Graft arteriosclerosis (GA) is characterized as a diffuse, usually concentric, proliferative lesion of uncertain pathogenesis that occurs in the coronary arteries of cardiac allografts involving both the microvasculature and epicardial vessels, and represents the major limitation to long-term recipient survival.
The whole length of the vessel is affected, including small distal intramyocardial branches, which precludes optimal treatment with routine revascularization procedures. The prevalence of GA at 5 years after transplantation is high. Early diagnosis of GA is limited by the lack of clinical symptoms for ischemia in the denervated allogaft, by the insensitivity of coronary angiography, which frequently underestimates the extent and severity of the disease, and by the exclusive or predominant involvement of small intramyocardial vessels in some cases.
The introduction of intracoronary ultrasound imaging supports earlier pathological data indicating that coronary angiography underestimates the severity of the disease. The use of intracoronary ultrasound has improved the early diagnosis of large vessel disease, but it lacks accessibility to distal lesions; thus, the extent of intramyocardial small artery disease remains relatively unexplored. Although it has been proposed that EMB could provide useful information on the diagnosis and development of allograft vasculopathy, less attention has been focused on the small intramyocardial vessels, as they appear in the endomyocardial biopsy (EMB), nor on the significance of the myocardial pathology resulting from the perfusion defects caused by GA.
The aim of this paper is to briefly review some of the pathogenic mechanisms responsible for the development of GA, and the pathological findings observed in the microvasculature of the myocardium with special attention to the lesions that can be noticed in EMBs.
CITATION Z Kardiol. 2000;89 Suppl 9:IX/54-7
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