Association of increased fibrin turnover and defective fibrinolytic capacity with leg atherosclerosis

M. Cortellaro, E. Cofrancesco, C. Boschetti, L. Mussoni, M. B. Donati, M. Catalano, L. Gabrielli, B. Lombardi, G. Specchia, L. Tavazzi, E. Tremoli, M. Turri, M. Rainisio, G. Gentile, G. Moreo, M. Cardillo, O. Bianchi, P. Leonardi, M. Columbi

Research output: Contribution to journalArticlepeer-review


Patients with peripheral arterial disease have a high risk of death from cardiovascular events. As defective fibrinolysis associated with leg atherosclerosis has been suggested as a predisposing factor, we sought a relation among decreased fibrinolysis, the presence of leg atherosclerosis and the incidence of thrombotic events in a case-control study nested in the PLAT. Fifty-eight patients with coronary and/or cerebral atherothrombotic disease, free of leg atherosclerosis at Doppler examination, were compared with 50 atherosclerotic patients with leg involvement. High D-dimer (153.0 vs 81.3 ng/ml, p <0.001) and tPA antigen before venous stasis (14.4 vs 11.8 ng/ml, p <0.03), and low tPA antigen (6.7 vs 15.6 ng/ml, p <0.01) and fibrinolytic activity released after venous stasis (fibrinolytic capacity: 113.2 vs 281.4 mm2, p <0.001) were found in patients with leg atherosclerosis. D-dimer and fibrinolytic capacity, in addition to age, were selected by stepwise discriminant analysis as characterizing patients with leg atherosclerosis. Moreover, higher D-dimer and tPA inhibitor characterized patients with leg atherosclerosis who subsequently experienced thrombotic events. These findings constitute evidence of high fibrin turnover and impaired fibrinolytic potential in patients with leg atherosclerosis. Thus impaired fibrinolysis may contribute to the prothrombotic state in these patients.

Original languageEnglish
Pages (from-to)292-296
Number of pages5
JournalThrombosis and Haemostasis
Issue number2
Publication statusPublished - 1994

ASJC Scopus subject areas

  • Hematology


Dive into the research topics of 'Association of increased fibrin turnover and defective fibrinolytic capacity with leg atherosclerosis'. Together they form a unique fingerprint.

Cite this