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An Urban Experience
J. Haggstrom1
1Swedish University of Agriculural Sciences, Department of Clinical Sciences, Uppsala, Sweden
Jens Häggström
Professor, DVM, PhD, DECVIM-CA (Cardiology)
Department of Clinical Sciences, Faculty of Veterinary Medicine and Animal Science
Swedish University of Agricultural Sciences, Uppsala, Sweden
The discovery of cardiomypathy in a cat often means that the veterinarian and the owner have to make a decision how to manage the condition. Preferably,
this decision should be based on results from clinical trials. Unfortunately, therapeutic clinical trials in cats
are few and this means that decisions and treatment recommendations are often based on extrapolation of results from human clinical trials, expert opinion, and own experience. In the absence of clinical trials, treatment strategies are bound to be controversial, and this is certainly the case for feline cardiomyopathy, particular
in managing cats with subclinical cardiomyopathy.
This presentation will outline the most commonly instituted treatments of cats with subclinical and clinical cardiomyopathy.
Subclinical cardiomyopathy
Feline cardiomyopathy is often discovered in clinically healthy cats as an incidental finding or as a consequence of screening for hypertrophic cardiomyopathy (HCM). Chronic therapy is often initiated in these cats to reverse or slow the progression of hypertrophy, in case of HCM, because there is a pressure on the veterinarian to do something, because of theoretical benefit, because
an absence of evidence of efficacy is not the same
as evidence of inefficacy, and because the rate of unwanted side reactions for the most common treatment choices are low. The drugs that are most commonly used in this setting are beta-blockers, ACE-inhibitors
and calcium channel blockers, but pimobendan has gradually become more frequently used. A finding of an enlarged left atrium with or without an atrial thrombus or spontaneous echocardiographic contrast (smoke) means
that antithrombotic therapy is indicated.
Several reasons have been suggested for using beta- receptor blockers in subclinical HCM. The tendency
for veterinary specialists to introduce beta-blockade in subclinical disease increases if systolic anterior motion (SAM) of the mitral valve is present. This phenomenon leads to a dynamic subaortic stenosis and mitral regurgitation, and it is a common finding in cats with HCM. Beta-receptor antagonism leads to a reduction
of the dynamic outflow obstruction and a slowed heart rate. Beta-blockers may be indicated in HCM for its anti- arrhythmic properties. The most commonly used beta- receptor antagonists used in veterinary medicine include: atenolol (6.25-12.5 mg/kg/cat q12h PO) and propranolol (0.4-1.2 mg/kg q8h PO). A recent study reported no long-term (5 years) benefit of atenolol on prolonging the pre-clinical period or survival compared to no treatment.
The rationale for using an ACE-inhibitor in subclinical HCM is to pharmacologically suppress the activity of the renin-angiotensin-aldosterone system (RAAS), and by doing so, counteract progressive myocyte hypertrophy and fibrosis. It has been shown that circulating levels of components of RAAS is increased in cats with HCM, especially after the onset of congestive heart failure. This data provides a theoretical background for efficacy of ACE-inhibitors in subclinical HCM, and ACE-inhibitors are widely used in this setting. The clinical studies concerning the effect of ACE-inhibitors on degree of hypertrophy in cats with HCM shows conflicting results, and there is no published study showing a beneficial effect of ACE-inhibitors on quality of life variables and survival.
Calcium channel blockers
Diltiazem is a drug with failing popularity among veterinary cardiology specialists. The rationale for
using calcium-channel blockers is subclinical HCM is that diltiazem has been suggested to lessen edema formation and decrease wall thickness in cats with HCM. Furthermore, calcium channel blockers have been suggested to improve diastolic function (improved relaxation) and reducing ischemia. Exactly how these drugs cause an improved diastolic function is currently not completely understood. However, both the systolic and diastolic abnormalities may be related to abnormal calcium kinetics, and drugs that block the inward transport of calcium over the myocardial cell membrane may be able change this abnormality in a positive way. The most commonly used calcium-channel blocker
in cats is diltaizem, which is also available as a slow-

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