Graft arteriosclerosis (GA) is characterized as a diffuse, usually concentr
ic, proliferative lesion of uncertain pathogenesis that occurs in the coron
ary arteries of cardiac allografts involving both the microvasculature and
epicardial vessels, and represents the major limitation to long-term recipi
ent survival. The whole length of the vessel is affected, including small d
istal intramyocardial branches, which precludes optimal treatment with rout
ine revascularization procedures. The prevalence of GA at 5 years after tra
nsplantation is high. Early diagnosis of GA is limited by the lack of clini
cal symptoms for ischemia in the denervated allogaft, by the insensitivity
of coronary angiography, which frequently underestimates the extent and sev
erity of the disease, and by the exclusive or predominant involvement of sm
all intramyocardial vessels in some cases. The introduction of intracoronar
y ultrasound imaging supports earlier pathological data indicating that cor
onary angiography underestimates the severity of the disease. The use of in
tracoronary ultrasound has improved the early diagnosis of large vessel dis
ease, but it lacks accessibility to distal lesions; thus, the extent of int
ramyocardial small artery disease remains relatively unexplored. Although i
t has been proposed that EMB could provide useful information on the diagno
sis and development of allograft vasculopathy, less attention has been focu
sed on the small intramyocardial vessels, as they appear in the endomyocard
ial biopsy (EMB), nor on the significance of the myocardial pathology resul
ting from the perfusion defects caused by GA.
The aim of this paper is to briefly review some of the pathogenic mechanism
s responsible for the development of GA, and the pathological findings obse
rved in the microvasculature of the myocardium with special attention to th
e lesions that can be noticed in EMBs.