Role of the Renin-Angiotensin System in the Pathogenesis of Intimal Hyperplasia: Therapeutic Potential for Prevention of Vein Graft Failure?

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• 作者：Michael J. Osgood¹ ; ^{michael.j.osgood@vanderbilt.edu} ; David G. Harrison² ; Kevin W. Sexton¹ ; Kyle M. Hocking¹ ; Igor V. Voskresensky¹ ; Padmini Komalavilas¹ ; ³ ; Joyce Cheung-Flynn¹ ; Raul J. Guzman¹ ; Colleen M. Brophy¹ ; ³
• 刊名：Annals of Vascular Surgery
• 出版年：2012
• 出版时间：November, 2012
• 年：2012
• 卷：26
• 期：8
• 页码：1130-1144
• 全文大小：495 K

文摘

The saphenous vein remains the most widely used conduit for peripheral and coronary revascularization despite a high rate of vein graft failure. The most common cause of vein graft failure is intimal hyperplasia. No agents have been proven to be successful for the prevention of intimal hyperplasia in human subjects. The renin-angiotensin system is essential in the regulation of vascular tone and blood pressure in physiologic conditions. However, this system mediates cardiovascular remodeling in pathophysiologic states. Angiotensin II is becoming increasingly recognized as a potential mediator of intimal hyperplasia. Drugs modulating the renin-angiotensin system include angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. These drugs are powerful inhibitors of atherosclerosis and cardiovascular remodeling, and they are first-line agents for management of several medical conditions based on class I evidence that they delay progression of cardiovascular disease and improve survival. Several experimental models have demonstrated that these agents are capable of inhibiting intimal hyperplasia. However, there are no data supporting their role in prevention of intimal hyperplasia in patients with vein grafts. This review summarizes the physiology of the renin-angiotensin system, the role of angiotensin II in the pathogenesis of cardiovascular remodeling, the medical indications for these agents, and the experimental data supporting an important role of the renin-angiotensin system in the pathogenesis of intimal hyperplasia.