[Treatment of heart arrhythmias with calcium antagonists].

The depressing effect of calcium antagonists on sinus node and AV node function is well documented in the experimental animal and in man. Other cardiac fibers may be depolarized to a level at which the slow inward current determines the rise of the action potential and may become sensitive to calcium antagonists, thus abolishing extrasystoles or tachycardias. However, effects of the drugs on heart rate, coronary perfusion, and pre- and afterload of the left ventricle must be taken into account, which may affect the electrophysiologic basis for the dysrhythmia. The conversion rate of atrial fibrillation to sinus rhythm (n = 200) amounted to 77% when quinidine was combined with verapamil. Monotherapy of these drugs or combination of quinidine with diltiazem or pindolol did not elevate the atrial fibrillation threshold compared to quinidine/verapamil. Reduced ventricular fibrillation thresholds in the experimental animal after coronary occlusion increased significantly during the early reperfusion period after verapamil and nifedipine by cardioprotection. Due to a reduced renal clearance the bio-availability of digoxin increased with a concomitant medication of quinidine and verapamil.