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Cardiogenic shock and coronary endothelial dysfunction predict cardiac allograft vasculopathy after heart transplantation
Author(s) -
LopezFernandez Silvia,
ManitoLorite Nicolas,
GómezHospital Joan Antoni,
Roca Josep,
Fontanillas Carles,
MelgaresMoreno Rafael,
AzpitarteAlmagro José,
CequierFillat Angel
Publication year - 2014
Publication title -
clinical transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 76
eISSN - 1399-0012
pISSN - 0902-0063
DOI - 10.1111/ctr.12470
Subject(s) - medicine , cardiogenic shock , cardiology , transplantation , heart transplantation , cardiac allograft vasculopathy , endothelial dysfunction , myocardial infarction
Cardiac allograft vasculopathy remains one of the major causes of death post‐heart transplantation. Its etiology is multifactorial and prevention is challenging. The aim of this study was to prospectively determine factors related to cardiac allograft vasculopathy after heart transplantation. This research was planned on 179 patients submitted to heart transplant. Performance of an early coronary angiography with endothelial function evaluation was scheduled at three‐month post‐transplant. Patients underwent a second coronary angiography after five‐yr follow‐up. At the 5‐ ± 2‐yr follow‐up, 43% of the patients had developed cardiac allograft vasculopathy (severe in 26% of them). Three independent predictors of cardiac allograft vasculopathy were identified: cardiogenic shock at the time of the transplant operation ( OR : 6.49; 95% CI : 1.86–22.7, p = 0.003); early coronary endothelial dysfunction ( OR : 3.9; 95% CI : 1.49–10.2, p = 0.006), and older donor age ( OR : 1.05; 95% CI : 1.00–1.10, p = 0.044). Besides early endothelial coronary dysfunction and older donor age, a new predictor for development of cardiac allograft vasculopathy was identified: cardiogenic shock at the time of transplantation. In these high‐risk patient subgroups, preventive measures (treatment of cardiovascular risk factors, use of novel immunosuppressive agents such as m TOR inhibitors) should be earlier and much more aggressive.

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