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concentric coronary artery disease that diffusely affects the larger epicardial and smaller intramyocardial coronaries. Cardiac veins are affected as well. Histologically CAV seems to begin as concentric intimal thickening and progresses with time to complex atherosclerotic plaque.

The incidence of CAV is very high. By one year posttransplant, 11% of patients are diagnosed with CAV by coronary angiography; it is found in 50% by five years. Most cardiac transplant recipients cannot experience angina because allograft reinnervation is incomplete. Thus, the clinical presentation of CAV is not angina, but is instead usually heart failure or sudden death. Occasionally CAV will present as ventricular dysrhythmias.

Cav Heart Transplant

Fig. 11.6. Coronary allograft vasculopathy. Histological section (A) and angiogram (B). Despite being the best diagnostic imagining modality, angiography is relative insensitive. From: Johnson DE. Transplant coronary artery disease: histopathologic correlations with angiographic morphology. J Am Coll Cardio. 1991; 17:449. Reprinted with permission from the American College of Cardiology.

Fig. 11.6. Coronary allograft vasculopathy. Histological section (A) and angiogram (B). Despite being the best diagnostic imagining modality, angiography is relative insensitive. From: Johnson DE. Transplant coronary artery disease: histopathologic correlations with angiographic morphology. J Am Coll Cardio. 1991; 17:449. Reprinted with permission from the American College of Cardiology.

The pathogenesis of CAV remains unclear. Following coronary vascular injury associated with ischemia/reperfusion at the time of transplantation, further coronary vascular endothelial and smooth muscle cell injuries are promoted by the local inflammatory response to rejection. Even subclinical allograft rejection may contribute to the development of CAV. Common risk factors for the development of atherosclerosis such as hyperglycemia, hypertension and hyperlipidemia are commonly noted following heart transplantation and may contribute to CAV. Furthermore, some investigators suggest an infectious etiology since human CMV infection has been associated with CAV.

All heart transplant recipients must be followed indefinitely for evidence of CAV. Unfortunately, noninvasive tests for myocardial ischemia such as radionuclide scintigraphy and exercise electrocardiography are neither sensitive nor specific for detection of CAV. Therefore most programs rely upon annual coronary angiography for follow-up. Because CAV is a diffuse rather than a localized process, it may be difficult to detect with certainty using angiography. Unfortunately, coronary angiography is quite specific but a relatively insensitive test (Fig. 11.6). Intravascular coronary ultrasound (IVUS) is becoming more widespread as a screening modality for the detection of CAV. Whether it will supplant coronary angiography as the study of choice is unknown.

Because of the diffuse nature of the disease, coronary artery bypass grafting and catheter-based revascularization procedures have limited effectiveness in the treatment of CAV. Following coronary balloon angioplasty, the restenosis rate is

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