Cardiac transplant vasculopathy

Coronary allograft vasculopathy (CAV) remains the major factor limiting long-term survival after heart transplantation. The purpose of this article is to review for the nontransplant physician the concept of CAV as a disease entity after heart transplantation.

A MEDLINE search from 1985 to 1999 was performed. Data on cardiac transplant vasculopathy were divided into pathology, pathophysiology, presentation, diagnosis, and treatment.

CAV manifests as a unique and unusually aggressive form of coronary artery disease that differs from traditional atherosclerosis. It is believed to be caused by immunologic mechanisms that combine with nonimmunologic factors to cause endothelial injury, resulting in smooth muscle proliferation and intimal thickening. This intimal hyperplasia leads to coronary obstruction, which ultimately results in allograft failure. Diagnosis of CAV can be difficult because transplant recipients have denervated hearts and rarely present with chest pain. Various noninvasive screening methods have not proved reliable. Therefore, most transplant centers perform periodic coronary angiography for routine CAV surveillance. Treatment of CAV involves modification of risk factors and the use of pharmacologic agents that alter vascular physiology. Revascularization procedures continue to play a role as palliative therapy, but are limited in their effectiveness by the diffuse nature of this disease.

Cardiac transplant vasculopathy continues to play a major dilemma regarding posttransplant care. Further research is needed to develop successful preventive and therapeutic strategies that may alter the course of this disease.