Coronary Microvasculopathy After Heart Transplantation

Abstract

A unique form of coronary artery disease remains the major limitation to long-term survival in heart transplant recipients, playing a major role in the current half-life of the graft of ≈10 years. Our understanding of the pathogenesis of cardiac transplantation coronary artery disease (TCAD) has evolved from the initial paradigm that it was due entirely to the host immune response or an antigen-dependent process. This belief was based on observations such as circumferential involvement of the allograft vessels throughout their length, the limitation of this process to the allograft vascular bed, and its appearance in recipients of all ages, including adolescents. However, unlike with kidney transplantations, the expected correlation between the number of HLA antigens matched between donor and recipient and the number or severity of rejection episodes and the development of TCAD has not been very consistent.1 Article p 1274 This inconsistency led to examination of antigen-independent factors.2 An abundance of data now demonstrates that an equally significant number of antigen-independent factors contribute to the pathogenesis of TCAD. These include the damage to the conduit arteries (of all organs) by the large catecholamine surge that often accompanies brain death in the donor that results in not only contraction band necrosis in the myocardium but also severe injury to the intima and media of the conduit vessels.1 The importance of this catechol-mediated injury was subsequently confirmed in a large clinical series in which the presence of contraction band necrosis, the hallmark of catecholamine injury, on early routine endomyocardial biopsies was the …