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Clin Transplant. 2020 Mar;34(3):e13794. doi: 10.1111/ctr.13794. Epub 2020 Feb 11.

Cardiac allograft vasculopathy: Insights on pathogenesis and therapy.

Clinical transplantation

Felicity Lee, Vidhya Nair, Sharon Chih

Affiliations

  1. Heart Failure and Transplantation, Division of Cardiology, Department of Medicine, University of Ottawa Heart Institute, Ottawa, ON, Canada.
  2. Department of Pathology and Laboratory Medicine, The Ottawa Hospital, Ottawa, ON, Canada.

PMID: 31991002 DOI: 10.1111/ctr.13794

Abstract

Cardiac allograft vasculopathy (CAV) is a unique accelerated form of coronary vascular disease affecting heart transplant recipients. This complication is a significant contributor to medium- to long-term post-transplant morbidity and mortality. There is a high prevalence of CAV with approximately one in three patients developing CAV by 5 years post-transplant. Morphologically, CAV is characterized by concentric coronary intimal hyperplasia in both the epicardial arteries and intramural microvasculature. Although several immune and non-immune factors have been identified, their precise pathogenic mechanisms, interactions, and relative importance in the development of CAV are not well defined. The advent of improved imaging surveillance modalities has resulted in earlier detection during the disease process. However, overall management of CAV remains challenging due to paucity of treatment. This review aims to discuss key concepts on the pathogenesis of CAV and current management strategies, focusing on the use of mammalian target of rapamycin inhibitors.

© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Keywords: cardiac allograft vasculopathy; heart transplant; mammalian target of rapamycin inhibitors

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