Usefulness of decreased levels of d-dimer in predicting progressive accelerated graft arteriosclerosis

Abstract

The classic metabolic risk factors for atherosclerosis such as hypercholesterolemia, hypertriglyceridemia, low high-density lipoprotein cholesterol, and diabetes mellitus are only weakly associated with the development of arteriosclerosis in coronary arteries of donor hearts after cardiac transplantation.1 Similarly, multiple nonimmune factors including donor age, sex, sex mismatch, pretransplant diagnosis, ischemic time, post-transplant hypertension, body mass index, and cytomegalovirus infection are not associated with the development of graft stenosis.2 A limitation of accelerated arteriosclerosis to the transplanted heart suggests that immune mechanisms may be involved because it is a form of vascular rejection. However, human leukocyte antigen class I or II mismatching does not appear to correlate with the subsequent development of graft stenosis.3 Fibrin deposition plays a role in the development and progression of atherosclerosis.4,5 Endothelial deposition of fibrin can be increased either by increased thrombotic activity or impaired fibrinolysis. Depletion of arteriolar tissue plasminogen activator measured by endomyocardial biopsy has been associated with the subsequent development of graft stenosis.6 There is also evidence from cross-sectional studies that elevation of both plasminogen activators and inhibitors is associated with accelerated graft arteriosclerosis.7,8 This study examines prospectively if plasma markers of thrombosis, fibrinolysis, or platelet activation can predict the development of accelerated graft arteriosclerosis.