Coronary artery disease in the transplanted heart

Coronary artery disease in the transplanted heart limits the long-term succ ess of cardiac transplantation. Intravascular ultrasound studies reveal a d ual morphology with donor-transmitted and de novo plaques. Coronary vasomot or dysfunction may occur independently of morphological alterations. The di sease is characterized by the interaction of activated T lymphocytes with c ytokines and donor epicardial and microvascular endothelium. Various noxiou s stimuli contribute to the continuing inflammatory response. Consequently, adhesion molecule expression is upregulated, leukocytes migrate into the a llograft, thrombocytes accumulate, and growth factors are expressed, finall y resulting in functional and morphological chronic allograft lesions. Bloc king the activation of T cells, CD4+ cytokines, and adhesion molecules may prevent endothelial injury and subsequent intimal thickening. Strategies to decrease the formation of antiendothelial and anti-HLA-DR antibodies may a lso be protective, as may antiproliferative drugs, augmentation of endogeno us nitric oxide bioactivity, and new immunosuppressive regimens. Revascular ization procedures have a limited role in treating significant focal lesion s. Retransplantation, the only definitive treatment, remains ethically cont roversial.