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Abstract

Blood clot formation is the key event in myocardial infarction. Besides increased coagulation, failure in blood clot lysis can induce undesired coronary thrombosis. Plasmin is essential for degradation of fibrin clots. Tissue-type plasminogen activator (t-PA) is the serine protease that converts plasminogen into plasmin. The association of the Alu insertion/deletion polymorphism in intron h of the t-pA gene to the risk of myocardial infarction was evaluated. Subjects with a documented history of myocardial infarction (n=162) and controls (n=258) were drawn from the Rotterdam Study, a population-based cohort study of 7983 subjects of 55 years or older. Allele frequencies were 0.54 for the insertion allele (t-PA Alu-h I) and 0.46 for the deletion allele, and were in Hardy Weinberg equilibrium. Among subjects that were homozygous for the insertion (n=138) were more than twice as many subjects with myocardial infarction compared to those homozygous (n=75) for the deletion (relative risk of 2.04, (95% CI 1.03-4.03), adjusted for age, gender, smoking, total cholesterol, HDL cholesterol, systolic and diastolic blood pressure and body mass index). Our results provide strong evidence for an association of a particular allele, t-PA Alu-h I, of the t-PA gene with the occurrence of myocardial infarction.

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