«FELINE CARDIOLOGY John D. Bonagura, DVM, DACVIM Cardiovascular diseases are common in cats.1- 3 Myocardial disorders are the major cause of heart ...»
John D. Bonagura, DVM, DACVIM
Cardiovascular diseases are common in cats.1- 3 Myocardial disorders are the major cause of
heart failure and thromboembolism, with idiopathic hypertrophic cardiomyopathy the most
important of the primary myocardial diseases. 4-7 Extensive myocardial fibrosis leading to a
restrictive cardiomyopathy or right ventricular cardiomyopathy is now recognized on a regular
basis in mature cats. Conversely, dilated cardiomyopathy is rare today because feline diets are supplemented with taurine. Nonsuppurative myocarditis is identified sporadically in cats;
however, the diagnosis is difficult and often based on suspicion (or necropsy). The cardiac manifestations of, hyperthyroidism, hypertension, and anemia are well known in this species, but these conditions must be distinguished from primary cardiomyopathies as management and prognoses differ. Primary acquired valvular disease is very rare in cats. Functional murmurs are common, including those related to ejection of blood into the dilated aorta found in older cats. Herein is a summary of clinical aspects of the most important of the feline myocardial diseases.
Clinical Pathophysiology - The cause of CHF in cats with HCM is thought to involve mainly ventricular diastolic dysfunction. 4,5,8,9 Abnormalities of ventricular filling are characterized by either abnormal myocardial relaxation (an active, oxygen-dependent process) or reduced left ventricular compliance (distensibility). These problems are related to abnormal cardiac muscle, myocardial ischemia or oxygen imbalance (reduced delivery relative to demand), increased chamber stiffness (thick wall to lumen ratio), and myocardial fibrosis. Higher than normalpulmonary venous and left atrial pressures are required to fill a stiff ventricle, predisposing to pulmonary edema. A vigorous atrial contraction may be needed for maintain ventricular preload; accordingly, the development of atrial fibrillation can be disastrous, causing severe CHF. The roles of myocardial ischemia and of stress (sympathetic activity) in the pathogenesis of diastolic dysfunction require further study. It is well known, however, that stress predisposes affected cats to CHF. Certainly protracted tachycardia increases myocardial oxygen demand, decreases coronary perfusion time, and elevates left atrial pressure. These factors may explain the sudden development of left-sided CHF (flash pulmonary edema) so often observed in this disorder.
Cats with HCM may also suffer from abnormal ventricular systolic function. 4,10 Dynamic and labile pressure gradients between the left ventricle (LV) and aorta ar e often found as blood is ejected rapidly across a bulging ventricular septum. Increased systolic pressure in the LV may stimulate further hypertrophy and predispose to ventricular subendocardial ischemia. These systolic gradients are due to the combination of septal hypertrophy and mitral-septal contact.
The latter stems from systolic anterior motion (SAM) of the mitral valve that begins once ejection has been initiated. The presence of significant SAM is invariably associated with mitral regurgitation (MR). Mitral incompetency also can be traced to geometric changes in the left ventricle, papillary muscle dysfunction, or possibly atrial dilatation.
Clinical features - Male cats are predisposed. Young cats (5 months to 6 years of age) are often affe cted, though cats of any age may have HCM. Breeds at risk include the Maine coon cat 10b, Persian cat, Ragdoll cat, and probably other breeds as well. The possibility of HCM may be prompted by auscultation of a cardiac murmur or gallop sound in a cat that has no other signs of heart disease. 2,4,11 When symptomatic, most cats are presented for tachypnea and dyspnea, attributable to CHF with pulmonary edema or pleural effusion. Stress, fever, moderate-to-severe anemia, thyrotoxicosis, anesthesia, or fluid therapy may precipitate congestive heart failure. Urgent presentation may follow arterial thromboembolism to the terminal aorta. More subtle or vague are signs related to embolism of the right forelimb or cerebrum. Sudden death is reported infrequently, and is likely to develop from a coronary embolus, a ventricular arrhythmia, or if signs of CHF are unrecognized and the cat succumbs to hypoxia. Nonspecific signs such as lethargy or anorexia are less common.
Typical physical examination features of HCM include various combinations of the following:
gallop, murmur of MR (along the left apical, sternal border), arterial thromboembolism, pulmonary edema or biventricular CHF (pleural effusion). When present, the systolic murmur can vary, often increasing in intensity with higher heart rates. This finding suggests dynamic outlet obstruction and SAM are present. The apical impulse can be prominent. Arrhythmias can occur but are not common. Arterial blood pressure is normal.
Laboratory tests can be useful. 2,3,5,12 The ECG may be abnormal but results are inconsistent.
Increased amplitude R-waves in lead II or a left axis deviation compatible with concentric hypertrophy or left anterior fascicular block may be observed. Radiographs can be normal, but in advanced cases demonstrate cardiomegaly (elongation) and left atrial enlargement (most evident as an auricular bulge on the VD view). Prominent pulmonary vascular patterns may indicate pulmonary hypertension secondary to elevated left ventricular diastolic pressure.
Increased lung densities are compatible with pulmonary edema. Pleural effusion is common in acute CHF and in chronic, longstanding cases of heart failure. Routine CBC and clinical chemistries are unremarkable in most cases unless there is thromboembolism or intercurrent disease. Serum thyroxine is normal.
Hypertrophic cardiomyopathy is characterized echocardiographically by increased ventricular thickness (generally 6 mm or more), normal to decreased intraluminal size, and normal or increased systolic shortening fraction. 3,5,10,10b,12 However, 2D echo may show regional LV hypertrophy that is not homogeneous; thus, over-reliance on one measurement (i.e. the LV wall between the papillary muscles) is discouraged. In some cats there is prominent ventricular septal hypertrophy with varying obstruction of the LV outlet. In others, prominent papillary muscles are observed (representing an early sign of HCM in some cats). The size of the left atrium bears prognostic significance as it usually relates to the severity of diastolic failure or MR, and can predict the risk for CHF and thromboembolism. In chronic HCM, LV contractility may decrease, the chamber can dilate, and there may be evidence of progression to restrictive disease (see Restrictive Cardiomyopathy below). Systolic anterior motion of the mitral valve is observed quite often and increases in severity with increased sympathetic tone.
Doppler studies may demonstrate abnormal relaxation or compliance of the LV, mitral regurgitation, or high velocity LV outflow caused by dynamic obstruction.
Drug Therapy for Hypertrophic Cardiomyopathy - A number of cardiovascular drugs are used in the management of feline HCM. These drugs may also be of valve for treatment of other feline CV disorders. It is emphasized that there are no large, controlled studies that indicate a superior treatment for asymptomatic disease, for cats with recurrent bouts of CHF, or for advancing heart failure. Prevention of arterial thromboembolism is a persistent problem.
Pharmacologic therapy of cats with HCM generally may include combinations of furosemide, diltiazem, a beta-adrenergic blocker, an angiotensin converting enzyme inhibitor, or drugs that impair coagulation. Relevant clinical pharmacology of these drugs in cats is discussed below.
Beta adrenergic blockers (atenolol 12.5 mg PO once or twice daily or propranolol 2.5 - 5 mg PO, t.i.d.) are most often used to block the adverse effects of sympathetic efferent traffic on the heart.13 Once daily atenolol often controls heart rate at 150/minute for almost 24 hours, though pharmacokinetic studies suggest that b.i.d. treatment may be better. Beta-blockers prevent sinus tachycardia and prolong diastole, increasing time for both coronary and ventricular filling. Myocardial oxygen demand is reduced through decreases in heart rate, contractility, and blood pressure. Beta blockade is especially helpful for reducing pressure gradients caused by dynamic left ventricular outflow obstruction. Once can administer the ultra-short beta-blocker, esmolol, at an initial 0.5 mg/kg loading followed by a 0.1 mg/kg/minute infusion as a provocative treatment during Doppler examination of the LV outlet. A simpler approach is to administer 12.5 mg of atenolol orally and repeat the Doppler study in 1-1/2 to 2 hours later. The murmur of mitral regurgitation when caused by SAM of the valve may partially abate with beta blockade. In a small European study, beta blockade with propranolol was associated with regression of LV hypertrophy, but this has not been a consistent finding. Unfortunately, the net effect of beta blockade on diastolic function in cats with HCM is unknown. The direct effect on myocardial relaxation is unfavorable; however, indirect effects, such as reduced myocardial oxygen demand, decreases in intraventricular gradients, and prolongation of diastole also should be important and could benefit diastolic function. Adverse effects include severe sinus bradycardia (examination HR 100/min), depression, and precipitation of CHF. Owing to the nonspecific blocking effects of propranolol, it is not recommended in cats with uncontrolled pulmonary edema or in cats with arterial thromboembolism until collateral circulation has been restored.
Diltiazem, a calcium channel antagonist, is a popular drug for chronic management of HCM based on the clinical report of Bright et al. 8,9 Calcium channel blockers are thought to improve left ventricular relaxation. The precise mechanism for this benefit has not been elucidated.
Indirect effects, by reducing blood pressure and reflexively increasing sympathetic tone, could be involved. Alternatively, myocardial perfusion may increase with diltiazem since the drug is a coronary vasodilator and also decreases resting heart rate, though not as effectively as a beta-blocker. Overall, diltiazem should reduce myocardial oxygen demand by decreasing heart rate, contractility, and blood pressure. Effects on reducing dynamic outflow tract gradients have been disappointing at the doses commonly used. Though the chronic administration of diltiazem has been reported to decrease LV hypertrophy in cats with very severe HCM, we rarely observe regression even after prolonged therapy with diltiazem, especially in the typical case. Overall, diltiazem is usually preferred in our practice when a cat has already experienced CHF, or when a cats has moderate to severe LV hypertrophy and left atrial dilatation as demonstrated by echocardiography. Diltiazem is also reasonable therapy for the cat with HCM and concurrent atrial fibrillation. Preparations of diltiazem vary and
include: (a) diltiazem (30 mg tablet; ¼ tablet PO tid); (b) Dilacor XR brand of diltiazem (note:
the 240 mg Dilacor XR capsule is opened to reveal four – 60 mg drug tablets which are split into halves using a pill cutter; the dose is 30 mg once or twice daily); or (c) Cardizem CD brand (120, 180, 240 mg capsules; compounded in capsules or in a palatable syrup to provide 30 mg once daily). Anorexia, skin reactions and erythema/edema have been observed in some cats receiving this drug. Depression, weakness, and hypotension may indicate sinus bradycardia, AV block, or arterial vasodilation from too high a dose or sensitivity to the drug (e.g., in older cats with inherent AV conduction disease). A combination of atenolol and diltiazem may be considered in cats with HCM and dynamic LV outflow tract obstruction (30 mg Dilacor in PM; 6.25 to 12.5 mg atenolol in the AM); however, heart rate and blood pressure should be monitored with this combination therapy because of the combined effect of these drugs on heart rate, contractility and blood pressure.
Furosemide is the initial treatment of choice for cats with pulmonary edema (2 – 4 mg/kg IV or IM as an initial dose; thereafter, 1 – 2 mg/kg IV, IM, SQ q8-12h for 24 to 48 hours). Oral therapy is prescribed for home care of cats that have experienced pulmonary edema; however, the maintenance dosage is often titrated down to a relatively low 1 – 2 mg/kg every second to third day. This can be accomplished over a period of two to three weeks. In some cases, furosemide can be discontinued completely. Conversely, doses of 2 mg/kg, b.i.d. to t.i.d., or higher, may be needed to treat progressive pulmonary edema or pleural effusion in cats with chronic CHF. These problems are detected by having clients monitor exercise activity and resting respiratory rate and through periodic examinations and thoracic radiographs. Dietary sodium restriction can be combined with furosemide provided the cat will eat a new diet.
Efficacy of diuretic therapy is monitored using respiratory rate, level of activity, thoracic examination, and the chest radiograph. Overzealous diuresis can be detected by periodic measurement of blood pressure, serum BUN, creatinine and electrolytes. Azotemia, hypokalemia, and hyponatremia are very common in cats taking furosemide on a daily basis.