Cardiomyopathy in cats comprises an incompletely understood group of diseases. The term cardiomyopathy means heart muscle disease, and encompasses multiple phenotypic variants. The most common and extensively studied type that is diagnosed in cats is hypertrophic cardiomyopathy (HCM), and is not the focus of this discussion. The other cardiomyopathies include dilated cardiomyopathy, restrictive cardiomyopathy, and unclassified or ischemic cardiomyopathy. Subcategories of these include moderator-band associated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy and left ventricular non-compaction. It is unclear what role myocarditis/endomyocarditis (inflammation of the heart muscle) plays in the development and/or exacerbation of cardiomyopathy in cats. Future studies may help delineate the etiologies of the different types of feline cardiomyopathy.
Dilated cardiomyopathy (DCM) in cats is characterized in much the same way that DCM is described in other species (i.e. dogs, humans). Most commonly, variable degrees of eccentric hypertrophy of the heart chambers is present along with a notable decrease in systolic dysfunction (dilated chambers with poor contractility). The ventricular walls themselves may be overtly and homogenously thinned. The left side of the heart may be predominately affected, and mild mitral regurgitation may occur secondary to annular dilation. Most cats with DCM present in congestive heart failure, showing symptoms of backward failure (dyspnea from pulmonary edema or pleural effusion) or occasionally forward failure (hypotension, hypothermia, bradycardia) or thromboembolism, and is generally associated with a poor prognosis. Taurine deficiency is a well-described potential cause of reversible DCM in cats, and should be suspected in cats being fed an exclusively dog-food, vegan or vegetarian home-cooked diet. Cats eating a commercial diet are highly unlikely to be taurine-deficient. Most cases of feline DCM diagnosed are idiopathic in etiology, and presumed to be the result of one or more genetic mutations.
Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a rarely-diagnosed condition in the cat. Cats with ARVC characteristically will have fibrofatty-replacement of the right ventricular myocardium, may present with right-sided congestive heart failure and ventricular arrhythmias from the right ventricular outflow tract with a characteristic right bundle-branch block pattern. The condition may progress to involve the left ventricle, but generally spares the interventricular septum. The right ventricle becomes markedly dilated, thin, with occasional aneurysms and has marked systolic dysfunction. This condition is commonly misdiagnosed as tricuspid dysplasia, as derangement of the tricuspid valve with associated insufficiency occurs with the progressive dilation of the right ventricle.
Restrictive cardiomyopathy (RCM) in cats is idiopathic in origin, may be myocardial, subendomyocardial or endomyocardial, is characterized by variable degrees (and typically mild) ventricular hypertrophy, may have normal to decreased left ventricular internal dimensions, with normal to mildly decreased myocardial contractility with often marked biatrial enlargement. The left ventricle may appear echocardiographically normal. Mitral/tricuspid insufficiency, if present, is disproportionately mild to the associated degree of atrial enlargement. The left and/or right ventricle becomes infiltrated with fibrous tissue, leading to a stiff myocardium that fails to relax appropriately. This in turn leads to elevated filling pressures and secondary, typically biatrial enlargement. Cats with RCM typically present in congestive heart failure with symptoms associated with pulmonary edema and/or pleural effusion, and may have thromboembolism. Presumptive diagnosis is made by echocardiography. Permanently elevated E wave velocities and E:A ratios (restrictive pattern) may found on mitral inflows, however they may be normal, have a decreased E:A ratio (relaxation abnormality), or pseudonormal. Doppler tissue interrogation of the mitral annulus shows reduced early diastolic waveforms. Invasive catheterization to document left ventricular diastolic dysfunction to definitively diagnose RCM is generally not performed.
Endocardial fibroelastosis and excessive moderator bands may result in phenotypic RCM. Generally the endocardium is hyperechoic and irregular and multiple, usually thickened moderator bands are identified in the left ventricle via echocardiography. Both of these conditions result in an endomyocardial form of RCM.
Unclassified cardiomyopathy (UCM) is cardiomyopathy that doesn’t fit neatly into the categories of hypertrophic, dilated or restrictive cardiomyopathies, and may have features of some or all of these. Ischemic cardiomyopathy is often lumped into this category as well. Many end-stage all-cause cardiomyopathic cats may develop myocardial infarctions leading to focal regions of hypocontractile, thin-walled ventricles +/- left ventricular dilation with some regression of hypertrophy leading to a diagnosis of UCM. Cats with UCM may have variable degrees of eccentric hypertrophy of the ventricles, may be hypocontractile or hypercontractile, often have evidence of prior infarctions, and may have hyperechoic/irregular endocardiums similar to cats with RCM. If they have left ventricular concentric hypertrophy, it is generally mild and disproportionate to the associated degree of left atrial enlargement (vs. HCM). Doppler tissue interrogation of the mitral annulus is generally normal. Left ventricular non-compaction is a congenital form of UCM in which large recesses within the left ventricle are present, and associated with myocardial dysfunction, secondary left atrial enlargement, etc.
Diagnosis of feline cardiomyopathy is typically made via echocardiography. Serum NT pro-BNP levels may be abnormally elevated. Thoracic radiographs may show cardiomegaly, pulmonary venous and arterial dilation, pulmonary edema or pleural effusion. Electrocardiography may show sinus tachycardia, premature beats, tachycardia, atrial fibrillation or ventricular arrhythmias.
Treatment is generally aimed at controlling fluid retention and enhancing inotropic support. Acute therapy may include oxygen administration, therapeutic thoracocentesis, injectable furosemide, topical nitroglycerine, injectable dobutamine, etc. Chronic oral therapy may include furosemide, enalapril, pimobendan, digoxin, clopridogrel or aspirin. Arrhythmias such as atrial fibrillation may be treated with digoxin and diltiazem. Ventricular arrhythmias may be treated with atenolol or sotalol.
The prognosis is generally determined by response to therapy and the presence of other comorbidities (i.e. renal failure, neoplasia, etc.). Generally speaking, uncomplicated congestive heart failure secondary to all-cause cardiomyopathy in cats can be expected to have a survival time of 1-2 years with lifelong medication. That said, some cats do poorly, and only survive for a few months. Negative prognostic indicators include biventricular failure, formed intracardiac thrombi or known thromboembolism, atrial fibrillation and ventricular arrhythmias. Some cats may live for 4-6+ years following an initial episode of congestive heart failure.