Hypertrophic Cardiomyopathy - in Other Animals

In Other Animals

Feline hypertrophic cardiomyopathy (HCM) is the most common heart disease in cats; the disease process and genetics are believed to be similar to the disease in humans. In Maine Coon and American Shorthair cat breeds, HCM has been confirmed as an autosomal dominant inherited trait. The first genetic mutation (in cardiac myosin binding protein C) responsible for feline hypertrophic cardiomyopathy was discovered in 2005 in Maine Coon cats. A test for this mutation is available. About one third of Maine Coon cats tested for the mutation have been shown to be either heterozygous or homozygous for the mutation, although many of these cats have no clinical signs of the disease. Some Maine Coon cats with clinical evidence of hypertrophic cardiomyopathy test negative for this mutation, strongly suggesting that a second mutation exists in the breed. The cardiac myosin binding protein C mutation identified in Maine Coon cats has not been found in any other breed of cat with HCM but more recently another myosin binding protein C mutation has been identified in Ragdoll cats with HCM.

While there is no cure for HCM, early detection and regular echocardiograms are key to trying to ward off life-threatening problems. Early signs may include a murmur or even heart failure. Unfortunately, death may occur without any other signs present, making the disease a difficult and often deadly one. While medication is commonly given to cats with HCM that have no clinical signs, no medication has been shown to be helpful at this stage and it has been shown that an ACE inhibitor is not beneficial until heart failure is present (at which time a diuretic is most beneficial). Diltiazem generally produces no demonstrable benefit. Atenolol is commonly administered when systolic anterior motion of the mitral valve is present.

Thromboembolic disease (TED) is relatively common sequelae of Feline HCM. The aetiology remains a little uncertain, but it is thought that ischemic damage to the hypertrophied left ventricular myocardium facilitates thrombus formation and subsequent embolism. Classically the embolus lodges at the iliac bifurcation of the aorta, occluding either one or both of the common iliac arteries. Clinically this presents as a cat with complete loss of function in one or both hindlimbs. The hindlimbs are cold, and the cat is in considerable pain. This pain derives from the exaggerated inflammatory response to the embolus at the point of impact, and the inflammatory mediators released generally have a vasoconstrictor effect further exacerbating the problem. Emboli may, rarely, lodge in other locations, typically the renal or ovarian/testicular arteries as they exit the abdominal aorta.

Treatment of TED is variable - typically very low doses of aspirin may be prescribed (aspirin however is extremely toxic to cats and should only be prescribed and administered by a veterinary surgeon). Plavix is also another widely used drug that may or may not prevent clot formation in HCM cats. The FATCAT study at Purdue University is addressing the efficacy of aspirin vs. Plavix for the prevention of a second clot in cats that have already experienced a clot. Thrombolytic agents (e.g., tissue plasminogen activators) have been used successfully, but their cost is usually prohibitively high in veterinary medicine. Despite the relative efficacy of treatment, the prognosis for cats with TED is poor as they are likely to have significant HCM already, and a recurrent bout of TED is very likely. For this reason euthanasia is often considered in TED cats.