Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE, Canada
Cardiomyopathies are "diseases of the myocardium associated with cardiac dysfunction."1 In cats, the spectrum of clinical severity of cardiomyopathy is extremely wide, ranging from lethal cases in young kittens to a seemingly large proportion of cases that show no overt signs and can live a normal lifespan.2-4
This subject is important to veterinarians because cardiomyopathies are the most common cardiac disorder of cats. For example, in one series of 425 cats examined at a referral hospital, 10 had congenital heart disease compared to ≈ 220 with cardiomyopathies.5 Even in young cats, where congenital heart disease might be thought to be more prevalent, cardiomyopathies predominate.
Cardiomyopathies classically have been categorized according to their effect on ventricular morphology and function. Hypertrophic (HCM), restrictive (RCM), unclassified (UCM), dilated (DCM), and arrhythmogenic right ventricular (ARVC) cardiomyopathies are recognized in cats.6 It is now understood that a great deal of overlap can occur between these categories, with certain patients having features of 2 cardiomyopathies simultaneously, for example. It was once believed that all of these cardiomyopathies represented individual stages in the continuum of one disease as it evolves over time, but this notion has not been supported by long-term observation.
Suspicion of cardiomyopathy occurs in one of three contexts: 1) a physical finding, such as a heart murmur, or a radiographic finding, like cardiomegaly, is identified in the course of an examination that was not primarily directed at the heart ("incidental finding"); 2) the patient shows overt physical signs consistent with congestive heart failure, arterial embolism, or syncope; or 3) sudden death, often without premonitory signs.
Clinically, cardiomyopathy is confirmed or excluded with echocardiography.2,3,5,6 Measurement of plasma NT-proBNP concentration can be considered as a screening test if echocardiography is unavailable; while a high result does not differentiate between cardiomyopathy types (a differentiation that is of unproven therapeutic importance in cats anyway), a low or normal value is strongly suggestive of the absence of cardiomyopathy.5,7
To date, only one treatment is known to specifically reverse cardiomyopathy in cats: taurine, for cats with taurine-deficient DCM. Other systemic treatments can reverse cardiac hypertrophy if the hypertrophy is part of a generalized disease state, such as hyperthyroidism or systemic hypertension. Mainly, treatment of cardiomyopathy is aimed at the consequences of the disease: medications are given to palliate congestive heart failure or thromboembolism.
Recent developments in the treatment of feline cardiomyopathies involve opposite ends of the spectrum of disease severity. In cats with subclinical ("asymptomatic") HCM, daily treatment for 5 years with the beta-adrenergic blocker atenolol did not produce a detectable benefit in one retrospective study.8 Such a finding calls this type of "prophylactic" treatment into question, especially - from a practical point of view - if the process of administering the drug every day is difficult or unappealing to the patient, the owner, or both. At the other extreme of disease severity, cats with severe clinical signs caused by HCM or RCM/UCM appear to have a much longer survival time if pimobendan is added to their treatment regimen, based on a recent retrospective study.9 This counterintuitive approach of giving a drug with positive inotropic properties to a patient with concentric ventricular hypertrophy might be explained by loss of systolic function in advanced HCM, RCM, or UCM, or some other property of pimobendan that remains to be elucidated in the context of feline cardiomyopathies.
1. Maron BJ, Towbin JA, Thiene G, Antzelevitch C, Corrado D, Arnett D, et al. AHA scientific statement: contemporary definitions and classification of the cardiomyopathies. An American Heart Association scientific statement from the Council on Clinical Cardiology, Heart Failure and Transplantation Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary Working Groups; and Council on Epidemiology and Prevention. Circulation. 2006;113:1807–1816.
2. Rush JE, Freeman LM, Fenollosa NK, Brown DJ. Population and survival characteristics of cats with hypertrophic cardiomyopathy: 260 cases (1990–1999). J Am Vet Med Assoc. 2002;220:202–207.
3. Wagner T, Fuentes VL, Payne JR, McDermott N, Brodbelt D. Comparison of auscultatory and echocardiographic findings in healthy adult cats. J Vet Cardiol. 2010;12:171–182.
4. Baty CJ, Malarkey DE, Atkins CE, DeFrancesco TC, Sidley J, Keene BW. Natural history of hypertrophic cardiomyopathy and aortic thromboembolism in a family of domestic shorthair cats. J Vet Intern Med. 2001;15:595–599.
5. Ettinger SJ. NT-proBNP: the cat is not a dog. In: Proceedings from the American College of Veterinary Internal Medicine Forum; Anaheim, CA; June, 2010.
6. Ferasin L, Sturgess CP, Cannon MJ, Caney SM, Gruffydd-Jones TJ, Wotton PR. Feline idiopathic cardiomyopathy: a retrospective study of 106 cats (1994–2001). J Feline Med Surg. 2003;5:151–159.
7. Fox PR, Rush JE, Reynolds CA, Defrancesco TC, Keene BW, Atkins CE, et al. Multicenter evaluation of plasma N-terminal probrain natriuretic peptide (NT-pro BNP) as a biochemical screening test for asymptomatic (occult) cardiomyopathy in cats. J Vet Intern Med. 2011;25:1010–1016.
8. Schober KE, Zientek J, Li X, Fuentes VL, Bonagura JD. Effect of treatment with atenolol on 5-year survival in cats with preclinical (asymptomatic) hypertrophic cardiomyopathy. J Vet Cardiol. 2013;15:93–104.
9. Reina-Doreste Y, Stern JA, Keene BW, Tou SP, Atkins CE, DeFrancesco TC, et al. Case-control study of the effects of pimobendan on survival time in cats with hypertrophic cardiomyopathy and congestive heart failure. J Am Vet Med Assoc. 2014;245:534–539.