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Which Drug for Which Disease?

INTRODUCTION ade, or others) and financial, temporal, or other client
limitations that ultimately lead the client to elect for
In a field with as few objective, evidence-based guide- premature discontinuation of monitoring, or even
lines as feline cardiology, this is no doubt the most dif- euthanasia, after misconstruing the importance of the
ficult chapter to write. Seemingly any conclusion on heart disease or its treatment:
cardiovascular therapeutics in the cat can be criticized
or dismantled if one tries hard enough. Yet as clinicians, • Beta blocker (atenolol 6.25–12.5 mg/cat PO q 12–24h).
we know that every patient represents the point at which Beta blockers appear to be the most useful drug to
concrete decisions must be made: treatment or no treat- reduce the severity of left ventricular outflow tract in
ment? If treatment, what is best, and for how long? Our cats with systolic anterior motion of the mitral valve,
clinical grounding makes it impossible for us to be satis- and cats with moderate or severe obstructions may
fied with criticizing a lack of evidence while streams of receive symptomatic benefit as well as reduced con-
cats with heart disease pass through our hands. We have centric hypertrophy associated with lessening the
written these treatment approaches as a work-in-prog- pressure overload to the left ventricle. Additional ben-
ress, fully aware—and hopeful—that, as we write these efits of beta blockade in cats with HCM may include
words, the data that prove us right or wrong are in the decreased myocardial oxygen demand via prevention
making. of tachycardia; increased diastolic filling time aug-
We are indebted to Dr. Lionel Opie and his seminal menting coronary blood flow; and reduction of direct
book, Drugs for the Heart, for providing the title and toxic effects of catecholamines on myocardium, which
concept for this chapter. may lessen concentric hypertrophy or development of

arrhythmias. Atenolol appears to reduce myocardial
HYPERTROPHIC CARDIOMYOPATHY—
COMPENSATED (“ASYMPTOMATIC”) damage short-term as evidenced by lower serum
cardiac troponin-I concentrations in treated cats
The cause of HCM in cats is proven to be one or more (Côté 2007). No studies have evaluated potential long-
genetic mutation(s) in some cats, and this pattern term benefit, however.
appears heritable. Therefore, in the absence of gene • Calcium-channel blocker, regular formulation (diltia-
therapy, treatment consists of selective breeding and, for zem hydrochloride 7.5 mg/cat PO q 8h). In one clini-
individual cats, drugs that slow or delay the cardiomyo- cal trial, there was reduced hypertrophy and improved
pathic process. There is either an absence of clinical diastolic relaxation in a small but significant number
studies of some commonly used cardiac drugs in the of cats with HCM and congestive heart failure (Bright
asymptomatic state, or a lack of evidence of benefit in et al. 1991). Based on preliminary findings in a small
some small-scale clinical reports. Therefore, two impor- number of asymptomatic cats, diltiazem had no mea-
tant considerations of treatment of compensated HCM surable benefit in structural or functional parameters
in the absence of proof of efficacy are safety and conve- (Schober et al. 2007). Currently, this drug is disfa-
nience. Contraindications to any of the following treat- vored because of frequency of dosage administration
ments include intolerance (patient’s resistance to (compliance) or adverse effects of the sustained
medication administration, adverse effect, exacerbation release formulations including sporadic changes in
of other disease states such as asthma with beta block- serum levels and high potential for side effects. The

Feline Cardiology, First Edition. Etienne Côté, Kristin A. MacDonald, Kathryn M. Meurs, Meg M. Sleeper.
© 2011 John Wiley & Sons, Inc. Published 2011 by John Wiley & Sons, Inc.

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