The role of beta-blockade therapy for ventricular tachycardia induced with isoproterenol: a prospective analysis

Isoproterenol is sometimes required for ventricular tachycardia (VT) induction. However, the role of beta-blockade for treatment of such VT has not been critically assessed. The use of beta-blockade was evaluated prospectively in 14 consecutive patients who required isoproterenol 2.4 +/- 1.3 (+/- S.D.) micrograms/min to induce sustained monomorphic VT (greater than 30 seconds, or requiring termination due to hemodynamic collapse) after a negative baseline study. The VT mechanisms were enhanced automaticity (group A, six patients), triggered automaticity (group B, three patients), and reentry (group C, five patients). Groups A and B had serial intravenous electropharmacologic tests with propranolol alone (0.2 mg/kg), verapamil alone (0.15 mg/kg), and propranolol plus verapamil, and group C had serial tests with propranolol alone, procainamide or quinidine (class Ia drug) alone, and propranolol plus a class Ia drug until VT could no longer be induced. All six patients in group A responded to propranolol alone. In group B, one patient responded to verapamil alone, and two patients responded to propranolol plus verapamil. In group C, three patients responded to propranolol alone, one patient responded to a class Ia drug alone, and one patient responded to propranolol plus a class Ia drug. During a follow-up of 7 to 37 (17.9 +/- 10.7) (+/- S.D.) months, VT has not recurred in any patient. Three patients treated initially with propranolol alone have required substitution of amiodarone due to refractory congestive heart failure. In patients requiring isoproterenol for VT induction, beta-blockade alone appears to be effective in preventing reinduction of VT caused by enhanced automaticity. A heterogeneous response occurs when the VT mechanisms are triggered automaticity or reentry.