| Abstract: | ![]()
Fibrinopeptide A (FPA) is a small polypeptide cleaved from fibrinogen by thrombin, has a short half-life, and is considered a sensitive biochemical marker of thrombin activity, fibrin generation, and ongoing thrombosis. Increased plasma levels of FPA have been reported in various procoagulable and thrombotic medical and cardiovascular disorders, including acute myocardial infarction, unstable angina, and sudden cardiac death. However, activation of thrombosis by the arterial injury incurred 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 obtained by venipuncture and measured by radioimmunoassay before, immediately after, 24 to 48 h later, and 1 and 3 months after uncomplicated coronary angioplasty. From December 1990 through June 1991, FPA was measured in 30 patients (28 men and 2 women, aged 54 ± 9 years) with coronary artery disease who were undergoing coronary angioplasty. The mean left ventricular ejection fraction was 55 ± 7%. The dilated vessel was the left anterior descending coronary artery in 20 patients (together 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 major complications in all patients. Before angioplasty the FPA levels averaged 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 FPA levels were significantly higher (32.33 ± 10.86 ng/ml) compared with baseline values (p = 0.025 ). At 1 month after the procedure, the FPA levels measured in 22 patients were lower but still elevated (20.25 ± 9.29 ng/ml), albeit nonsignificantly, compared with baseline values, 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 period 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 generates ongoing coronary thrombosis, which is not suppressed by heparin or aspirin and appears to extend at least through the first month after the procedure. |
