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

Bethany L. Jackson, Darcy B. Adin, Linda B. Lehmkuhl
Journal of veterinary cardiology 2015 v.17 pp. S296
arrhythmia, cardiomyopathy, cats, death, echocardiography, electrocardiography, heart rate, monitoring, systolic blood pressure, therapeutics
To investigate the negative chronotropic, antiarrhythmic, and obstruction-relieving effects of atenolol in cats with subclinical hypertrophic cardiomyopathy (HCM).Seventeen cats with HCM.Results 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).The 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).Atenolol 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.