title: Plasma levels of tissue plasminogen activator and plasminogen activator inhibitor-1 are correlated with the presence of transplant coronary artery disease in cardiac transplant recipients.
abstract: Hemostatic factors are involved in the pathogenesis of native coronary artery disease. However, their role in transplant coronary artery disease is less established. To assess the role of hemostatic factors in transplant coronary artery disease we studied 52 consecutive cardiac transplant patients. The presence of transplant coronary artery disease was determined by angiography. Plasma levels of tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), von Willebrand Factor (vWF), and fibrin D-dimer were determined by enzyme-linked immunosorbent assays. Serum lipids were measured by enzymatic methods. Patients with transplant coronary artery disease had higher circulating t-PA (8.6 +/- 0.8 vs. 5.4 +/- 0.6 ng/ml, p = 0.021) and PAI-1 antigen concentrations (38.0 +/- 3.4 vs 25.8 +/- 2.2 ng/ml, p = 0.037). t-PA and PAI-1 antigen concentrations correlated with the severity of angiographic disease (R = 0.34; p = 0.014 for t-PA, and R = 0.45; p = 0.001 for PAI-1). Serum cholesterol levels were higher in patients with transplant coronary artery disease (221 +/- 7.6 vs 191 +/- 9.2 mg/dl, p = 0.039). Serum triglycerides were also higher in patients with transplant coronary artery disease by angiography (246 +/- 38.3 vs 139 +/- 20.8 mg/dl, p = 0.050). Multivariate analysis identified t-PA antigen (p = 0.003) and triglyceride levels (p = 0.038) as independent predictors for the presence of transplant coronary artery disease. We conclude that cardiac transplant patients with evidence of transplant coronary artery disease on coronary angiography have altered hemostatic function which is reflected by elevated levels of circulating t-PA and PAI-1 antigens. The interaction of the hemostatic system and serum lipids in the development of transplant coronary artery disease warrants further study.
authors.affiliation: Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
authors.forename: M K
authors.initials: MK
authors.lastname: Warshofsky
authors.forename: H S
authors.initials: HS
authors.lastname: Wasserman
authors.forename: W
authors.initials: W
authors.lastname: Wang
authors.forename: P
authors.initials: P
authors.lastname: Teng
authors.forename: R
authors.initials: R
authors.lastname: Sciacca
authors.forename: M
authors.initials: M
authors.lastname: Apfelbaum
authors.forename: A
authors.initials: A
authors.lastname: Schwartz
authors.forename: R E
authors.initials: RE
authors.lastname: Michler
authors.forename: D M
authors.initials: DM
authors.lastname: Mancini
authors.forename: P J
authors.initials: PJ
authors.lastname: Cannon
authors.forename: L E
authors.initials: LE
authors.lastname: Rabbani
mesh_terms: D002784:Cholesterol / Q000097:blood; D003327:Coronary Disease / Q000097:blood*; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D016027:Heart Transplantation / Q000502:physiology*; D006801:Humans; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D010959:Tissue Plasminogen Activator / Q000097:blood*; D014280:Triglycerides / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D005338:Fibrin Fibrinogen Degradation Products; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides; C036309:fibrin fragment D; D014841:von Willebrand Factor; D002784:Cholesterol; D010959:Tissue Plasminogen Activator