Thrombin-activatable fibrinolysis inhibitor genetic polymorphisms as markers of the type of acute coronary syndrome.

INTRODUCTION In patients with coronary disease at risk of acute coronary events it is unclear which biological factors could predict the type of acute coronary syndrome clinical presentation. The aim of the study was to investigate the role of genetic polymorphisms in key proteins in fibrinolysis in the type of acute coronary syndrome. MATERIALS AND METHODS 248 patients with acute coronary syndrome (unstable angina or myocardial infarction) (77% male, mean age 60.75 SD 13.30years) were prospectively recruited. PAI-1 (type-1 plasminogen activator inhibitor) 4G/5G and TAFI (thrombin-activatable fibrinolysis inhibitor) Ala147Thr, C+1542G, and Thr325Ile polymorphisms were determined by PCR. RESULTS 147 (59.3%) patients presented with ST-segment elevation acute coronary syndrome (all Q-wave myocardial infarction), and 101 (40.7%) with non-ST-elevation acute coronary syndrome (52 non-Q wave myocardial infarction, and 49 unstable angina). Homozygous TAFI +1542G and TAFI 325Ile genotypes were less prevalent in patients with ST elevation acute coronary syndrome (p<0.001, OR: 0.22, 95% CI 0.10-0.50 and p<0.001, OR: 0.25, 95% CI 0.11-0.55, respectively). There were no differences in TAFI Ala147Thr or PAI genotype distribution between ST elevation and non-ST elevation acute coronary syndrome. In the multivariate analysis including clinical variables, the best model for ST elevation acute coronary syndrome included TAFI +1542GG (p<0.001, OR: 0.17, 95% CI 0.07-0.30), age (in years, p<0.005, OR: 0.97, 95% CI 0.94-0.98) and dyslipidemia (p<0.005, OR: 2.33, 95% CI 1.42-3.80). CONCLUSION TAFI polymorphism C+1542G and Thr325/Ile are related to the type of acute coronary syndrome. Patients with coronary disease would benefit from individualized cardiovascular prophylaxis based on genetic risk.