Comparative clinical electrophysiologic effects of diltiazem, verapamil and nifedipine: a review.
The slow channel blocking agents--diltiazem, verapamil and nifedipine--have generated clinical interest for the treatment of a variety of cardiovascular disorders. These agents, despite a similar basic mechanism of action, produce disparate clinical cardiac electrophysiologic effects in human beings. In usual doses, the acute administration of diltiazem slows heart rate. Verapamil and nifedipine, however, increase heart rate. Although diltiazem and verapamil produce equivalent slowing of atrioventricular (A-V) nodal conduction, verapamil prolongs A-V nodal refractoriness to a greater degree. In contrast, nifedipine facilitates A-V nodal conduction and shortens A-V nodal refractoriness. Knowledge of these differences may aid in the appropriate selection of specific slow channel blocking agents in specific clinical situations.
D001283:Atrioventricular Node / Q000187:drug effects; D001552:Benzazepines / Q000627:therapeutic use*; D003327:Coronary Disease / Q000188:drug therapy; D004110:Diltiazem / Q000627:therapeutic use*; D004562:Electrocardiography; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007473:Ion Channels / Q000187:drug effects; D009543:Nifedipine / Q000627:therapeutic use*; D011725:Pyridines / Q000627:therapeutic use*; D012849:Sinoatrial Node / Q000187:drug effects; D014700:Verapamil / Q000627:therapeutic use*
D001552:Benzazepines; D007473:Ion Channels; D011725:Pyridines; D014700:Verapamil; D004110:Diltiazem; D009543:Nifedipine