Efficacy of nadolol alone or in combination with a type IA antiarrhythmic drug in sustained ventricular tachycardia: a prospective study.

We examined the clinical efficacy and safety of intravenous nadolol acutely, as well as chronic nadolol alone or combined with a type IA antiarrhythmic drug in 19 patients with sustained ventricular tachycardia and heart disease, mean age 62 +/- 15 years, and mean left ventricular ejection fraction 39 +/- 8%. Patients underwent electrophysiological studies in the drug-free state (control), after intravenous nadolol (dose = 0.05 mg/kg), and oral nadolol (dose = 80 mg/day) for 5 days alone or in combination with a type IA antiarrhythmic drug. Electrocardiographic and electrophysiological effects as well as ventricular tachycardia induction at electrophysiological study were analyzed. Long-term therapy with oral nadolol alone or in combination with a type IA antiarrhythmic drug was evaluated in responders. Intravenous nadolol prolonged RR and QRS intervals but had no effect on PR and QTc intervals. Oral nadolol alone tended to prolong RR intervals (P = 0.08). Oral nadolol with type IA antiarrhythmic drug prolonged RR and QTc intervals (P less than 0.001). The mean right ventricular effective refractory period tended to prolong after intravenous nadolol alone (from 251 +/- 29 to 263 +/- 25 msec, P = 0.08). Oral nadolol and type IA antiarrhythmic drugs did not prolong right ventricular effective refractory period (P = 0.3). Eighteen patients had inducible sustained ventricular tachycardia at control electrophysiological study. After intravenous nadolol, ventricular tachycardia was no longer inducible in seven patients. Ventricular tachycardia did not recur and remained noninducible in two of six patients who tolerated oral nadolol alone. Mean right ventricular effective refractory period prolonged from baseline values (from 249 +/- 30 to 271 +/- 30 msec, P less than 0.02) in patients who became noninducible on intravenous nadolol. In patients who remained inducible, mean right ventricular effective refractory period remained unchanged (from 253 +/- 29 to 258 +/- 22 msec, P greater than 0.2). In nonresponders to intravenous or oral nadolol, oral nadolol, and type IA antiarrhythmic drug suppressed ventricular tachycardia induction in two of ten patients. During follow-up, three patients continued on oral nadolol alone (one patient) or oral nadolol and type IA antiarrhythmic drug (two patients). Adverse effects resulting in nadolol discontinuation occurred in five patients. Therefore, we concluded that intravenous nadolol is effective in acute suppression of inducible ventricular tachycardia in selected patients. Oral nadolol alone or in combination with type IA antiarrhythmic drug is infrequently effective and poorly tolerated by this patient population. In addition, electrophysiological studies on intravenous nadolol do not predict the outcome of oral nadolol therapy.