Electrophysiologic properties of cimetidine in man

Severe bradycardia has been reported with the use of cimetidine. This observation has been explained by histamines' known action in increasing the contraction rate of the spontaneously beating right atrium, strips of ventricular muscle, and whole heart of guinea pigs. Histamine can also produce cardiac arrhythmias in animals. There is evidence for H2 receptors in the heart. Black and his associates have shown that the characteristic effect of histamine on isolated guinea pig atrium could be selectively blocked by anti-H2 drugs. Thus cimetidine probably can produce a sinus bradycardia by blocking the H2-receptor site in the heart. Recently Engel and Luck reported that 300 mgs of intravenously administered cimetidine did not affect heart rate, sinus node recovery time, or sinoatrial conduction time. These workers concluded that there is insufficient evidence to demonstrate that cimetidine caused appreciable sinus node dysfunction in man. In view of the disparity in these reports, we investigated the effects of 300 mgs of intravenously administered cimetidine on the human conduction system.