Low-dose aspirin in patients recovering from myocardial infarction. Evidence for a selective inhibition of thromboxane-related platelet function.
The adequacy, selectivity and long-term persistence of inhibition in cyclooxygenase-dependent platelet function by a daily low-dose (0.45 mg kg-1 day-1) aspirin treatment have been evaluated in 15 patients after a recent (less than 17 days) acute myocardial infarction. Serum thromboxane (TX) B2, an index of platelet TXA2 production, was decreased by 94-98% (P less than 0.001) by aspirin, while urinary excretion of 6-keto-prostaglandin F1 alpha, as an index of extraplatelet cyclooxygenase activity, remained unchanged. Compared to placebo, aspirin induced a persistent increase in bleeding time (% difference 45.6 +/- 21.4, mean +/- SD) and a decrease in platelet aggregation by ADP, epinephrine, collagen and arachidonic acid. No tendency towards an attenuation of the effects was apparent for the period of aspirin administration (4 weeks). Aspirin 0.45 mg kg-1 day-1 is adequate and selective in the long-term inhibition of TX-related platelet function in patients after acute myocardial infarction. The clinical effectiveness of such a regimen remains to be proven in clinical trials.
D000328:Adult; D000368:Aged; D001241:Aspirin / Q000008:administration & dosage* / Q000627:therapeutic use; D001760:Bleeding Time; D001792:Blood Platelets / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D016861:Cyclooxygenase Inhibitors; D004311:Double-Blind Method; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D013928:Thromboxane A2 / Q000037:antagonists & inhibitors* / Q000502:physiology; D013929:Thromboxane B2 / Q000037:antagonists & inhibitors* / Q000096:biosynthesis
D016861:Cyclooxygenase Inhibitors; D013929:Thromboxane B2; D013928:Thromboxane A2; D011451:Prostaglandin-Endoperoxide Synthases; D001241:Aspirin