Artery wall structure, showing intimal layer Immunological (innate and adaptive) and nonimmunological factors contribute to the complex pathogenesis of<unk> . In those nontransplanted people who develop coronary artery disease due to atherosclerosis, progression of disease is slow, histological changes are confined mainly to the main coronary arteries and arterial dilatation is observed as a form of compensatory remodelling. However, in<unk> , histology specimens typically show concentric thickening of the intimal layer of the main coronary arteries on the surface of the heart and in intramyocardial arteries which can become obliterated within a few years. There is smooth muscle cell migration, foamy macrophages and lymphocytic infiltrates. This can be seen to affect the whole length of the coronary arteries and often the smaller arteries. Calcification does not always occur in<unk>  and if it does appear, it happens late. The compensatory arterial dilation does not occur in<unk> . Unlike in nontransplanted people with coronary artery disease due to atherosclerosis, in<unk>  occlusion with thrombus of the vessel lumen is rare. Inflammation and endothelial injury can be triggered by the donor arrest, organ procurement, and allograft ischaemia and reperfusion.
Cardiac allograft vasculopathy
Graft-versus-host disease
Chronic allograft nephropathy
Transplant rejection
Cardiac amyloidosis
Extrapulmonary tuberculosis
Vasculogenic mimicry
Transplant glomerulopathy