Impairment of fibrinolytic potential in long-term steroid treatment after heart transplantation

• Published in: Transplantation Vol. 64; no. 11; p. 1610
• Main Authors: Patrassi, G M, Sartori, M T, Livi, U, Casonato, A, Danesin, C, Vettore, S, Girolami, A
• Format: Journal Article
• Language: English
• Published: United States 15.12.1997
• Subjects: Adolescent; Adult; Aged; Azathioprine - therapeutic use; Cyclosporine - therapeutic use; Female; Fibrinolysis - drug effects; Heart Transplantation; Humans; Immunosuppressive Agents - therapeutic use; Male; Middle Aged; Plasminogen Activator Inhibitor 1 - analysis; Prednisone - therapeutic use; Tissue Plasminogen Activator - analysis
• ISSN: 0041-1337
• DOI: 10.1097/00007890-199712150-00021

Thrombotic complications constitute an important risk in transplant recipients, in whom a hypercoagulable state and hypofibrinolysis have been associated with immunosuppressive treatment, especially with cyclosporine. In no case have clotting and fibrinolytic abnormalities been correlated with steroid immunosuppression, even though steroids were always administered. Previous studies found a relationship between hypercorticism and hypofibrinolysis both in Cushing's disease and after renal transplantation. The aim of this investigation was to compare fibrinolytic potential using the venous occlusion test in two similar groups of heart transplant patients treated with or without steroids. Euglobulin lysis time, tissue-type plasminogen activator and plasminogen activator inhibitor-1 (PAI-1) activities, and antigens were determined before and after the venous occlusion test. A reduced fibrinolytic potential (significant prolongation of lysis time) due to a significant increase in PAI-1 activity and antigen levels was found in heart transplant patients treated with steroids, as compared with patients without steroid treatment and control subjects. The prevalence of reduced fibrinolytic potential was 69.2% (18 cases) in the steroid-treated group and 34.8% (8 cases) in the non-steroid-treated group. In every case, the impaired fibrinolytic potential was due to high basal PAI-1 levels. Our results are compatible with the presence of a hypofibrinolytic state secondary to long-term steroid treatment. In heart transplant recipients, steroid-induced hypofibrinolysis may constitute a further risk factor for thrombotic disease.