Jackson B, Adin DB, Lehmkuhl LB. Effect of atenolol on heart rate, arrhythmias, blood pressure, and dynamic left ventricular outflow tract obstruction in cats with subclinical hypertrophic cardiomyopathy. J Vet Cardiol. 2015 Dec;17 Suppl 1:S296-305.

Hypertrophic cardiomyopathy (HCM) is the most common heart disease of cats. In HCM, the myocardium of the left ventricle hypertrophies concentrically and stiffens, which results in diastolic dysfunction and ultimately increased left atrial pressures and distension of the left atrium. This disease may be subclinical throughout some or all of an affected cat’s life, but when it progresses to clinically evident dysfunction, congestive heart failure (CHF), thromboembolic disease, and even sudden cardiac death may be the result. When subclinical HCM is detected in a cat, both clinicians and owners experience great concern as there are no evidence-based prophylactic therapies that are clinically proven to prevent progression to clinical disease, and once clinical disease does occur, even the short-term prognosis may be poor to grave.

Atenolol, a beta-1 adrenergic receptor antagonist, has often been used empirically in the treatment of cats with subclinical HCM, and is thought by many clinicians to be of benefit to these animals. In this study of client-owned cats with subclinical HCM, cats were included if they had echocardiographic evidence of diffuse or segmental left ventricular hypertrophy, but were excluded if they were found to have systemic hypertension or hyperthyroidism. In addition to echocardiography and Doppler blood pressure measurement, the cats were also evaluated with cardiac auscultation, electrocardiography and 24-hour Holter monitoring. Seventeen cats (14 neutered males and 3 spayed females) completed the study; the median age of the animals was 7.0 years (range, 4 years-17 years). Of the 17 cats, 11 had left ventricular outflow tract obstruction (LVOTO) secondary to systolic anterior motion (SAM) of the mitral valve, and 6 did not have this echocardiographic abnormality.

Results of the above-described clinical evaluations were compared in the subjects before and then 2-4 weeks after starting atenolol therapy at 6.25-12.5 mg PO q 12 hours. Echocardiography demonstrated that LVOT velocity, and therefore LVOT obstruction, decreased in the patients after at least 2 weeks of atenolol administration. Cardiac arrhythmias were not found in many of the patients until Holter monitoring was performed. In humans, there is a known association between the occurrence of non-sustained ventricular tachycardia and risk of sudden cardiac death, and also in humans with HCM, 88% had ventricular arrhythmias demonstrated by Holter monitoring, and 31% had ventricular tachycardia. One previous study showed that 100% of cats with subclinical HCM have arrhythmias.

Atenolol was also found to decrease heart rate, heart murmur grade, and to a lesser degree, ventricular ectopy, in cats with subclinical HCM. The frequency and complexity of ventricular arrhythmias in the study cats was reduced with atenolol use; atenolol is also a ventricular and supraventricular antiarrhythmic agent. It is still unknown if administration of this drug results in reduced incidence of sudden cardiac death in cats with HCM, or a longer period of time before subclinical HCM progresses to CHF. As only cats with mild subclinical HCM were included in the study it is unknown if atenolol adminstration also positively affects cardiac function parameters in cats with more severe HCM or actual clinically evident heart disease. Given the promise atenolol has shown in improvement of cardiac function in this small population of cats with subclinical HCM, additional studies in cats with more severe or clinically evident disease are warranted. [PJS]