Treatment and Prophylaxis of Cardiac Allograft Vasculopathy
Journal
Transplantation Proceedings
Journal Volume
40
Journal Issue
8
Pages
2609-2610
Date Issued
2008
Author(s)
Abstract
Cardiac allograft vasculopathy (CAV) remains a life-threatening complication after heart transplantation (HT). Recipients with severe intimal thickening are 10-fold more likely to suffer cardiac events than those without severe hyperplasia. From July 1987 to July 2007, we performed 323 HTs with 5-year actuarial freedom from CAV of 69%, similar to the data reported by the International Society for Heart and Lung Transplantation, namely, 68% at 5 years. Therefore, CAV is not uncommon in Asia. The pathogenesis of CAV is initial endothelial injury followed by intimal hyperplasia and proliferation of vascular smooth muscle cells. It may be caused by both immunological events (involving T or B cells in response to donor major histocompatibility antigens, or natural killer [NK] cell-triggered recruitment of T cells not responsive to donor alloantigen) and nonimmunologic factors, such as older age, ischemia-reperfusion injury, viral infection (particularly cytomegalovirus [CMV] infection), immunosuppressive drugs, and classic risk factors, such as hyperlipidemia, insulin resistance, and hypertension. The therapy for CAV has been disappointing, despite prescriptions of statin lipid-lowering agents, calcium-channel blockers, angiotensin-converting enzyme inhibitors, and antiproliferative drugs. Patients with CAV are often not amenable to successful revascularization (medical or surgical) because of the diffuse obliterative process. Prophylaxis of CAV starts with modification of risk factors: hypertension, hyperlipemia, hyperglycemia, obesity, and smoking, as well as promotion of exercise programs. The HMG-CoA reductase inhibitors and antiproliferative drugs may slow the progression of CAV by various immunologic and nonimmunologic effects. Prevention of CMV infection reduces CAV. Mycophenolate mofetil and signal transduction inhibitors, such as everolimus, reduce intimal thickening and CAV. ? 2008 Elsevier Inc. All rights reserved.
SDGs
Other Subjects
alloantigen; calcium channel blocking agent; dipeptidyl carboxypeptidase inhibitor; everolimus; hydroxymethylglutaryl coenzyme A reductase inhibitor; major histocompatibility antigen; mycophenolic acid 2 morpholinoethyl ester; artery intima proliferation; article; Asia; B lymphocyte; cardiac allograft vasculopathy; cell proliferation; Cytomegalovirus; disease course; endothelium injury; exercise; heart transplantation; human; hyperglycemia; hyperlipidemia; hypertension; immunosuppressive treatment; insulin resistance; major clinical study; natural killer cell; obesity; organ donor; pathogenesis; priority journal; reperfusion injury; revascularization; risk factor; signal transduction; smoking; smooth muscle fiber; virus infection; B-Lymphocytes; Heart Transplantation; Humans; Major Histocompatibility Complex; Postoperative Complications; T-Lymphocytes; Transplantation, Homologous; Tunica Intima; Vascular Diseases
Type
journal article