The incidence of hypertrophic cardiomyopathy (HCM) is higher in the cat than it is in the dog. hypertrophic cardiomyopathy can be classified as primary or secondary. The aetiology of the primary or idiopathic form is unknown. A recent survey of 74 cases of hypertrophic cardiomyopathy showed no apparent breed predilection ; others have suggested that the Persian breed may be predisposed. The disease rarely occurs in the Siamese. Burmese and Abyssinian breeds in which there is a much higher incidence of dilated cardiomyopathy. Secondary hypertrophic cardiomyopathy most commonly occurs in association with hyperthyroidism.
Idiopathic hypertrophic cardiomyopathy typically occurs in young to middle-aged cats (mean age 6,5 years) and males are more commonly affected.
Hypertrophic cardiomyopathy is characterized by symmetrical hypertrophy of the interventricular septum and left ventricular free wall. Occasionally there may be evidence of left ventricular outflow obstruction especially if there is disproportionate hypertrophy of the septum. Partial aortic outflow obstruction may also be caused by anterior motion of the mitral valve during early systole but this appears to be a rare occurrence in feline hypertrophic cardiomyopathy. Indeed, echocardiographic studies have shown that most cats with hypertrophic cardiomyopathy do not have left ventricular outflow gradients and it appears therefore that obstructive hypertrophic cardiomyopathy, as occurs in dogs, is rare in cats.
Left ventricular hypertrophy results in decreased myocardial compliance, interference with normal diastolic filling due to impaired myocardial relaxation, and an increase in left ventricular end-diastolic pressure (despite a normal or often reduced end-diastolic volume). Decreased myocardial compliance may be aggravated by focal or diffuse endocardial fibrous tissue deposition. Pressure overload within the left ventricle may also be associated with mitral valve dysfunction and regurgitation leading to left atrial enlargement.
The decrease in stroke volume ultimately leads to a reduction in cardiac output and decreased coronary perfusion resulting in myocardial ischaemia. Abnormal myocardial handling of calcium may be a factor in the pathogenesis of hypertrophic cardiomyopathy (an increase in intracellular calcium inhibits complete myocardial relaxation which may explain why calcium blocking drugs have been shown to improve diastolic function significantly in affected cats.
More recently, excessive circulating levels of growth hormone has been implicated in the pathogenesis of hypertrophic cardiomyopathy. Cats with acromegaly due to functional pituitary tumours have hypertrophic cardiomyopathy (Q). It has also been shown that non-acromegalic cats with hypertrophic cardiomyopathy have significantly increased levels of growth hormone compared to normal cats and cats with other forms of cardiac disease but whether this is cause or effect is not clear.
Hypertrophic cardiomyopathy: Clinical signs
Recent studies have demonstrated the heterogeneity of feline hypertrophic cardiomyopathy with regard to the wide spectrum of clinical, electrocardiographic, radiographic and echocardiographic features of the disease. Some cases of hypertrophic cardiomyopathy remain asymptomatic until the cat is stressed. The clinical signs of hypertrophic cardiomyopathy are typically those of left-sided congestive heart failure. Bright and others showed that 61 % of cats with hypertrophic cardiomyopathy had a history of respiratory distress characterized by the acute onset of dyspnoea progressing to mouth breathing. Affected cats become lethargic, anorexic and may cough. Occasionally heart sounds may be muffled due to the presence of pleural or pericardial fluid, Clinical examination may reveal diffuse pulmonary crackles and the presence of a gallop rhythm and / or systolic murmur. Other more variable signs include prolonged capillary refill time and pallor or cyanosis of the tongue and mucous membranes- Animals showing severe signs of cardiac failure are often hypothermic with weak femoral pulses. The increased tendency towards thrombus formation may result in acute onset of hindlimb (less frequently forelimb) paralysis or lameness with cold limb extremities (see section on arterial thromboembolism).
Almost 70% of cases may be expected to have an abnormal ECG. Abnormalities reported include increased amplitude and width of P and R waves (P waves >0.04 s and >0,2 mV; QRS complexes >0.04 s and R waves >0.9 mV in lead II), arrhythmias (atrial or ventricular premature contractions) and conduction disturbances. Left anterior fascicular bundle branch block, with deep S waves in leads 1, 11 and 111 and left axis deviation, is particularly common.
Radiographic abnormalities consisting of mild to moderate left atrial and left ventricular enlargement or biventricular enlargement with evidence of pulmonary venous congestion and / or oedema are present in more than 80% of cases. Biventricular enlargement may lead to elevation of the trachea and increased sternal contact and, on the dorsoventral view, the enlarged atria may result in a ‘valentine-shaped’ heart. Occasionally there may also be radiographic signs of right heart failure (right ventricular enlargement, hepatomegaly and ascites.
Hypertrophic cardiomyopathy is characterized by symmetric or less frequently asymmetric hypertrophy of the inter-ventricular septum and left ventricular free wall, and enlarged hypertrophied papillary muscles which contribute to a marked reduction in left ventricular internal dimensions. Most cases show evidence of a moderate degree of left atrial dilation and fractional shortening is usually normal or increased. Occasionally there is systolic anterior motion of the septal mitral valve leaflet and Doppler studies may show mitral regurgitation. Mild pericardial effusion may be evident.
With the increased use of ultrasound angiocardiography is rarely required. In the absence of ultrasound facilities, non-selective angiocardiography (injection of the contrast agent via the jugular vein) can be used to demonstrate the hypertrophied left ventricle and papillary muscles and regurgitation of contrast into the dilated left atrium. Circulation time is usually normal.
Prognosis of Hypertrophic cardiomyopathy
The prognosis for hypertrophic cardiomyopathy is guarded and other causes of left ventricular hypertrophy such as systemic hypertension, hyperthyroidism, acromegaly, chronic anaemia and congenital subaortic stenosis (rare in the cat) should be excluded. Plasma T3 and T4 concentrations should always be determined even when no thyroid nodules can be palpated in the neck.
Hypertrophic cardiomyopathy: Treatment
Cats presented with severe respiratory distress should be given oxygen and confined to a cage in the first instance. Initially frusemide may be given intravenously or intramuscularly (1-2 mg kg-1 body weight); thereafter it may be given orally at a dose rate of 1 mg kg-1 body weight two or three times daily. One of the main aims of therapy should be to reduce the heart rare to less than ISO beats per minute in order to improve cardiac filling.
Diltiazem not only decreases the heart rate in cats with hypertrophic cardiomyopathy but increases myocardial relaxation, decreases myocardial oxygen demand and dilates the coronary vasculature. It has minimal negative inotropic and peripheral vasodilating properties compared to other calcium blocking agents such as verapamil. A dose of 1.75-2.4 mg kg-1 body weight per os three times daily (mean effective dose 1.78 mg kg-1) has been shown to effectively reduce pulmonary congestion and improve left ventricular filling with no apparent side effects.
Recent work has shown that the survival times of cats with hypertrophic cardiomyopathy may be prolonged with the use of calcium Mocking agents such as diltiazem. About 94% of cats in one study receiving diltiazem survived longer than 6 months. Cats which show no clinical signs on initial presentation and those with heart rates less than 200 beats per minute survive significantly longer than do cats with emboli or congestive heart failure, 60% of which fail to survive 6 months.
Beta-blocking drugs such as propranolol (2,5-5,0 mg per os twice or three limes daily) slow the heart rate and improve diastolic filling. Propranolol is the antidysrhythmic drug of choice for cats but its effects on myocardial compliance in cases of feline hypertrophic cardiomyopathy have not been documented.
Although vasodilators are generally contra-indicated in cats with hypertrophic cardiomyopathy, captopril (3.12-6.20 mg twice or three times daily) may be useful In cases with severe mitral regurgitate on and signs of refractory congestive heart failure.
The administration of digoxin is contraindicated in cats with hypertrophic cardiomyopathy since myocardial contractility is often normal or increased. Aspirin (25 mg kg-1 body weight every 72 h) should be given to minimize the risk of throntboembolic disease although there is no evidence to date to suggest that aspirin, if given prophylactically, decreases the incidence of arterial thrombosis in cats with hypertrophic cardiomyopathy.