Schober KE, Zientek K, Li XB, et al. Effect of treatment with atenolol on 5-year survival in cats with preclinical (asymptomatic) hypertrophic cardiomyopathy. Journal of Veterinary Cardiology 2013;15:93-104.
When an asymptomatic cat is found to have hypertrophic cardiomyopathy (HCM), there arises a natural desire on the part of both owners and clinicians to take steps that might pre-empt progression of disease. At this time there is no clear evidence-based recommendation for treatment of these patients, principally due to the lack of prospective controlled studies. Serial monitoring only of such patients is recommended by some cardiologists, while others will treat cats with preclinical HCM with negative inotropes and/or negative chronotropes. Beta-adrenergic receptor blockers, usually atenolol, because of its modest cost and low frequency of administration, are the most popular drugs used empirically in cats with preclinical HCM, although there is currently no evidence supporting the long-term benefits of these agents.
In this prospective, observational, open-label, clinical cohort study, 63 client-owned cats with preclinical (asymptomatic) HCM diagnosed by echocardiography and 31 healthy control cats with similar body weight, age, gender, and breed to the HCM cats were enrolled. Hypertrophic cardiomyopathy was diagnosed echocardiographically if the patient had diffuse or segmental left ventricular end-diastolic wall thickness > 6 mm, which is diagnostic for idiopathic left ventricular hypertrophy and therefore HCM. Cats with cardiac disease other than HCM and any systemic diseases, cats in congestive heart failure (CHF), and cats with repeated systolic blood pressures > 170 mm Hg as evaluated using a Doppler unit, were excluded. All of the control and HCM cats had cardiac murmurs but no evidence of cardiac disease; the HCM group had a median heart murmur intensity of 3/6, while the control cats had a median heart murmur intensity of 2/6. Cats in the HCM group had a higher frequency of gallop sounds (25% of HCM cats versus 3% of controls), were more likely to have ventricular premature complexes (30% in the HCM group versus 0 controls), had a greater frequency of left ventricular diastolic dysfunction (65% of the HCM cats versus 19% of the controls) and a greater incidence of dynamic left ventricular outflow tract obstruction (48% of the HCM cats versus 0 controls).
Patients with HCM were placed into one of two treatment groups, partially based on the owner’s willingness to give tablets twice daily. The cats were not randomized and a placebo group was not used, as the investigators did not want to ask an owner to give a blank pill twice daily. Atenolol at 6.25 or 12.5 mg PO q 12 hours was given to 42 of the HCM cats, and the dose was adjusted to meet a target heart rate of 120-160 bpm. The remainder of the HCM cats (n =21) were not treated. Some of the treated cats also received enalapril (n=9), 0.25-0.5 mg/kg PO q 12 hours, starting at a mean of 3.6 years after enrollment, and some received clopridogrel (n=5), 18.75 mg PO q 24 hours, starting at a mean of 4.2 years after enrollment. All cats were observed for 5 years following enrollment in the study, and death due to any cause was the end point.
Of the 63 cats with HCM, 27 died during the observational period; 14 (22%) died of cardiac disease, while 13 (21%) died of non-cardiac disease. Ten of the 31 control cats (32%) died of non-cardiac disease during the same period. These investigators concluded that there was no significant difference found in all-cause mortality between the control and HCM cats, but cardiac mortality was significantly higher in the HCM cats than the control cats. There was also no significant difference in all-cause mortality or cardiac mortality between untreated and atenolol-treated HCM cats; based on the results of this research, use of atenolol in cats with preclinical HCM does not influence 5-year survival. The only parameters that predicted the 5-year outcome for a patient were age at the time of diagnosis, and left atrial size (LA:Ao; ratio of maximum left atrial size in systole to maximum aortic root diameter in diastole) at the time of diagnosis. [PJS]
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