title: Cardiac allograft vasculopathy: a review.
abstract: Cardiac allograft vasculopathy (CAV) is a major factor limiting long-term survival after cardiac transplantation. CAV is an accelerated form of coronary artery disease (CAD) that is characterized by concentric fibrous intimal hyperplasia along the length of coronary vessels. Both immunologic and nonimmunologic risk factors contribute to the development of CAV by causing endothelial dysfunction and injury eventually leading to progressive intimal thickening. The diagnosis of CAV remains a challenge as angiography, the standard method for detecting focal plaques, lacks sensitivity in detecting CAV, and intravascular ultrasonography, a more sensitive method, lacks the ability to evaluate the entire coronary tree. The disease is difficult to treat and results in significant morbidity and mortality. Since treatment of CAV is limited and usually involves repeat transplantation, prevention or mitigation of immunologic and nonimmunologic risk factors is critically important. CAV prevention may involve therapy that provides protection against endothelial injury implemented just before transplantation, during storage and transplantation as well as after transplantation. This review addresses the frequency of occurrence, pathophysiology, diagnosis and treatment of CAV, highlighting areas of active research.
authors.affiliation: Heart Transplant Program, Toronto General Hospital, University Health Network, Division of Cardiac Surgery, University of Toronto, Toronto, ON.
authors.forename: Danny
authors.initials: D
authors.lastname: Ramzy
authors.forename: Vivek
authors.initials: V
authors.lastname: Rao
authors.forename: Julie
authors.initials: J
authors.lastname: Brahm
authors.forename: Santiago
authors.initials: S
authors.lastname: Miriuka
authors.forename: Diego
authors.initials: D
authors.lastname: Delgado
authors.forename: Heather J
authors.initials: HJ
authors.lastname: Ross
mesh_terms: D003324:Coronary Artery Disease / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*; D016027:Heart Transplantation / Q000009:adverse effects*; D006801:Humans; D014184:Transplantation, Homologous / Q000009:adverse effects*