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.

Effects of Helicobacter pylori eradication on platelet activation and disease recurrence in patients with acute coronary syndromes.

BACKGROUND: Platelet activation is consistently observed in animal models of Helicobacter pylori infection and could help to explain the alleged epidemiological association between H. pylori and coronary heart disease. MATERIALS AND METHODS: Ninety-two patients with recent acute coronary syndromes were enrolled. Helicobacter pylori-positive patients were randomized to receive a 7-day course of omeprazole, amoxycillin and metronidazole or placebos. Two months later, H. pylori status was reassessed and baseline parameters, including soluble P-selectin and platelet surface expression of CD62P, CD63 and CD41, were measured again. Patients were followed-up for 1 year or until death or readmission. RESULTS: No baseline differences were observed between H. pylori-positive and -negative cases. Among H. pylori-positive patients, 18 received placebo and 31 received active medication resulting in eradication in 21 cases. No differences were observed in inflammatory parameters or platelet activation markers between patients with persistent or resolved H. pylori infection. However, coronary events recurred at 6 and 12 months, respectively, in 35% and 55% of patients with persisting H. pylori infection compared with 10% and 25% of patients in whom H. pylori was either absent or eradicated (p = .01). Only final H. pylori status [RR 3.07 (95% CI 1.35-98)] and number of coronary risk factors [RR 2.58 (95% CI 1.51-4.41)] were independent predictors of recurrence. CONCLUSIONS: Infection with H. pylori does not induce significant platelet activation in patients treated for coronary disease. Helicobacter pylori-infected patients, however, may have an increased risk of recurrence of coronary events.