CYTOMEGALOVIRUS-INFECTION AND ACCELERATED CARDIAC ALLOGRAFT VASCULOPATHY IN HUMAN CARDIAC ALLOGRAFTS

Cardiac allograft vasculopathy is a major limiting factor of the long- term survival of heart transplant patients. An association of cytomega lovirus infection and cardiac allograft vasculopathy has been describe d. We analyzed 104 endomyocardial biopsy specimens obtained from 53 he art transplant recipients and correlated the histologic findings with 115 angiograms obtained from the same patients during 4 postoperative years. The frequency of vascular changes in endomyocardial biopsy spec imens was significantly higher than in angiograms during the first 3 p osttransplantation years (P < 0.001, P < 0.005, P < 0.03, respectively ). Also, in patients with angiographically documented cardiac allograf t vasculopathy, significantly higher scores of capillary and arteriola r endothelial cell accumulation and arteriolar intimal thickness were recorded when compared with the recipients with normal angiograms (P < 0.02, P < 0.05, P < 0.005, respectively). Altogether, 29 of 53 recipi ents underwent cytomegalovirus infection during the first posttranspla nt year. Cytomegalovirus infection was associated with arteriolar endo thelial cell accumulation and with increased intimal thickness of intr amyocardial vessels of 1-year endomyocardial biopsy specimens when com pared with cytomegalovirus-free recipients (P < 0.02 and P < 0.005, re spectively). After the second year, the cytomegalovirus-associated end othelial cell response subsided, but the thickness of intima had incre ased when compared with cytomegalovirus-free patients (P < 0.05). Ther eafter, the cytomegalovirus-associated histologic changes reached a pl ateau. In coronary angiography, the cardiac allograft vasculopathy cha nges were detected in a slower pace. Thus only after 2 posttransplanta tion years, cytomegalovirus-associated acceleration of cardiac allogra ft vasculopathy was observed, compared with cytomegalovirus-free patie nts (P < 0.05). Early diagnosis and active treatment of cytomegaloviru s infection may be important steps in avoiding cardiac allograft vascu lopathy.