Letter to the Editors-in-Chief

Cyclooxigenase (COX)-1, formally known as prostanglandin endoperoxideH synthetase-1,mediates synthesis of prostaglandin H2,which is subsequently converted to various biologically active metabolites including thromboxane (TX) A2 [1]. TXA2 is synthesized and released by activated platelets and strongly reinforces thrombus formation, a critical pathway in the pathogenesis of myocardial infarction (MI). Inhibition of COX-1-derived TXA2 in platelets by low-dose aspirin administration reduces incidence of MI [2]. Hypothetically, MI-risk could also be modified by genetic variants that affect activity or expression of COX-1. Many single nucleotide polymorphisms (SNP) in the gene encoding COX-1 (PTGS1) have been described; including functional alterations in both coding and non-coding regions [3,4].We have evaluated if two of such variations are related to the risk ofMI in a historic cohort of patients with coronary artery disease (CAD)