Delgado Jiménez, Juan Francisco García Reyne, Ana Dios Pérez, Santiago de López Medrano, Francisco Jurado Román, Alfonso San Juan Garrido, Rafael Ruiz Cano, María José Folgueira López, María Dolores Gómez Sánchez, Miguel Ángel Aguado García, José María Lumbreras Bermejo, Carlos
Influence of cytomegalovirus infection in the development of cardiac allograft vasculopathy after heart transplantation. [artículo] - The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2015 - 34(8):1112-9.
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.
Influence of cytomegalovirus infection in the development of cardiac allograft vasculopathy after heart transplantation. [artículo] - The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2015 - 34(8):1112-9.
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.
