Abstract

Objectives. This study assessed the influence of donor age and preexisting donor coronary artery disease on the later development of allograft coronary artery disease, ischemic events and overall survival.Background. The increasing demand for heart donors has led to a tendency to liberalize age criteria for donor acceptability.Methods. A total of 233 consecutive heart transplant recipients who had baseline, early postoperative and follow-up coronary angiograms, as well as a subset of 47 patients with baseline intracoronary ultrasound imaging recordings, were analyzed (mean 3.8 years of follow-up). Patients were subclassified according to the presence of donor coronary artery disease on the baseline angiogram and stratified at age 40 years.Results. Patients without evidence of preexisting coronary artery disease on a baseline angiogram (n = 219) were significantly less likely to develop new disease than the 14 patients with preexisting coronary artery disease (p = 0.002). Although older donors exhibited earlier coronary artery disease than younger donors at 3 years of follow-up, there was no difference by 5 years (p = 0.25). There was no difference in survival or probability of developing ischemic events between the groups. Baseline ultrasound imaging revealed substantial disease in 7 of 9 older donated hearts, and in only 7 of 38 younger donated hearts (p = 0.002). Preexisting coronary artery disease, nonuse of calcium channel blocking agents, older donor age, posttransplantation cytomegalovirus infection, elevated very low density lipoprotein levels and previous ischemic heart disease in the recipient were significant predictors of allograft coronary artery disease.Conclusions. Heart donors with angiographic evidence of pre-existing coronary artery disease and older donors are more likely to develop new allograft coronary artery disease by 3 years. However, there is no difference in patient survival or freedom from ischemic events between younger and older donors at a mean follow-up of 3.8 years.(J Am Coll Cardiol 1997;29:623–9)

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