[Coronary endothelial dysfunction and graft atheromatosis following heart transplantation].
Graft atheromatosis is the most important limiting factor on long-term survival after heart transplantation. Histologically it involves so-called myointimal proliferation occurring in either circumscribed or diffuse form. Endothelial dysfunction with impaired release of nitric oxide represents an early stage of graft atheromatosis. Progression of the disease typically leads to a diffuse narrowing of the coronary tree; however, focal stenoses may also occur. Endothelial dysfunction results in a decrease in physiological coronary flow reserve during exercise, whereas pharmacological flow reserve after papaverine or adenosine administration is maintained. This functional disturbance can be enhanced by transplantation-related (e.g., vascular graft rejections, cytomegalovirus infections, etc.) as well as by cardiovascular risk factors (e.g., hypercholesterolemia, hypertension). The occurrence of endothelial dysfunction and graft atheromatosis may be delayed, although probably not prevented, by elimination of risk factors and optimization of immunosuppressive treatment. Preliminary data suggest that long-term administration of the calcium-antagonist diltiazem may have a protective effect.
D003324:Coronary Artery Disease / Q000503:physiopathology* / Q000517:prevention & control; D003326:Coronary Circulation; D003586:Cytomegalovirus Infections / Q000503:physiopathology; D004110:Diltiazem / Q000627:therapeutic use; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006084:Graft Rejection / Q000503:physiopathology; D016027:Heart Transplantation; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology; D011183:Postoperative Complications / Q000209:etiology*; D012307:Risk Factors
D009569:Nitric Oxide; D004110:Diltiazem
Koronare Endotheldysfunktion und Graft-Atheromatose nach Herztransplantation.