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(Circulation. 2000;101:221.)
© 2000 American Heart Association, Inc.

Editorials

Vascular Matrix and Vein Graft Failure

Is the Message in the Medium?

Joseph Loscalzo, MD, PhD

From the Whitaker Cardiovascular Institute and Evans Department of Medicine, Boston University School of Medicine, Boston, Mass.

Correspondence to Joseph Loscalzo, MD, PhD, Boston University School of Medicine, Whitaker Cardiovascular Institute, 715 Albany St, W507, Boston, MA 02118. E-mail jloscalz@bu.edu

Key Words: Editorials • veins • revascularization • atherosclerosis • grafting

The pioneering work of Favaloro¹ established the era of surgical revascularization for the treatment of ischemic heart disease. The benefits of this procedure were recognized early, and the use of the saphenous vein as a bypass conduit rapidly gained widespread acceptance as an effective treatment for angina. However, surgical revascularization has significant shortcomings, principal among which is the high rate of accelerated atherosclerosis that develops in vein grafts: at 10 years after surgery, 40% of grafts are occluded and only 50% are free of significant disease.²

Vein graft failure is a consequence of three related processes. Early after implantation, thrombosis plays a critical role, both by predisposing to acute occlusion and by serving as a stimulus for neointima formation and, ultimately, graft atherosclerosis. Within 6 weeks after implantation, virtually all arterialized vein grafts develop intimal hyperplasia, which, although it only modestly compromises the lumen of the graft, renders the graft susceptible to atherosclerosis.³ The cellular events that account for this intimal response include migration and proliferation of vascular smooth muscle cells, perhaps derived from adventitial fibroblasts (myofibroblasts),⁴ followed by extracellular matrix synthesis and deposition. This latter process ultimately leads to progressive intimal fibrosis with relatively reduced intimal cellularity.⁵

Vein grafts are susceptible to intimal hyperplasia and atherosclerosis for two main reasons. First, explanted vein grafts are prone to vessel wall ischemia owing to a loss of functional vasa vasorum; regrowth of these nutrient vessels appears as early as 5 days after graft placement, but a rich network sufficient to provide . . . [Full Text of this Article]

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