Does aspirin and tourniquet-induced ischaemia affect platelet function and aggregation in survivors of myocardial infarction compared to healthy controls?
Platelet function is increased and the proaggregatory threshold is decreased in MI survivors, and short-term aspirin fails to inhibit spontaneous platelet aggregation following ischaemia in these patients.
Platelet number, plasma beta-thromboglobulin (beta-TG), spontaneous platelet aggregation (SPA), serum thromboxane B2 (TXB2), and 6-keto-PGF101 were assessed in 9 males with proven atherosclerosis (survivors of myocardial infarction, (MI) in a stable condition) and compared with values for 9 young, healthy controls. Results were obtained before and after 3-day treatment with aspirin. In addition, SPA was assessed before and after a tourniquet test. MI survivors had higher beta-TG (p < 0.01) and SPA values (p < 0.05), and a lower platelet count (p < 0.05) than controls. Aspirin significantly attentuated all these changes. These data suggest that platelet function is increased in survivors of MI. Tourniquet-induced ischaemia significantly (p < 0.05) enhanced SPA in MI survivors but not in controls. Aspirin did not inhibit SPA following ischaemia in contrast to its effect under pre-ischaemic conditions or in controls. It seems that the proaggregatory threshold is decreased in MI survivors. The results challenge the assumption that an acute coronary event with underlying atherosclerosis is due to an interaction between atherosclerosis plaque and normal platelets.
Spławińska et al. (Wed,) studied this question.