Abstract |
Cardiac allograft hypertrophy is associated with persistent expression of cardiac tumor necrosis factor ( TNF)-alpha. We investigated whether TNFalpha antagonism would impact allograft hypertrophy. EFECT (EFfect of Etanercept on Cardiac Transplantation) was a randomized, controlled, double-blind trial evaluating the effect of etanercept versus placebo treatment immediately posttransplant. The primary end-point was change in left ventricular (LV) mass after 6 months. Secondary endpoints included degree of collagen deposition at 6 months and incidence of adverse events. Forty-nine patients were randomized to either etanercept or placebo. LV mass increased significantly in both arms at 6 months, with a smaller increase in the etanercept group (19% vs. 33%, P=ns). Myocardial collagen content increased in the placebo, but not the etanercept, group (+39.8%, P<0.08 vs. -7.0%, P=NS). Allograft hypertrophy develops posttransplant with a corresponding increase in extracellular matrix. Etanercept appeared to decrease LV hypertrophy by decreasing extracellular matrix deposition.
|
Authors | Guillermo Torre-Amione, Cynthia K Wallace, James B Young, Michael M Koerner, Vinay Thohan, Susan McRee, Roberta C Bogaev |
Journal | Transplantation
(Transplantation)
Vol. 84
Issue 4
Pg. 480-3
(Aug 27 2007)
ISSN: 0041-1337 [Print] United States |
PMID | 17713431
(Publication Type: Journal Article, Randomized Controlled Trial)
|
Chemical References |
- Immunoglobulin G
- Immunosuppressive Agents
- Receptors, Tumor Necrosis Factor
- Tumor Necrosis Factor-alpha
- Collagen
- Etanercept
|
Topics |
- Collagen
(metabolism)
- Double-Blind Method
- Etanercept
- Extracellular Matrix
(metabolism, pathology)
- Female
- Heart Transplantation
(adverse effects, immunology, pathology)
- Heart Ventricles
(metabolism, pathology)
- Humans
- Hypertrophy, Left Ventricular
(etiology, pathology, prevention & control)
- Immunoglobulin G
(adverse effects, therapeutic use)
- Immunosuppressive Agents
(adverse effects, therapeutic use)
- Male
- Middle Aged
- Myocardium
(metabolism, pathology)
- Receptors, Tumor Necrosis Factor
(metabolism, therapeutic use)
- Transplantation, Homologous
- Tumor Necrosis Factor-alpha
(antagonists & inhibitors, metabolism)
|