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To investigate the association of thrombophilia and coronary artery disease (CAD) in patients with myocardial infarction (MI).Under the age of 45 years, 129 patients with MI and 107 control subjects were included into the study. Traditional risk factors of CAD and protein C, S, antithrombin III deficiencies, factor V Leiden (FV Leiden), prothrombin G20210A and methylenetetrahydrofolate reductase (MTHFR) C677T mutations were investigated.There were statistically significant differences in terms of obesity, smoking, triglyceride, total cholesterol, high-density lipoprotein, high-density lipoprotein, and very-low-density lipoprotein cholesterol, family history, hypertension, diabetes, and left ventricular hypertrophy between patients and controls. None of the patients and controls had protein C, protein S, and antithrombin III deficiencies. Ten patients (7.8%) and 4 controls (3.7%) had heterozygote FV Leiden mutation. Homozygous prothrombine G20210A gene mutation was detected in one patient (1.1%). Homozygous MTHFR C677T mutation was observed in 7.8% (patients) and in 6.5% (controls). Heterozygous MTHFR C677T mutation was detected 36.4% in patients and 31.7% in controls. The difference was not statistically significant in terms of carriage of thrombophilic mutations.We found that traditional risk factors increased the risk of CAD. Prothrombin G20210A, FV Leiden and MTHFR C677T mutations, protein C, S and AT-III deficiencies did not increase the risk of CAD in our young population.
Adult, Male, Antithrombin III, Myocardial Infarction, Factor V, DNA, Protein S, Logistic Models, Risk Factors, Case-Control Studies, Mutation, Humans, Thrombophilia, Female, Prothrombin, Methylenetetrahydrofolate Reductase (NADPH2), Protein C
Adult, Male, Antithrombin III, Myocardial Infarction, Factor V, DNA, Protein S, Logistic Models, Risk Factors, Case-Control Studies, Mutation, Humans, Thrombophilia, Female, Prothrombin, Methylenetetrahydrofolate Reductase (NADPH2), Protein C
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