The role of blood platelets in the pathogenesis of experimental sudden death was evaluated in dogs. Coronary artery embolization resulted in acute myocardial ischemia that was followed by sudden death (death within 15 min of embolization) in 51% of anesthetized control animals. Pretreatment with carbenicillin, which markedly inhibited platelet aggregation, or estradiol cypionate, which induced severe thrombocytopenia, significantly reduced the incidence of sudden death to 9% and zero, respectively. Pretreatment with aspirin, which uniformly inhibited platelet aggregation, was associated with a reduced incidence of sudden death (25%), but the difference between aspirin-treated and control animals lacked statistical significance. Drug treatment did not prevent myocardial infarction, and the sizes of myocardial infarcts observed in animals that survived 30 days were not different from those of control animals. Sudden death was preceded by a significantly greater fall in mean arterial pressure than that observed in survivors, but the frequency of ventricular ectopic beats did not differ in survivors and nonsurvivors. These studies suggest that (1) platelets play an important role in experimental sudden death which follows acute coronary embolization and (2) inhibition of platelet function protects against experimental sudden death by a mechanism that prevents severe hypotension but is not antiarrhythmic. Drug-induced platelet dysfunction and thrombocytopenia may protect against experimental sudden death by preventing intravascular platelet aggregation and embolization.
|Original language||English (US)|
|Number of pages||13|
|Journal||The Journal of laboratory and clinical medicine|
|State||Published - Nov 1981|