Many aspects of chronic therapy of hypertrophic cardiomyopathy are controversial. All therapy is palliative. Furosemide is the only drug that has a clearly beneficial effect chronically on survival in cats with hypertrophic cardiomyopathy.
Many cats with hypertrophic cardiomyopathy are dyspneic because of pleural effusion that reaccumulates despite appropriate medical therapy. These cats need periodic pleurocentesis ().
In cats with congestive heart failure due to hypertrophic cardiomyopathy, rurosemide administration, once initiated, should usually be maintained for the rest of the cat’s life. In a few cases, furosemide can be discontinued gradually once the cat has been stabilized. This usually only occurs in a cat that has had a precipitating stressful event.
As for dilated cardiomyopathy, the maintenance dose of furosemide in cats usually ranges from 6.25 (one half of a 12.5 mg tablet) once a day to 12.5 mg orally every 8 hours, although the dose may be increased further if the cat is not responding to a conventional dose. The author and colleagues have administered higher doses (up to 37.5 mg every 12 hours) than commonly recommended to a few cats with severe heart failure without identifying severe consequences as long as the cats were eating and drinking. Cats on high-dose furosemide therapy are commonly mildly dehydrated and mildly to moderately azotemic. However, they often continue to maintain a reasonable quality of life.
The furosemide dose needs to be titrated carefully in each patient. The owner should be taught how to count the resting respiratory rate at home and instructed to keep a daily written log of the respiratory rate as oudined previously under dilated cardiomyopathy. This is highly beneficial for making decisions regarding dose adjustment in individual patients.
Angiolensin-Converting Enzyme Inhibitors
Although furosemide has been used to treat heart fadure secondary to feline hypertrophic cardiomyopathy for decades, the use of angiotensin-converting enzyme inhibitors in cats with hypertrophic cardiomyopathy is relatively recent, because veterinarians, like their colleagues who treat humans, feared that the use of angiotensin-converting enzyme inhibitors would worsen systolic anterior motion in their patients. Over the past 10 years it has become obvious to most veterinary cardiologists that angiotensin-converting enzyme inhibitors do not worsen the clinical signs referable to hypertrophic cardiomyopathy, and a recent study has documented that systolic anterior motion is not worsened by enalapril administration in cats. Many have believed and one study has suggested that angiotensin-converting enzyme inhibitors improve the quality and quantity of life of cats with hypertrophic cardiomyopathy. Preliminary evidence from a recent placebo-controlled and blinded clinical trial suggests that enalapril produces little to no benefit when compared with furosemide alone in cats with heart failure due to hypertrophic cardiomyopathy. However, this study also included cats with unclassified (restrictive) cardiomyopathy and both cats with and without SAM. Subgroup analysis failed to change the conclusions of the study but die subgroups were small. Consequendy, it is the recommendation of this author to continue to use an angiotensin-converting enzyme inhibitor in cats in heart failure due to hypertrophic cardiomyopathy at a dose of 1.25 to 2.5 mg orally every 24 hours.
In cats with severe hypertrophic cardiomyopathy that have or have had evidence of CHF, diltiazem or a beta-adrenergic blocking agent are often administered. Both provide symptomatic benefit in human patients. Their use in cats with hypertrophic cardiomyopathy is controversial; however, little doubt exists that neither drugs produces dramatic benefits. Diltiazem, however, appears to produce no harm.M
Diltiazem is a calcium channel blocker previously reported to produce beneficial effects in cats with hypertrophic cardiomyopathy when dosed at 7.5 mg every 8 hours. Beneficial effects that have been reported include lessened edema formation and decreased wall thickness in some cats. In the author’s experience only a few cats appear to experience a clinically significant decrease in wall thickness, and it is impossible to tell ii this is due to drug effect or time. Rarely does it appear clinically that diltiazem controls congestive heart failure on its own or helps control pulmonary edema or pleural effusion when added on to furosemide therapy. Diltiazem does improve the early diastolic relaxation abnormalities seen in feline hypertrophic cardiomyopathy. Whether this helps decrease diastolic intraventricular pressure and so decrease edema formation is unknown. Theoretically it should have little benefit in the resting cat with a slow heart rate. Slower myocardial relaxation during rapid heart rates may not allow the myocardium enough time to relax, resulting in increased diastolic intraventricular pressure. Diltiazem may help protect a cat that undergoes a stressful event. Incomplete relaxation and decreased compliance, however, are more plausible explanations for increased diastolic pressure due to diastolic dysfunction in feline hypertrophic cardiomyopathy. In humans, diltiazem does not change left ventricular chamber stiffness and so does not alter passive diastolic function. In cats it also appears not to alter late diastolic filling properties. Diltiazem decreases SAM, which may decrease the amount of mitral regurgitation, but beta blockers generally produce a greater decrease in the amount of SAM. Recent evidence suggests that diltiazem has no effect on survival time in cats with severe hypertrophic cardiomyopathy and heart failure.
Dilacor XR is dosed at 30 mg per cat orally every 12 hours and produces a significant decrease in heart rate and blood pressure in cats with hypertrophic cardiomyopathy for 12 to 14 hours.
Beta-Adrenergic Receptor Blockers
Beta blockers are primarily used to reduce systolic anterior motion and heart rate in cats with hypertrophic cardiomyopathy. At this stage, beta blockers should probably be reserved for cats with severe systolic anterior motion at rest or with tachyarrhythmias and not routinely administered to the affected population as a whole, because a recent study has suggested that atenolol shortens the survival of cats with diastolic dysfunction, including cats with hypertrophic cardiomyopathy. Beta blockade is questionable for systolic anterior motion and tachycardia observed in a clinical situation. Cats spend 85% of their life asleep, and sleep probably reduces sympathetic activity better than a beta-adrenergic blocking drug. Consequently, many cats with mild to moderate systolic anterior motion in a veterinary clinic probably have no or milder systolic anterior motion at home, and the same can be said for tachycardia. Beta blockers are effective for reducing SAM. Two studies have examined the effects of esmolol, a short-acting Bradrenergic blocking drug, in cats with hypertrophic cardiomyopathy and obstruction to left ventricular outflow due to SAM; both showed a reduction in the pressure gradient across the outflow tract In both studies the degree of outflow tract obstruction decreased and the heart rate slowed, and in one esmolol was more effective than diltiazem. If the data on esmolol can be translated to atenolol’s effects in cats (which seems reasonable), one would predict that atenolol would decrease SAM.
Atenolol is a specific pVadrenergic blocking drug that needs to be administered twice a day, usually at a total dose of 6.25 to 12.5 mg orally every 12 hours. In the cat, atenolol has a half-life of 3.5 hours. When administered to cats at a dose of 1.4 mg/lb, atenolol attenuates the increase in heart rate produced by isoproterenol for 12 but not for 24 hours.