The efficacy of intravenous propranolol for suppression of inducibility of sustained ventricular tachyarrhythmias (VT) was studied in 24 patients who had failed ≥1 membrane-active antiarrhythmic drug (mean 2.2 ± 1.2 drugs/patient). The response to propranolol was compared in 13 patients who had only stable monomorphic VTs inducible at baseline and another 11 patients who had ≥1 episode of electrically unstable VTs (polymorphic VT, ventricular flutter or ventricular fibrillation) at baseline. Seven patients (29%) became noninducible (responders) and 17 patients (71%) remained inducible to sustained VT (nonresponders) after propranolol. The basal heart rate was faster in responders than in nonresponders (101 ± 14 vs 86 ± 11 beats/min, p < 0.01). The magnitude of heart rate reduction was also greater after propranolol in responders (from 101 ± 14 to 80 ± 9 beats/min, p < 0.001) than in nonresponders (from 86 ± 11 to 74 ± 9 beats/min, p < 0.01) (p < 0.05 between the groups), despite equal plasma propranolol concentrations (84 ± 50 vs 88 ± 43 ng/ml, difference not significant). Seven of 11 patients (64%) who had ≥1 episode of unstable VTs inducible at baseline responded to intravenous propranolol, whereas none of the patients with only stable monomorphic VTs became noninducible after β blockade (p < 0.001). Responders had shorter cycle length of inducible VTs than nonresponders (225 ± 38 vs 302 ± 66 ms, p < 0.001). Thus, intravenous propranolol appears to be efficacious in suppressing fast, electrically unstable VTs, compared to monomorphic VTs with slower rates.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine