Welt Frederick G P, Rogers Campbell
Department of Medicine, Cardiac Catheterization Laboratory and Coronary Care Unit, Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass, USA.
Arterioscler Thromb Vasc Biol. 2002 Nov 1;22(11):1769-76. doi: 10.1161/01.atv.0000037100.44766.5b.
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.
再狭窄的病理生理学涉及平滑肌细胞直接损伤、内皮剥脱和血栓沉积等早期因素。随着时间的推移，这会导致平滑肌细胞增殖/迁移以及细胞外基质沉积。越来越多的证据表明，炎症在将早期血管损伤与内膜增生和管腔狭窄的最终后果联系起来方面起着关键作用。冠状动脉支架的广泛应用通过引发更强烈和持久的炎症状态，从根本上改变了血管对损伤的反应。许多负责白细胞募集的细胞和分子因素已被阐明，为再狭窄提供了潜在的治疗靶点。本综述旨在提供一个再狭窄病理生理学的综合观点，以解释炎症的核心作用。
