(Circulation. 2000;102:2100.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY.
Correspondence to LeRoy E. Rabbani, MD, Division of Cardiology, Department of Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th St, New York, NY 10032. E-mail ler8{at}columbia.edu
BackgroundInflammation may be involved in the origin of transplant coronary artery disease. We hypothesized that plasma levels of C-reactive protein (CRP) and interleukin-6 (IL-6), markers for systemic inflammation, would correlate with cardiac transplant graft survival.
Methods and ResultsWe studied 99 consecutive cardiac transplant recipients who were referred for routine endomyocardial biopsy and/or surveillance coronary angiography. Plasma levels of CRP and IL-6 were measured by their respective ELISAs. Patients were divided into 2 groups: those who died or required retransplantation and those who survived without the need for retransplantation. During the follow-up period of 5.0±2.7 years (range, 0.2 to 15.1 years) after transplant, 20 patients died and 9 required retransplantation. There was no significant difference in age, race, sex, cause of native myopathy, presence of diabetes, or use of aspirin, statins, or calcium channel blockers between the 2 groups. Although IL-6 did not relate to graft failure, CRP level was predictive of allograft failure (P=0.003). The risk of allograft failure increased 36% for every 2-fold increase in CRP level. Moreover, CRP levels also correlated significantly with the frequency of grade 3 rejection (P=0.02). In multivariate analysis, when combined with other significant predictors such as donor age and sex mismatching of the graft, CRP still significantly predicted graft failure (P=0.025) with a 32% increase in the risk of graft failure for every 2-fold increase in CRP level.
ConclusionsThese findings suggest that elevated plasma levels of CRP are associated with subsequent allograft failure in cardiac transplant recipients.
Key Words: transplantation inflammation proteins survival
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