PLASMA-LEVEL CHANGES OF FIBRINOPEPTIDE A AFTER UNCOMPLICATED CORONARYANGIOPLASTY

Fibrinopeptide A (FPA) is a small polypeptide cleaved from fibrinogen by thrombin, has a short half-life, and is considered a sensitive bioc hemical marker of thrombin activity, fibrin generation, and ongoing th rombosis. Increased plasma levels of FPA have been reported in various procoagulable and thrombotic medical and cardiovascular disorders, in cluding acute myocardial infarction, unstable angina, and sudden cardi ac death. However, activation of thrombosis by the arterial injury inc urred during coronary angioplasty has not been systematically examined with use of plasma FPA measurements. To detect and monitor activation of thrombosis by coronary angioplasty, plasma levels of FPA were obta ined by venipuncture and measured by radioimmunoassay before, immediat ely after, 24 to 48 h later, and 1 and 3 months after uncomplicated co ronary angioplasty. From December 1990 through June 199 1, FPA was mea sured in 30 patients (28 men and 2 women, aged 54 +/- 9 years) with co ronary artery disease who were undergoing coronary angioplasty. The me an left ventricular ejection fraction was 55 +/- 7%. The dilated vesse l was the left anterior descending coronary artery in 20 patients (tog ether with a second vessel in 2), the right coronary artery in 9, and the left circumflex in 1. The procedure was successful and free of maj or complications in all patients. Before angioplasty the FPA levels av eraged 6.50 +/- 1.18 ng/ml. Shortly after angioplasty they rose to 20. 20 +/- 7.91 ng/ml (p = 0.08) despite intravenous heparin. At 24 to 48 h and after heparin had been discontinued for at least 4 h, the mean F PA levels were significantly higher (32.33 +/- 10.86 ng/ml) compared w ith baseline values (p = 0.025 ). At 1 month after the procedure, the FPA levels measured in 22 patients were lower but still elevated (20.2 5 +/- 9.29 ng/ml), albeit nonsignificantly, compared with baseline val ues, and at 3 months they had fallen to baseline values (4.84 +/- 2.20 ng/ml, n = 11). No patient developed restenosis during the study peri od of 1 to 3 months, during which all patients were receiving aspirin. We conclude that, as reflected by increased FPA levels, angioplasty, most likely due to arterial injury incurred, activates thrombin and ge nerates ongoing coronary thrombosis, which is not suppressed by hepari n or aspirin and appears to extend at least through the first month af ter the procedure.