Hypertrophic cardiomyopathy is the most common primary heart disease diagnosed in cats. It is familial in certain breeds of cats such as Maine Coon cats and American Shorthairs. The disease occurs in cats from 3 mo to 17 yr of age, although most patients are middle aged; male cats are predisposed. The etiology is believed to be genetic mutations resulting in abnormalities of the sarcomeric proteins. Although not proved in cats, it has been documented in humans with this disease.

 

    Affected cats may be asymptomatic or may have signs of acute dyspnea, collapse, or hindlimb paresis/paralysis. Cough is uncommon in cats with heart failure. Physical examination frequently demonstrates abnormal heart sounds, including soft to prominent systolic cardiac murmurs and gallop heart sounds. Increased respiratory sounds may suggest pulmonary edema, and decreased respiratory sounds may indicate pleural effusion. Pulses may be normal, weak, or absent if distal aortic thromboembolism has developed. Distal aortic embolization commonly leads to rear limb paresis or paralysis.  

 

    Radiographically, there may be pronounced left atrial enlargement and variable left ventricular enlargement. The cardiac silhouette often appears relatively normal even in the presence of moderate left ventricular hypertrophy. Echocardiography allows confirmation of the diagnosis and assessment of additional therapy needed (eg, anticoagulants are most beneficial in cats with severe left atrial enlargement). Systolic anterior motion of the mitral valve, concentric left ventricular hypertrophy, or variable hypertrophy of other portions of the left ventricle such as papillary muscle hypertrophy or asymmetric septal hypertrophy can be noted. ECG abnormalities may include atrial premature complexes, ventricular premature complexes, and ventricular tachycardia. With severe atrial enlargement, atrial fibrillation may develop. Conduction disturbances such as left anterior fascicular block may also be noted.

    

    Treatment is directed at controlling signs of CHF, improving diastolic function, and reducing the incidence of systemic thromboembolism. Furosemide administration, oxygen, and nitroglycerin administration should be considered when acute CHF is present. Diltiazem (7.5 mg, PO, tid), a calcium-channel blocker, improves diastolic function and may also reduce wall thickness and edema formation. Use of β-blockers such as atenolol (6.25-12.5 mg, PO, sid-bid) or propranolol may also be considered. Humans with hypertrophic cardiomyopathy have shown improvement in angina, dyspnea, and exercise intolerance when given β-blockers. If calcium channel blockers are ineffective, switching to β-blockers may be considered. ACE inhibitors may be considered in some cats (enalapril, 0.25-0.5 mg/kg, PO, sid), especially where CHF has developed and activation of the RAAS is a concern. Either aspirin (80 mg, PO, every third day) or warfarin (0.2-0.5 mg, PO, sid) may reduce the incidence of further thrombus formation in cats with thromboembolism or a propensity to develop thrombi (such as a large left atrium on echocardiographic examination).  

 

    Efficacy has not been well documented, however. Prognosis is highly variable, with many mildly affected cats having a good long term prognosis. Cats in CHF have a poorer prognosis, with a median survival time of 3 months. Up to 20% of CHF cats survive for more prolonged periods.

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