INFREQUENCY OF CYTOMEGALOVIRUS GENOME IN CORONARY ARTERIOPATHY OF HUMAN HEART ALLOGRAFTS

In heart transplantation, long-term engraftment success is severely li mited by the rapid development of obliterative disease of the coronary arteries, Data from various groups have been suggestive of a pathogen etic role of herpesviruses, particularly human cytomegalovirus, ill ac celerated allograft coronary artery disease; however, results are not yet conclusive, This study examines the hypothesis that human cytomega lovirus infection of allograft tissues is related pathogenetically and directly to accelerated coronary artery disease Using in situ DNA hyb ridization and polymerase chain reaction, we examined particular coron ary artery segments from 41 human heart allografts (ranging from 4 day s to greater than 4 years after transplantation mean, 457 days) and 22 donor age- and gender-comparable, coronary site-matched trauma victim s for presence of human cytomegalovirus DNA, Human cytomegalovirus gen ome was detected in 8 of 41 (19.5%) allografts and ill I of 22 (4.5%) control hearts, This difference in positivity, was not statistically s ignificant (P = 0.10). In the human cytomegalovirus-positive hearts, v iral genome was localized to perivascular myocardium or corollary arte ry media or adventitia, Human cytomegalovirus genome was not detected in arterial intima of any allograft ol control heart, although human c ytomegalovirus genome was readily identified within intima of small pu lmonary arteries from lung tissue with human cytomegalovirus pneumonit is. By statistical analyses, the presence of human cytomegalovirus gen ome was not associated with the nature or digitized extent of transpla nt arteriopathy, evidence of rejection, allograft recipient or donor s erological data suggestive of human cytomegalovirus infection, duratio n of allograft implantation, or causes of death or retransplantation T hus, our data indicate a low frequency of detectable human cytomegalov irus genome in accelerated coronary artery disease and do not support a direct role for human cytomegalovirus in vascular wall infection or in the development of accelerated coronary artery disease.