Vagally mediated suppression of premature ventricular contractions in man.

Twelve patients with PVC's were studied to assess the possible role of the vagus nerves in suppressing PVC's. All were without significant heart disease and under forty years of age. A series of five autonomically active drugs, including vagotonic and vagolytic agents, was administered intravenously, each drug being given after the effects of the previous one had abated. Two of the patients did not have PVC's at the time of study. Of the remaining ten patients, five showed vagally mediated suppression of PVC's. Phenylephrine (40 to 60 mug per minute) reduced HR, from an average of 63.2 bpm to 48.5 bpm by a vagally mediated reflex, and decreased PVC incidence in all five patients. The per cent of ventricular heart beats which were PVC's (per cent PVC) decreased from an average of 18.2 per cent to 3.2 per cent in these patients (p smaller than 0.005 in each case). Edrophonium (10 mg.) produced less bradycardia and less reliable PVC suppression. In two of these five patients, atropine (1.5 mg.) increased PVC incidence markedly, although the per cent PVC did not change significantly because of the concomitant tachycardia. These data suggest that strongly increased vagal tone can suppress PVC's in a significant percentage of such patients. This finding in man extends previous animal work which has shown a protective role of the vagus against ventricular arrhythmias under certain conditions.