Influence of cytomegalovirus infection in the development of cardiac allograft vasculopathy after heart transplantation. [artículo]
Por: Delgado Jiménez, Juan Francisco [Cardiología]
| García Reyne, Ana [Medicina Interna] | Dios Pérez, Santiago de [Cardiología] | López Medrano, Francisco [Enfermedades Infecciosas] | Jurado Román, Alfonso [Cardiología] | San Juan Garrido, Rafael [Medicina Interna] | Ruiz Cano, María José [Cardiología] | Folgueira López, María Dolores [Microbiología y Parasitología] | Gómez Sánchez, Miguel Ángel [Cardiología] | Aguado García, José María [Enfermedades Infecciosas] | Lumbreras Bermejo, Carlos [Medicina Interna].
Colaborador(es): Servicio de Cardiología | Servicio de Medicina Interna | Servicio de Microbiología y Parasitología | Instituto de Investigación imas12.
Tipo de material: 
ArtículoEditor: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2015Descripción: 34(8):1112-9.Recursos en línea: Solicitar documento Resumen: Background: Cardiac allograft vasculopathy (CAV) is a major cause of long-term morbidity and mortality after heart transplantation (HTx), whose relationship with CMV infection is uncertain. This study evaluated the influence of CMV infection in the development of CAV.
Methods: We enrolled 166 consecutive HTx recipients who underwent their first transplant from January 1995 to July 2002. All patients received 14 days of intravenous ganciclovir and were prospectively monitored for CMV infection during the first year after HTx. CAV was diagnosed by coronary angiography performed at 1, 5, and 10 years after HTx, following the new criteria of the International Society for Heart and Lung Transplantation. We collected all variables potentially related with the development of CAV. Risk factors were studied using a complementary log-log model.
Results: After a median follow-up of 11 years (range, 1-17 years), 72 patients (43%) developed CAV (63.8% CAV(1), 15.2% CAV(2), 20.8% CAV(3)). Symptoms secondary to CAV were present in 32% of these patients, and 8% died because of it. In the regression multivariate analysis, independent variables associated with the development of CAV were donor age (hazard ratio [HR], 1.028; 95% confidence interval [CI], 1.002-1.053; p < 0.028), presence of cellular acute rejection ≥ 2R (HR, 1.764; 95% CI, 1.011-3.078; p < 0.0414), CMV infection (HR, 2.334; 95% CI, 1.043-5.225; p < 0.0354), and not having been treated with a calcium channel blocker (HR, 0.472; 95% CI, 0.275-0.811; p < 0.0055).
Conclusions: Standardized angiographic criteria show CMV infection is associated with the development of CAV.
| Tipo de ítem | Ubicación actual | Signatura | Estado | Fecha de vencimiento |
|---|---|---|---|---|
Artículo
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PC17100 (Navegar estantería) | Disponible |
Navegando Hospital Universitario 12 de Octubre Estantes Cerrar el navegador de estanterías
Formato Vancouver:
Delgado JF, Reyne AG, de Dios S, López Medrano F, Jurado A, Juan RS et al. Influence of cytomegalovirus infection in the development of cardiac allograft vasculopathy after heart transplantation. J Heart Lung Transplant. 2015 Aug;34(8):1112-9.
PMID: 25940077
Contiene 40 referencias
Background: Cardiac allograft vasculopathy (CAV) is a major cause of long-term morbidity and mortality after heart transplantation (HTx), whose relationship with CMV infection is uncertain. This study evaluated the influence of CMV infection in the development of CAV.
Methods: We enrolled 166 consecutive HTx recipients who underwent their first transplant from January 1995 to July 2002. All patients received 14 days of intravenous ganciclovir and were prospectively monitored for CMV infection during the first year after HTx. CAV was diagnosed by coronary angiography performed at 1, 5, and 10 years after HTx, following the new criteria of the International Society for Heart and Lung Transplantation. We collected all variables potentially related with the development of CAV. Risk factors were studied using a complementary log-log model.
Results: After a median follow-up of 11 years (range, 1-17 years), 72 patients (43%) developed CAV (63.8% CAV(1), 15.2% CAV(2), 20.8% CAV(3)). Symptoms secondary to CAV were present in 32% of these patients, and 8% died because of it. In the regression multivariate analysis, independent variables associated with the development of CAV were donor age (hazard ratio [HR], 1.028; 95% confidence interval [CI], 1.002-1.053; p < 0.028), presence of cellular acute rejection ≥ 2R (HR, 1.764; 95% CI, 1.011-3.078; p < 0.0414), CMV infection (HR, 2.334; 95% CI, 1.043-5.225; p < 0.0354), and not having been treated with a calcium channel blocker (HR, 0.472; 95% CI, 0.275-0.811; p < 0.0055).
Conclusions: Standardized angiographic criteria show CMV infection is associated with the development of CAV.
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