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J Thorac Cardiovasc Surg 2006;131:1065-1072
© 2006 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Pharmacologic inhibition of vein graft neointimal hyperplasia

Thomas Schachner, MD *

Department of Cardiac Surgery, Innsbruck Medical University, Innsbruck, Austria

Received for publication September 9, 2005; accepted for publication November 16, 2005.

* Address for reprints: Thomas Schachner, MD, Anichstrasse 35, 6020 Innsbruck, Austria (Email: Thomas.Schachner{at}uibk.ac.at).

Although arterial conduits are widely used and have improved the long-term results of coronary artery bypass grafting, vein grafts remain important additional conduits in coronary surgery. Newer studies show a saphenous vein graft patency of 60% or more at 10 years postoperatively. The pathology of vein graft disease consists of thrombosis, neointimal hyperplasia, and vein graft atherosclerosis, which limit graft longevity. Therapeutic strategies to prevent vein graft disease include external stenting, pharmacotherapy, and gene therapy. The potential benefits of a pharmacologic approach are as follows: (1) Drugs with a broad clinical experience can be used; (2) side effects of systemic application can be minimized by local therapy; and (3) no vascular injury, such as pressurizing the vein for a viral transfection approach, is necessary. The different sites for pharmacotherapy in vein graft disease are reviewed in this article.

Abbreviations and Acronyms ACE = angiotensin-converting enzyme; CABG = coronary artery bypass graft; ET = endothelin; ICAM-1 = intercellular adhesion molecule-1; MMP = matrix metalloproteinase; NIH = neointimal hyperplasia; NO = nitric oxide; ODN = oligodeoxynucleotide; PDGF = platelet-derived growth factor; PGI2 = prostacyclin; SMC = smooth muscle cell; TIMP = tissue inhibitor of metalloproteinase; VSMC = vascular smooth muscle cell




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