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Title: [Comparative studies on the anti-arrhythmic and anti-fibrillatory effectiveness of verapamil and nifedipine following acute coronary artery occlusion and reperfusion]. Author: Gülker H, Thale J, Brisse B, Bender F. Journal: Z Kardiol; 1984 Aug; 73(8):515-24. PubMed ID: 6495811. Abstract: The ability of the two calcium-antagonists Verapamil and Nifedipine to reduce ventricular electrical instability following acute transient coronary artery occlusion and release and to prevent ventricular arrhythmias, particularly fibrillation, was evaluated on a total of 25 anaesthetized and artificially ventilated dogs. In all animals repeated coronary occlusions, lasting 20 min each, with a reperfusion period of 120 min between subsequent ligations, were performed. Time course and extent of ventricular ectopic activity were continuously registered, and the changes in ventricular vulnerability were assessed by measuring the ventricular fibrillation threshold at different times both after coronary artery occlusion and reperfusion. Verapamil displayed strong antiarrhythmic and antifibrillatory action on ventricular arrhythmias during occlusion. Ventricular tachycardia and fibrillation were completely prevented during phase la of arrhythmia (2nd to 10th min after coronary artery occlusion) and significantly reduced during phase lb (15th to 20th min after coronary artery occlusion). By contrast, Nifedipine failed to exert any antiarrhythmic and antifibrillatory effect, respectively. Following release of coronary artery occlusion, none of the compounds proved to reduce the frequency of ventricular fibrillation immediately after the onset of reperfusion. However, either drug was able to accelerate significantly the increase in the ventricular fibrillation threshold during the early post-reperfusion period. The different antiarrhythmic and antifibrillatory action of Verapamil and Nifedipine after coronary artery occlusion can be assumed to result from differences in the electropharmacological properties of these compounds, whereas the enhancement of the electrical stability of the myocardium after release of coronary artery occlusion may be due to "cardio-protective" effects of these drugs.[Abstract] [Full Text] [Related] [New Search]