Effect of atenolol on heart rate, arrhythmias, blood pressure, and dynamic left ventricular outflow tract obstruction in cats with subclinical hypertrophic cardiomyopathy

Abstract

ObjectiveTo investigate the negative chronotropic, antiarrhythmic, and obstruction-relieving effects of atenolol in cats with subclinical hypertrophic cardiomyopathy (HCM). AnimalsSeventeen cats with HCM. MethodsResults for echocardiography, electrocardiography, Doppler blood pressure, and 24 h Holter monitoring were compared in cats before and 2–4 weeks after atenolol therapy (6.25–12.5 mg PO q 12 h). ResultsThe left ventricular outflow tract maximum velocity (LVOT Vmax) decreased after atenolol administration (mean Vmax pre-treatment 3.3 m/s ± 1.8 m/s; post-treatment 1.6 m/s ± 1.0 m/s, p < 0.0001). Heart rate (HR) decreased after atenolol for all HR modalities. The total number of ventricular origin complexes (TotVent) and ventricular premature complexes (VPCs) decreased after atenolol. The VPCs decreased from a geometric mean of 61 complexes/24 h (range, 11–620 complexes/24 h) to 15 complexes/24 h (range, 1–1625 complexes/24 h) (p < 0.0001). Murmur grade decreased after atenolol from a median grade of 3/6 to 2/6 (p < 0.0001). The systolic blood pressure did not change (mean pre-treatment 130 mmHg ± 16 mmHg, mean post-treatment 123 mmHg ± 20 mmHg, p = 0.2). ConclusionAtenolol decreases HR, murmur grade, and LVOT obstruction, and to a lesser degree, frequency of ventricular ectopy, in cats with subclinical HCM. Further studies are needed to determine if sudden cardiac death or long-term outcome is influenced by atenolol administration.