Why the study?
Does sulfinpyrazone have direct antiarrhythmic electrophysiological effects in patients with impulse-formation and conduction defects?
Does sulfinpyrazone have direct antiarrhythmic electrophysiological effects in patients with impulse-formation and conduction defects?
Sulfinpyrazone lacks direct electrophysiological effects; challenges antiarrhythmic classification and supports antiplatelet mediation of post-MI sudden death reduction.
To determine whether a direct antiarrhythmic effect could explain the claimed beneficial effect of sulfinpyrazone on the sudden death rate in postmyocardial infarction patients, we performed a double-blind, randomized trial in 20 patients with impulse-formation and conduction defects. The patients were studied by intracardiac electrocardiography and programmed stimulation before and after an intravenous bolus injection of either 500 mg sulfinpyrazone or a placebo. We found no consistent clinical or statistical effects of sulfinpyrazone on sinus rate, sinus node recovery time, sinoatrial conduction time, conduction intervals during spontaneous cardiac activity and atrial pacing. Wenckebach point and refractory periods of the atrium, AV node, His Purkinje system and right ventricle. We conclude that sulfinpyrazone has no clinical electrophysiological effects comparable with those of known antiarrhythmic agents and that a direct antiarrhythmic action is an unlikely explanation for the reduction of sudden death in postinfarction patients treated with this drug. Antiarrhythmic activity by an indirect mechanism, related to the antiplatelet properties of the drug, or by metabolites of sulfinpyrazone, remains a possibility requiring further investigation.
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Roos et al. (1982) studied this question.
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