Conclusions from this review, based primarily on study of 39 cardiac allografts in place for >2 months, but also on a study of 37 grafts in place for </=2 months, might include the following: (1) allograft vascular disease affects all layers of the epicardial coronary arteries and usually the intramural coronary arteries in the outer one-half of the left ventricular wall; (2) the resulting intimal lesion is relatively uniform, consisting mainly of cellular and acellular fibrous tissue; it is diffuse, affecting all segments of the major and minor epicardial coronary arteries; (3) the degree of resulting luminal narrowing is similar in most 5-mm coronary segments, making coronary angiography hazardous in reliably predicting accurately the degree of luminal narrowing; (4) the extensive adventitial fibrosis and the extensive fibrous tissue infiltration of the subepicardial tissues probably inhibit dilation and remodeling of the epicardial coronary arteries and indeed may constrict them; (5) luminal narrowing of the epicardial coronary arteries after transplantation may be the consequence of both intraluminal lesions and exterior compression from the surrounding fibrous tissue; (6) intraluminal and intralesion thrombus is commonly observed as are multiluminal channels in coronary plaques, suggesting that organization of thrombi plays some role in the progression of post-transplant epicardial coronary disease; (7) the coronary lesions developing after cardiac transplantation are morphologically quite different in composition than those occurring in natural (nontransplantation) atherosclerosis; and (8) inflammatory cellular infiltrates are often extensive in the subepicardial tissues and the infiltrates in this area may be extensive even when interstitial myocardial inflammatory infiltrates are minimal or absent.