Transplant Coronary Vasculopathy.

Because the transplanted heart is denervated, classic angina as a symptom of allograft coronary vasculopathy rarely is perceived. Any cardiac transplant patients who presents with decreased exercise capacity, shortness of breath, or syncope should be assessed thoroughly. Unfortunately, the initial presenting symptom of transplant vasculopathy may be acute myocardial infarction, heart failure, or even sudden death. Patients should be evaluated on an annual basis for the presence of transplant coronary vasculopathy in addition to when clinical suspicion warrants. Coronary angiography has been the main modality of invasive assessment, although it is insensitive. Recently, intracoronary ultrasound has been used in conjunction with angiography to detect the first evidence of transplant vasculopathy, manifested as thickening of the intimal layer of the vessel wall due to smooth muscle cell proliferation, which ultimately leads to luminal narrowing. Patients with evidence of vasculopathy should undergo functional evaluation with dobutamine echocardiography to document ischemic burden. Preventive measures include traditional coronary risk factor modification. Patients are started on statins early in the post-transplantation period and hypertension is treated aggressively using calcium channel blockers and angiotensin-converting enzyme (ACE) inhibitors. Because of their deleterious metabolic effects, steroids may be withdrawn under close surveillance for rejection. After transplant vasculopathy has developed, it is difficult to treat and options are limited. Patients with discrete luminal obstructions may undergo angioplasty, stenting, or coronary artery bypass. However, these procedures are palliative, and the only definitive therapy is retransplantation.