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Ann Thorac Surg 1997;64:1330
© 1997 The Society of Thoracic Surgeons
Section of Cardiology, Rush-Presbyterian-St. Luke's Medical Center, 1653 W Congress Parkway, Chicago, IL 60612
Cardiac allograft vasculopathy (CAV) is the leading cause of death in transplant recipients who survive more than 1 year, and is also a major cause of long-term morbidity. Cardiac allograft vasculopathy is typically concentric and diffuse, and thus continues to present a substantial diagnostic and therapeutic challenge. Concentric CAV can be inapparent by angiography even in the presence of substantial disease; intravascular ultrasound is much more sensitive. The diffuse coronary involvement limits the utility of revascularization, and medical therapies have been only minimally effective at best. Because of this, the importance of efforts to identify CAV early and characterize its pathogenesis is clear.
Vascular endothelial function is a promising area for research in CAV, for a number of reasons. Cardiac allograft vasculopathy is most likely immunologically mediated, and vascular endothelial cells, situated at the interface between the circulating immune cells and the vessel wall, are an early target of the immune system. Endothelial dysfunction is not only likely to be an early marker for the development of CAV, but may play a role in its pathogenesis. The endothelium is an important regulator of vasomotor tone and vascular smooth muscle cell proliferation, and thus abnormalities of the endothelium could potentiate vascular injury caused by circulating immune cells. Accurate characterization of endothelial dysfunction after transplantation could also permit diagnosis of CAV earlier, when therapeutic interventions might be more efficacious. Another important issue in the pathogenesis of allograft vasculopathy is the relative role of acute and chronic rejection. Although CAV is considered a form of chronic rejection, the degree to which bouts of acute rejection potentiate vascular damage is uncertain.
In this context, the study by Bouchard and associates is interesting because it elucidates the mechanisms of endothelial dysfunction in acute allograft rejection. Heterotopic heart transplantation was performed in a canine model; histologic evidence of acute rejection was found despite treatment with cyclosporine. Acute rejection decreased vasodilation in response to thrombin, but vasomotor responses to acetylcholine and adenosine diphosphate were preserved, and responses to serotonin were actually potentiated. That acute rejection affects only some specific endothelial responses strengthens the case that endothelial dysfunction is not merely a marker for CAV, but precedes it and plays a causal role. More precise characterization of the mechanisms of endothelial dysfunction in allograft rejection could point the way toward innovative preventive and therapeutic approaches.
Related Article
Ann. Thorac. Surg. 1997 64: 1325-1330.
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