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Selective inhibition of thromboxane-related platelet function by low-dose aspirin in patients after myocardial infarction

1985; Elsevier BV; Volume: 55; Issue: 5 Linguagem: Inglês

10.1016/0002-9149(85)90258-9

1879-1913

Raffaele De Caterina, Daniela Giannessi, W Bernini, P Gazzetti, Claudio Michelassi, Antonio LʼAbbate, L Donato, Paola Patrignani, Paola Filabozzi, Carlo Patrono,

Acute Myocardial Infarction Research

Aspirin inhibits thromboxane (TX) A2-dependent platelet function by irreversibly acetylating platelet cyclooxygenease.1 Acetylation of the enzyme and inhibition of TXB2 production are both dose- and time-dependent. In healthy subjects, inhibition of platelet aggregation and prolongation of bleeding time by aspirin are seen after chronic dosing with as low as 20 to 40 mg/day, without concomitant changes in urinary 6-keto-prostaglandin (PG) F1α and 2,3-dinor-6-keto-PGF1α excretion, i.e., in vivo indexes of renal and extrarenal prostacyclin (PGI2) production.2,3 Inasmuch as the cumulative nature of aspirin-induced inhibition of cyclooxygenase activity is a function of the different rates of daily acetylation and turnover of the enzyme (cell turnover and de novo synthesis), altered platelet survival or endothelial damage may decrease efficacy or selectivity of low-dose aspirin. Therefore, we evaluated the biochemical and functional effects of low-dose aspirin in a small sample of patients surviving acute myocardial infarction (AMI).