Prognostic significance of elevated hemostatic markers in patients with acute myocardial infarction

OBJECTIVES The purpose of this study was to determine whether the elevated levels of hemostatic markers in the early phase of myocardial infarction may serve as risk factors for subsequent cardiac mortality. BACKGROUND Increased plasm hemostatic markers were noted in acute myocardial infarction, indicating that the blood coagulation system is highly activated in those patients. However, there are few clinical dat concerning the association between the elevated hemostatic markers and survival in patients with myocardial infarction. METHODS Blood samples were obtained from 64 patients (mean age 67 ± 11 years; 49 male) with acute myocardial infarction within 12 h after the onset of symptoms and before the initiation of any antithrombotic treatment. We measured plasm concentrations of fibrinopeptide (FPA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) using the enzyme-linked immunosorbent assay method, and examined the associations between the level of these markers and survival with Cox proportional hazards models. RESULTS The follow-up time was 27 ± 17 months, and 19 patients died of cardiac causes during the follow-up. Univariate survival analysis identified Killip class IV (hazard ratio 4.86; 95% confidence interval [CI] 1.55–15.19), left ventricular ejection fraction (hazard ratio 0.94; 95% CI 0.90–0.99), FP (hazard ratio 1.54; 95% CI 1.13–2.10), F1+2 (hazard ratio 2.03; 95% CI 1.17–3.53) and TAT (hazard ratio 1.88; 95% CI 1.27–2.79) as significant factors associated with cardiac mortality. In multivariate analyses, only FP level (hazard ratio 1.84; 95% CI 1.03–3.30) and left ventricular ejection fraction (hazard ratio 0.93; 95% CI 0.88–0.98) were independent predictors of cardiac mortality. CONCLUSIONS Elevated FP in the early phase of myocardial infarction identifies patients with increased risk for subsequent cardiac death. This association appears to be independent of residual left ventricular function after infarction.