Coagulation activity and clinical outcome in unstable coronary artery disease

In the current study, we investigated molecular markers of coagulation acti vity, ie, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin (TAT) comp lex, soluble fibrin (SF), and D-dimer, and their relation to death, myocard ial infarction, and refractory angina during and after anticoagulant treatm ent in unstable coronary artery disease, Patients with unstable coronary ar tery disease (N=320) were randomized to a 72-hour infusion with either inog atran, a low-molecular-mass direct thrombin inhibitor, or unfractionated he parin. During the 30-day follow-up, a 40% lower event rate was seen in pati ents with high compared with low baseline levels of TAT or SF. High baselin e levels of coagulation activity were correlated with a larger decrease dur ing treatment. Patients with decreased compared with raised F1+2 or TAT lev els after 6 hours of treatment had a 50% lower event rate at 30 days (F1+2, P=0.04; TAT, P=0.02). At the cessation of antithrombin treatment, there wa s a clustering of cardiac events that tended to be related to a rise in the levels of TAT and the other markers. During long-term follow-up (median, 2 9 months), there was a relation between higher baseline levels of D-dimer ( P=0.003) and increased mortality. High baseline levels of molecular markers of coagulation activity might identify patients with a thrombotic conditio n las the major cause of instability) who are good responders to anticoagul ant therapy, with a larger decrease in coagulation activity during treatmen t and a decreased risk of ischemic events. However, this early benefit is l ost during long-term follow-up when high baseline levels of coagulation act ivity are associated with a raised risk of early reactivation and increased mortality.