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.