Characteristics of left bundle branch block morphology, interiorly directed frontal plane QRS axis and repetitive nonsustained salvos were used to define a discrete subgroup of patients with ventricular tachycardia (VT). The origin of this tachycardia was thought to be the right ventricular outflow tract. Twenty-six patients with this definition (group 1) were compared with 29 consecutive patients with all other forms of VT (group 2). When compared with patients in group 2, group 1 patients were younger (average age 37 vs 51 years, p < 0.005), had less structural heart disease (2 of 26 vs 25 of 29 patients, p < 0.005) and had a better prognosis (no deaths) after an average follow-up time of 28 months in comparison with 5 deaths after an average follow-up of 35 months (p < 0.05). Induction of VT was possible using isoproterenol infusion in 14 of 20 group 1 patients, but no VT could be induced in 9 group 2 patients (p < 0.05). Exercise stress testing induced VT in 11 of 21 group 1 patients and 2 of 9 group 2 patients (p > 0.05). Programmed electrical stimulation failed to induce VT in 9 group 1 patients, but did induce H in 15 of 20 group 2 patients (p < 0.005). Successful therapy in group 1 patients was achieved by β blockers alone (7 patients), β blockers plus type 1A antiarrhythmic drugs (9 patients), procainamide alone (2 patients), sotalol (3 patients) and amiodarone (2 patients). Three patients were not treated. Evaluation of the relation of the initiating coupling interval to the first tachycardia interval permitted insight into the mechanism. Most had an inverse relation, suggesting that triggered automaticity may be the mechanism of this arrhythmia.