Ischemic cardiomyopathy (ICM) is the clinical endpoint of coronary heart disease and a leading cause of heart failure. Despite growing demands to develop personalized approaches to treat ICM, progress is limited by inadequate knowledge of its pathogenesis. Since epigenetics has been implicated in the development of other chronic diseases, the current study was designed to determine whether transcriptional and/or epigenetic changes are sufficient to distinguish ICM from other etiologies of heart failure.
View Article and Find Full Text PDFBackground: We have previously shown that lack of plasminogen activator inhibitor-1 (PAI-1) expression in donor tissue greatly increases intimal proliferation (IP) after allogeneic transplantation. We sought to determine the relative role of PAI-1 and other fibrinolytic proteins in the development of IP.
Methods: We used an abdominal aortic transplant model in mice to investigate IP in 3 groups of 6 recipients.
J Heart Lung Transplant
October 2009
Background: Cytokine gene polymorphisms regulate cytokine expression. We analyzed transforming growth factor-beta (TGF-beta) allelic variation in codon 25 in susceptibility to acute rejection episodes in cardiac transplant recipients.
Methods: Between June 1997 and December 2001, 123 de novo heart transplants were performed at UAB with analysis based on 109 patients.
Background: Changes in the fibrinolytic system that occur after cardiac transplantation (CTx) and the factors that influence such changes have been poorly described, yet may be important in determining the varying morphologic features of transplant-related coronary artery disease (TxCAD).
Methods: Baseline demographic as well as serial clinical information and plasma fibrinolytic levels were prospectively recorded pre-CTx and at multiple time-points post-CTx in 110 de novo cardiac transplant recipients.
Results: We noted a biphasic change in fibrinolytic activity over the first year of CTx with an early immediate decline in plasminogen activator inhibitor-1 (PAI-1) activity (p > 0.