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Transplant atherosclerosis: the clinical syndrome, pathogenesis and possible model of spontaneous atherosclerosis.

OBJECTIVE
To summarize the clinical syndrome of transplant atherosclerosis, including the clinical risk factors, pathological features and known pathophysiological mechanisms. The review also examines transplant atherosclerosis and naturally occurring atherosclerosis to delineate common pathophysiological mechanisms and to promote transplant atherosclerosis as a model for the more commonly occurring spontaneous process.


STUDY SELECTION
Information gathered includes studies related to transplantation, endothelium, atherosclerosis, macrophages, lipoproteins and vascular smooth muscle. All studies cited were published prior to 1992.


CONCLUSIONS
Transplant atherosclerosis appears to result from a 'response to injury' of the endothelium, similar to naturally occurring atherosclerosis. The injury is diffuse, chronic and related to immune and nonimmune factors. Cellular and antibody-mediated rejection, cytomegalovirus infection and cytokine-induced vessel wall cell proliferation provide potential targets for future pharmacological and biological therapy.