Enhanced coagulation activation in troponin T-positive unstable angina pectoris.

Intracoronary thrombus formation and systemic activation of coagulation have been demonstrated in unstable angina pectoris. Circulating troponin T as a marker of minor myocardial cell injury is associated with adverse outcome in this condition. Little information exists about the interrelation of coagulation activation and myocardial cell injury in unstable angina. We quantitatively assessed systemic activation of coagulation and myocardial cell injury in serial blood samples obtained up to 10 days from 22 patients with angiographically documented coronary heart disease and unstable angina pectoris at rest. In the nine patients with increased maximal levels of serum troponin T, maximal concentrations of fibrin monomers during the first 48 hours were higher than those in patients with persistently normal troponin T concentrations (6.3+/-4.8 vs. 2.9+/-2.3 mg/L; p = 0.04). The proportion of patients with at least one blood sample showing an increased concentration of plasma fibrin monomer was also higher in the group with increased troponin T (67% vs. 15%; p = 0.04). Plasma prothrombin fragment F1+2 levels showed a nonsignificant trend toward higher values in troponin T-positive patients. Enhanced activation of coagulation in patients with troponin T-positive unstable angina may contribute to the adverse outcome associated with this condition.