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

被引:20
作者
Warshofsky, MK
Wasserman, HS
Wang, WZ
Teng, P
Sciacca, R
Apfelbaum, M
Schwartz, A
Michler, RE
Mancini, DM
Cannon, PJ
Rabbani, LE
机构
[1] COLUMBIA UNIV COLL PHYS & SURG,DEPT MED,DIV CARDIOL,NEW YORK,NY 10032
[2] COLUMBIA UNIV COLL PHYS & SURG,DEPT SURG,NEW YORK,NY 10032
关键词
D O I
10.1016/S0002-9149(97)00308-1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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-I), van 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-I 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-I antigens. The interaction of the hemostatic system and serum lipids in the development of transplant coronary artery disease warrants further study. (C) 1997 by Excerpta Medica, Inc.
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页码:145 / 149
页数:5
相关论文
共 29 条
[1]   FUNCTIONAL-SIGNIFICANCE OF INTIMAL THICKENING AS DETECTED BY INTRAVASCULAR ULTRASOUND EARLY AND LATE AFTER CARDIAC TRANSPLANTATION [J].
ANDERSON, TJ ;
MEREDITH, IT ;
UEHATA, A ;
MUDGE, GH ;
SELWYN, AP ;
GANZ, P ;
YEUNG, AC .
CIRCULATION, 1993, 88 (03) :1093-1100
[2]  
BILLINGHAM ME, 1989, TRANSPLANT P, V21, P3665
[3]   ABNORMALITIES IN INTRAMYOCARDIAL ARTERIES DETECTED IN CARDIAC TRANSPLANT BIOPSY SPECIMENS AND LACK OF CORRELATION WITH ABNORMAL INTRACORONARY ULTRASOUND OR ENDOTHELIAL DYSFUNCTION IN LARGE EPICARDIAL CORONARY-ARTERIES [J].
CLAUSELL, N ;
BUTANY, J ;
MOLOSSI, S ;
LONN, E ;
GLADSTONE, P ;
RABINOVITCH, M ;
DALY, PA .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1995, 26 (01) :110-119
[4]   Early endothelial dysfunction predicts the development of transplant coronary artery disease at 1 year posttransplant [J].
Davis, SF ;
Yeung, AC ;
Meredith, IT ;
Charbonneau, F ;
Ganz, P ;
Selwyn, AP ;
Anderson, TJ .
CIRCULATION, 1996, 93 (03) :457-462
[5]  
EICH D, 1991, J HEART LUNG TRANSPL, V10, P45
[6]   CARDIAC ALLOGRAFT VASCULOPATHY ASSESSED BY INTRAVASCULAR ULTRASONOGRAPHY AND NONIMMUNOLOGICAL RISK-FACTORS [J].
ESCOBAR, A ;
VENTURA, HO ;
STAPLETON, DD ;
MEHRA, MR ;
RAMEE, SR ;
COLLINS, TJ ;
JAIN, SP ;
SMART, FW ;
WHITE, CJ .
AMERICAN JOURNAL OF CARDIOLOGY, 1994, 74 (10) :1042-1046
[7]  
EVERETT JP, 1994, J HEART LUNG TRANSPL, V13, P142
[8]  
GAO SZ, 1993, J HEART LUNG TRANSPL, V12, P1029
[9]  
GAO SZ, 1989, CIRCULATION, V80, P100
[10]   ACCELERATED CORONARY VASCULAR-DISEASE IN THE HEART-TRANSPLANT PATIENT - CORONARY ARTERIOGRAPHIC FINDINGS [J].
GAO, SZ ;
ALDERMAN, EL ;
SCHROEDER, JS ;
SILVERMAN, JF ;
HUNT, SA .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1988, 12 (02) :334-340