Investigation of the fibrinolytic activity in patients with atherosclerotic coronary artery disease and the effects of Fraxiparine therapy

Abstract

Hypofibrinolysis is one of the important risk factors in the progress of atherosclerosis. Blood heparin levels reportedly decrease in atherosclerosis. It has also been stated that heparin activates the fibrinolytic system. Therefore, in our study, the fibrinolytic activity in patients with atherosclerotic coronary artery disease (ACAD) and the effects of Fraxiparine, a low molecular weight heparin, on the fibrinolytic activity were investigated. The study group consisted of 12 volunteer patients, aged between 40 and 60, whose atherosclerotic coronary had been verified by coronary angiography. The control group consisted of 11 healthy volunteer men aged between 30 and 40. The fibrinolytic activity was determined by the detection of t-PA, PAI-1, ELT, the fibrin plate lysis area, fibrinogen and FDP. The patients with atherosclerosis showed significantly higher t-PA and PAI-1 levels than the control values. The disparity in PAI-1 was greater than that in t-PA. There were no significant differences in fibrinogen and FDP. These data show that fibrinolytc activity is inhibited in atherosclerosis. After administration of Fraxiparine in a single dose and in repeated doses for seven days, there was a significant increase in t-PA, a decrease in PAI-1, a shortening ELT and an extension in the fibrin plate lysis area, compared with the control values. These findings show that Fraxiparine increases the fibrinolytic activity in atherosclerosis.