decrease the heart rate and must, where necessary, be supplemented by potassium and magnesium substitution. In dogs presenting with WPW syndrome, catheter ablation by means of radiotherapy is necessary to ensure the long-term elimination of accessory bundles.


Syncope as a result of organic heart disease In dogs with structural changes in the heart or the large blood vessels in direct proximity to the heart (Table 1), and therefore with organic heart diseases, syncope predominantly occurs under physical or mental strain and is nearly always accompanied by a heart sound. Clinical symptoms of cardiac insufficiency, or signs of the underlying disease can be observed to varying degrees just before the seizure. The most common causes for syncope are aortic (AS) and pulmonary (PS) stenoses with obstruction of the ventricular outflow tracts, as well as dilated cardiomyopathies and severe mitral insufficiency resulting from reduced minute volume. In , cardiac seizures resulting from heartworm disease with right ventricular outflow tract obstruction are rare. Similarly, hypertrophic obstructive cardiomyopathy (HCM, HOCM) in dogs is hardly ever diagnosed. Causes of isolated syncope can be baroreflex afferent mismatch in a more pronounced obstruction of the left ventricular outflow tract induced by exertion, and




Table 4. Therapeutic treatment of heart rhythm disturbances in dogs Indication

Drug Vagolytic drug

Side effects

Bradycardia arrhythmia

Use only in life-threatening situations, hence relative contra-indications

Atropine in emergencies 0.02-0.4 mg/kg i.v., s.c.

Local anesthetic

Ventricular tachycardia

Ventricular fibrillation, CNS disturbances (syncope, coma)

AV block (2nd and 3rd°), bradycardia


Negative inotropic effects!

Congestive heart insufficiency, increased QT time, SA-, AV- or intraventricular performance disturbances

Lidocaine in emergencies 2-4 (-6) mg/kg, i.v. CRI*: 50-80 µg/kg/min in the first 24 hrs, i.v. Sodium channel blocker Mexiletin in emergencies 30 µg/kg/min in the first 24 hrs. i.v., thereafter CRI* 5 µg/kg/min, i.v. Long-term therapy: 3-5 (-10) mg/kg 2-3x daily, oral

Digitalis Digoxin 0.01 mg/kg/d i.v., oral Calcium channel blocker

Cardiac insufficiency, bradycardiac arrhythmia, bundle branch block, polymorphous v tachyc., gastrointestinal or CNS disturbances AF, Supraventricular tachycardia

AV block, bundle branch block, anorexia, vomiting, apathy

Sick Sinus syndrome, AV block (1st, 2nd and 3rd°), WPW syndrome, HCM, HOCM, AS

AF

Bradycardia, asystole, AV block, increased cardiac insufficiency, drop in blood pressure, loss of appetite, nausea, dizziness, constipation

Congestive cardiac insufficiency, shock, bradycardia, sick sinus syndrome, SA block, AV block, WPW syndrome, Atrial fibrillation with hypotonia, Simultaneous istration of ß blockers, liver diseases

AF

as Verapamil

as Verapamil

Supraventricular tachycardia

Cardiodepressive effect, cardiac insufficiency, hypotonia, bronchial obstruction, gastrointestinal disturbances

Congestive cardiac insufficiency, sick sinus syndrome, highgrade AV block obstructive respiratory diseases

AF, Ventricular arrythmia

as Propranolol

as Propranolol

AF, Ventricular arrythmia

Brady- and tachyarrhythmia, CNS disturbances, bronchial obstruction

Cardiogenic shock, bradycardia, AV block (2nd and 3rd°), obstructive bronchitis

Verapamil 0.1 mg/kg 3x daily, i.v. 1.0 mg/kg 3x daily, oral

Calcium channel blocker

Contra-indications

Diltiazem 0.5-1.5 (-2) mg/kg 3x daily, oral ß receptor blocker Propranolol 0.2-1.0 mg/kg 3x daily, oral ß receptor blocker


Atenolol 0.25-1.0 mg/kg 2x daily, oral ß receptor blocker (not selective) Sotalol 1-2 (-2.5) mg/kg 2 x daily, oral

CRI*: constant rate infustion; AF: atrial fibrillation.





also an arrhythmogenic trigger, which generally manifests itself as ventricular tachycardia.

failure. In the final stages, ventricular fibrillation can lead to sudden death.

In patients presenting with Tetralogy of Fallot, hypoxic seizures can occur as an indication of pronounced cyanosis.

In aortic stenosis there is a fixed obstruction of the left ventricular outflow tract, generally with a subvalvular, less commonly a valvular, and extremely rarely a supravalvular location. Depending upon the degree of severity of the change, there can be increased pressure load on the left ventricle. In order to maintain cardiac output, a concentric left hypertrophy develops, which is often connected with a disturbed ventricular diastolic function. A critical decrease in cardiac output is not only the result of the constant obstruction of the left ventricular outflow tract, it is also mainly caused by paradoxical baroreflex vasodilation. Invasive examinations could at least be conducted in humans to demonstrate this. There is a special form of neurocardiogenic syncope, which amounts to a discrepancy in the baroreflex afferents of the ventricle (high pressure) and the vessels (low pressure) with vasodilatation in the non-working muscles. Increasing cardiac output during exertion in severe cases of aortic stenosis is generally not adequately possible. The high pressure overload and the reduced coronary flow lead to myocardial oxygen deficit with greater left ventricular insufficiency and induce severe ventricular arrhythmia.

Atrial myxoma is generally located in the left atrium. Dependant upon the size and position of the mass, it can lead, owing to an intermittent displacement of the mitral valve opening area, to a sudden decrease in the left ventricular filling volume and therefore heart minute volume, together with syncopal episodes. In cases of pericardial tamponade, certain symptoms resulting from impaired right ventricular filling predominate, including right-sided heart failure with inefficiency and syncope. Aside from sinus tachycardia, atrial and ventricular tachycardia are also recorded. In patients presenting with cardiac insufficiency and reduced heart minute volume resulting from dilated cardiomyopathy (DCM) or severe mitral valve insufficiency, the most common cause of syncopal episodes are malignant heart rhythm disturbances. As a result of severe ventricular arrhythmia, syncope or collapse occur more frequently in Dobermans and Boxers presenting with DCM than in other breeds of dog. Cardiomyopathy in Boxers corresponds to a large degree to arrhythmogenic right ventricular cardiomyopathy in humans. In this form of DCM, probably of autosomal heredity, the steady replacement of the right ventricular muscles by adipose tissue leads, among other things, to loss of function and disturbances in electrical conduction. While at first only isolated ventricular extrasystoles occur, the development of the disease can lead to severe ventricular tachycardia with syncope and left-sided heart

FURTHER

The increasingly weak contractility of the myocardium leads, on its own or together with an aortic valve and/or mitral valve insufficiency, to congestive left-sided insufficiency. In some cases, heart rhythm disturbances occur only at this point, and arrhythmia already in existence become more pronounced. Breed disposition is seen in Boxers, Golden Retrievers, St. Bernard's, German Shepherds, Newfoundlands, Bull Terriers, German Shorthaired Pointers, Great Danes and Rottweilers.

READING

Hainsworth R. Syncope and fainting: classification and pathophysiological basis. In: Mathias CJ, Bannister R, Hrsg.: Autonomic failure. A textbook of clinical disorders of the autonomic nervous system, 4th edition Oxford: Oxford University Press 1999, pp. 428-436.


Schaller B, Lyrer Ph. Synkopen bei neurologischen Erkrankungen. Geriatrie Praxis 2001; 5: 36-41 Tobias R, M Skrodzki, M. Schneider. Kleintierkardiologie Kompakt; 1 Auflage: Schlütersche Verlagsgesellschaft, 2008.



CUT-OUT AND KEEP GUIDE

Electrocardiography in dogs Michael Johnson, MRCVS, MVB, DVC, Veterinary Cardiorespiratory Centre, Kenilworth, UK Michael Johnson graduated from UCD Dublin. He spent the next 10 years in mixed, mainly large animal practice in Ireland, Wales, Australia and Canada. This was followed by 6 years in small animal practice in Manchester, UK. He obtained the certificate examinations in small animal medicine and veterinary cardiology during this time. For the past 7 years Mike Johnson has specialised in cardiorespiratory medicine at a referral practice in the UK, Martin Referrals, during which time he was awarded his Diploma in veterinary cardiology.

n ECG recording is most commonly of 2 types. A standard recording records a rhythm over several minutes. A Holter recording, requiring a strap on device, can provide a recording over 1-7 days.

A

provide information if an abnormality is clearly present on auscultation. More useful in such cases would be a prolonged ECG such as a Holter recording over one or more days.

Single or multi-channel recordings may be used. The latter typically record 3 or 6 leads simultaneously. The most useful paper speed settings are 25 or 50 mm/second. Most useful sensitivity settings are 1 cm/ mV (standard setting (Figure 110)) with 1/2 cm/ mV for large complexes and 2 cm/ mV for very small complexes (often seen in cats).

If there is marked bradycardia or tachycardia present on auscultation, an ECG can determine the etiology. Chaotic rhythms usually represent atrial fibrillation but all such rhythms should be documented with an ECG. Premature or missed beats may also be characterized on ECG. If the arrhythmia is quite infrequent, it is unlikely to be detected on a standard recording and a prolonged or Holter recording may be necessary.

Indications to performing an ECG

Contra-indications to performing an ECG

In general ECGs are probably performed more frequently than necessary. They are not of benefit for example in the diagnosis of the cause of a murmur in small animals. They are also unlikely to be of benefit where the rate and rhythm appear normal on auscultation. The ECG is not usually an accurate guide to heart size. If cardiomegaly is suspected, other tests particularly radiology should be considered. In cases of collapse where a cardiac origin is suspected, a standard ECG is only likely to

Positioning for ECG recording The conventional recording is obtained in right lateral recumbency. Recording in other positions is quite acceptable. The standing position may be preferred in nervous or large dogs for example. Varying the position will lead to some alteration in the morphology of the complexes recorded. This is not clinically important however and the rhythm, which is the most important aspect of the recording, will remain unaffected.




ELECTROCARDIOGRAPHY IN DOGS

Figure 1. This ECG shows normal sinus rhythm at 140 beats per minute.

Figure 2. A West Highland White Terrier with marked depression and anorexia had a marked bradycardia on auscultation. Heart rate averages 35/minute. No P waves are visible. This represents atrial standstill. This occurred secondary to hyperkalemia caused by hypoadrenocorticism.

Figure 3. St Bernard with atrial fibrillation due to DCM. Note the rapid rate at 180/minute, chaotic rhythm and absence of P waves.

Figure 4. Sometimes altered morphology of complexes provides useful information. Note that the QRS complexes alternate markedly in amplitude. This dog had a pericardial effusion, which often leads to electrical alternans as noted here.

Figure 5. A 7-year-old Shetland Sheepdog presented for lethargy. The overall heart rate is low at 45/minute. P waves are unrelated to QRS complexes, representing third degree AV block.

Figure 6. Figure 7. Persistent sinus tachycardia at 180/minute in a dog with heart failure.

A single supraventricular premature beat in a dog with atrial enlargement. Such complexes resemble the normal QRS complexes but occur early.

Figure 8. Dog with DCM showing initially 2 ventricular premature beats, VPCs, followed later by a run of rapid ventricular tachycardia. Note that VPCs appear quite different from the normal sinus complexes.

Figure 9.

Figure 10.

Normal dog showing wandering pacemaker. The P wave varies in amplitude and conformation from beat to beat. This is not an abnormality however.

West Highland White Terrier presented with occasional collapse. Note the sinus arrest/ pauses which occur, in this case due to sick sinus syndrome. This is well recognized in older Westies.


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