RESUMEN
BACKGROUND: In acute coronary syndromes (ACS) interaction among several haemostatic (S and C protein, antitrhombin Ill, C protein resistance, plasminogen, alpha 2-antiplasmi and inflammatory factors (white cell blood count, fibrinogen, reactive C protein) could have association with recurrent thrombosis and recurrence ischemia, reinfarction, shock and cardiovascular mortality. METHODS: Prospective, controlled, with a six-year follow-up trial. END-POINT: Prove in acute phase and in a follow-up association among inflammatory, coagulation and fibrinolysis markers with cardiovascular adverse events. INCLUSION: a) ischemic chest pain at rest > 20 minutes with ST depression or elevation ACS, b) clinical stability. EXCLUSION: a) > 75 years-old, b) ACS secondary stress, hypertensive crisis, aortic stenosis, c) another acute vascular syndromes suggesting acute ischemia, d) Killip and Kimbal III o IV, e) ejection fraction < 35%, f) pre-hospital treatment with any medication that modify coagulation or fibrinolysis, c) inflammatory acute or chronic process. CONTROL GROUPS: Healthy individuals and stable chronic heart disease patients whose were matched by age and sex. In all patients with ischemic heart disease angiography, nuclear medicine or echocardiography stress tests were done. STATISTICS: Chi square, student t-test. Lineal, logistic and multivariate regression. Kaplan-Meier and Cox survival curves. Statistical significance: p < 0.05. RESULTS: 50 patients with non- or ST elevation ACS were enrolled. Regression logistic analysis indicated association among plasminogen, antithrombin III and C reactive-protein (p < 0.00001) with death. Protein C and S, protein C resistance and antithrombin III had correlation with death (p 0.0001) and recurrent ischemia (p < 0.0001). Multivariate analysis showed that antithrombin III, plasminogen, C reactive-protein and fibrinogen had significant correlation with death (p 0.001), cardiogenic shock (0.001), new ST-elevation myocardial infarction (0.001). CONCLUSION: These findings suggesting that in acute phase and in a follow-up of an ACS abnormal coagulation, inflammation and fibrinolysis markers had independent and direct relationship with cardiovascular adverse events.