Dilated cardiomyopathy (DCM) is characterized by the progressive loss of myocyte number and/or function, along with a decrease in cardiac contractility. DCM is most prevalent in dogs and is especially prevalent in certain breeds; it typically occurs in middle-aged to older male dogs. Causes of DCM include chemical (eg, doxorubicin), viral (eg, parvovirus), nutritional (taurine deficiency), genetic (in Doberman Pinschers and Boxers), or idiopathic. DCM most commonly affects large-breed dogs; Doberman Pinschers, Boxers, Great Danes, German Shepherd Dogs, Irish Wolfhounds, Scottish Deerhounds, Newfoundlands, Saint Bernards, and Labrador Retrievers are particularly at risk. DCM has a protracted subclinical phase in dogs, with clinical signs evident for a relatively short time. As cardiac contractile function is progressively lost, cardiac output decreases and then is normalized again due to RAAS compensation. After years of initial benefit from this mechanism, fluid retention causes deleterious effects during the late phases of the disease: excessive activation of the RAAS causes continued retention of sodium and water even in the face of edema or effusion.
The incidence of DCM in cats has decreased dramatically since the discovery in 1987 that taurine deficiency was responsible for most cases (taurine-responsive DCM). Since then, taurine has been added to all commercial cat foods. Most cases in cats today are not taurine responsive and reflect primary (or idiopathic) disease; however, the disease occurs occasionally in cats fed noncommercial diets (eg, vegetarian food, baby food, home-cooked food). As noted above in Nutritional Considerations, some dogs (usually small breeds or those on grain-free diets) can also have taurine-responsive DCM. Cats with DCM typically present with severe respiratory signs due to pulmonary edema and/or pleural effusion, and clinical signs are often rapidly progressive and refractory to treatment.
A soft systolic heart murmur, best heard at the left cardiac apex, is often present. A gallop sound may also be present but is subtle and usually identified in dogs only by an experienced examiner. It is often more obvious in cats. The femoral pulse may be weak, and an arrhythmia with associated pulse deficits may be noted. The arrhythmia is most commonly ventricular ectopy (eg, premature ventricular contractions, ventricular tachycardia) in Doberman Pinschers and Boxers, and atrial fibrillation in giant-breed dogs. Ascites, tachypnea, dyspnea, or cough may also be noted, depending on the type of heart failure that develops.
Echocardiography is the best test to definitively diagnose DCM: the left atrium and left ventricle in particular are dilated, and contractility is markedly decreased. Mitral insufficiency typically develops as progressive left ventricular chamber dilation results in separation of the valve leaflets. Abnormal ECG findings may include ventricular premature complexes, ventricular tachycardia and atrial fibrillation (especially in giant breeds); the occurrence of ventricular premature complexes on a routine ECG in a Doberman Pinscher is highly suggestive of DCM.
CHF, which may be severe, should be treated as discussed elsewhere (see Heart Failure Heart Failure in Dogs and Cats The three primary functions of the cardiovascular system are to maintain 1) normal blood pressure and 2) normal cardiac output, both at a 3) normal venous/capillary pressure. Heart failure is... read more ). As severe pulmonary edema resolves, furosemide can be administered orally, with oxygen continued until clinical signs are controlled. Pimobendan and an ACE inhibitor (eg, enalapril, benazepril) should be started. Pimobendan treatment may be indicated in Doberman Pinschers with DCM before the onset of heart failure, and concurrent antiarrhythmic treatment is also frequently indicated in this breed especially.
The prognosis is grave for cats with DCM (not taurine responsive); the median survival time is 2 weeks. Cats that are taurine responsive also have an initial high risk of death. However, cats that survive long enough for taurine to become effective (2–3 weeks) have an excellent prognosis because the disease is completely reversible. Dogs that are taurine responsive also have a fair to good prognosis once clinical signs of CHF abate. The short-term prognosis for other dogs with DCM depends primarily on the severity of the heart failure on presentation, but the longterm prognosis is poor and most die within 6 months of diagnosis. Dogs with severe heart failure, particularly left heart failure, have a worse prognosis than those with milder clinical signs or signs of right heart failure at presentation.