Managing feline cardiomyopathies (Proceedings)


Managing feline cardiomyopathies (Proceedings)

Apr 01, 2010

Etiology and epidemiology

Myocardial disease is the most frequently diagnosed type of heart disease in the cat. Until recently, the two most common forms of cardiomyopathy in the cat were idiopathic dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM). The discovery in 1987 that most cases of DCM in cats resulted from inadequate amounts of available dietary taurine caused most cat food manufacturers to increase the taurine content in their cat diets. Since then, the prevalence of DCM in cats has drastically declined.

In the past, all cats with concentrically hypertrophied ventricles were considered to have HCM. It is now obvious that many of these cats suffer from hyperthyroidism or from systemic hypertension, and that their myocardial disease is secondary to these conditions. The term hypertrophic cardiomyopathy should be reserved for those patients with idiopathic left ventricular hypertrophy. Cats with HCM may range from one to 16 years of age, with a large percentage ranging from 4 to 7 years. Neutered male cats were found to be at increased risk for HCM compared to neutered female cats, but significant breed predilections are more difficult to identify. A colony of Maine Coon cats has been identified that display a severe and rapidly progressive form of HCM. A genetic alteration in cardiac myosin binding protein C (single base pair change from G to C) has been identified as a cause of familial HCM in some Maine Coon cats. This base pair change alters the protein confirmation and results in sarcomeric disorganization. Similarly an alteration in cardiac myosin binding protein C (base pair change A to T) has been found in Ragdolls with familial hypertrophic cardiomyopathy. There are over 200 genetic alterations that have been identified in humans with familial HCM, therefore it is likely there are many additional genetic modifications responsible for feline HCM.

History and clinical signs

Labored respiration (tachypnea, open-mouthed breathing) is the most common owner complaint, developing either as a consequence of pleural effusion or pulmonary edema. Other common clinical signs include lethargy and anorexia. Some cats present for sudden paralysis, usually of the hindleg, due to arterial thromboembolism. Syncope and sudden death are uncommon signs and are most frequent in cats with HCM. Sudden death is likely the consequence of terminal ventricular arrhythmias that have developed subsequent to myocardial ischemia.

Physical examination

Systolic murmurs are common in all types of feline cardiomyopathy. They usually result from systolic anterior motion of the mitral valve/mitral insufficiency or from dynamic right ventricular outflow tract obstruction. Audible disturbances of rhythm and pulse deficits are also common. Gallop heart sounds are audible in most cases where ventricular gallops, S3 sounds, are most common in DCM and atrial gallops, S4 sounds, are more common in HCM. Rapid heart rates make precise identification of these sounds impossible by auscultation and difficult by phonocardiography. Summation gallops may also be auscultated. Rales, dyspnea, and open mouth breathing are common in cats with left-sided heart failure, but coughing is very uncommon. Heart sounds and lung sounds may be muffled due to pleural effusion. Jugular distension and jugular venous pulses are frequently noted in cats with pleural effusion. Hypothermia, weak arterial pulses, and other signs of cardiogenic shock may be present with advanced heart failure. Physical evidence of systemic thromboembolism includes posterior paresis or paralysis with cool, stiff, and usually painful hindlimbs. The gastrocnemius muscles are very hard, and femoral pulses are absent or unequal. Nonpigmented pads may be obviously cyanotic. Evidence of embolism to other systemic sites, such as a foreleg, may also be noted.

Heart murmurs in cats are almost dynamic in nature, meaning that rather than organic valvular insufficiencies or valvular stenoses, their heart murmurs arise from two structures encroaching on one another. This encroachment decreases the diameter through which blood can flow, resulting in turbulence and the development of an audible murmur. Unfortunately physical examination, electrocardiography, and thoracic radiography cannot differentiate between these two types of heart murmurs. Only Doppler echocardiography can identify where the murmur originates.