Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1769-1776
Published online before print September 12, 2002, doi: 10.1161/01.ATV.0000037100.44766.5B
Published online before print September 12, 2002, doi: 10.1161/01.ATV.0000037100.44766.5B
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© 2002 American Heart Association, Inc.
Brief Reviews |
Inflammation and Restenosis in the Stent Era
From the Department of Medicine (F.G.P.W., C.R.), Cardiac Catheterization Laboratory and Coronary Care Unit, Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass; the Harvard-MIT Division of Health Sciences and Technology (F.G.P.W., C.R.), Massachusetts Institute of Technology, Cambridge, Mass; and the West Roxbury Veteran’s Affairs Medical Center (F.G.P.W.), West Roxbury, Mass.
Correspondence to Frederick G.P. Welt, MD, Harvard-MIT Division of Health Sciences and Technology, MIT, 16-343, 77 Massachusetts Ave, Cambridge, MA 02139. E-mail welt{at}mit.edu
The pathophysiology of restenosis involves early elements of direct injury to smooth muscle cells, deendothelialization, and thrombus deposition. Over time, this leads to smooth muscle cell proliferation/migration and extracellular matrix deposition. There is an increasing body of evidence to suggest that inflammation plays a pivotal role linking early vascular injury to the eventual consequence of neointimal growth and lumen compromise. The widespread use of coronary stents has fundamentally altered the vascular response to injury by causing a more intense and prolonged inflammatory state. Many of the cellular and molecular elements responsible for leukocyte recruitment have been elucidated, providing potential therapeutic targets for restenosis. This review seeks to provide an integrated view of the pathophysiology of restenosis that explains the central role of inflammation.
Key Words: stenting • balloon angioplasty • restenosis • inflammation
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