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Pathogenesis of and risk factors for cardiac allograft vasculopathy

Author
Howard J Eisen, MD
Section Editor
Sharon A Hunt, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC

INTRODUCTION

Cardiac transplantation is the definitive therapy for eligible patients with end-stage heart failure. The major limitations to survival in the early post-transplant period (first year) are nonspecific graft failure, multiorgan failure, acute rejection, and infection [1]. Beyond the first year, cardiac allograft vasculopathy (CAV, also called transplant coronary artery disease or cardiac transplant vasculopathy) is among the top three causes of death [1]. Approximately 30 percent of patients have angiographic coronary artery disease at five years and 50 percent at 10 years, with the incidence increasing progressively with time [1]. (See "Prognosis after cardiac transplantation", section on 'Causes of death' and "Diagnosis and prognosis of cardiac allograft vasculopathy".)

The pathogenesis of CAV will be reviewed here. The diagnosis, prevention, and treatment of this disease are discussed separately. (See "Prevention and treatment of cardiac allograft vasculopathy" and "Diagnosis and prognosis of cardiac allograft vasculopathy".)

PATHOLOGY

Cardiac allograft vasculopathy (CAV) is a panarterial disease confined to the allograft and is characterized by diffuse concentric longitudinal intimal hyperplasia in the epicardial coronary arteries (figure 1) [2-4] and concentric medial disease in the microvasculature [5-7]. In contrast, traditional atherosclerosis is focal, noncircumferential, and most often observed proximally in the epicardial vessels.

Transplant recipients also frequently develop proximal coronary artery disease. However, these lesions more closely resemble traditional atherosclerosis pathologically and probably evolve from pre-existing disease in the donor heart that is accelerated by the plethora of cardiac risk factors after transplantation [4].

Serial intravascular (intracoronary) ultrasound testing has shown that most of the intimal thickening occurs during the first year after transplantation [8]. Lumen loss is also due to arterial remodeling, with early expansion and late constriction of the external elastic membrane area. (See "Diagnosis and prognosis of cardiac allograft vasculopathy", section on 'Epidemiology'.)

                       

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Literature review current through: Nov 2016. | This topic last updated: Mon Dec 21 00:00:00 GMT 2015.
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References
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