Holm A M, Haunsø S, Hansen P R
Medicinsk afdeling B, H:S Rigshospitalet, Hjertecentret.
Ugeskr Laeger. 1998 Feb 23;160(9):1302-6.
Symptomatic restenosis occurs in approximately 30-40% of patients after percutaneous transluminal coronary angioplasty (PTCA). Despite intensive research, the primary pathophysiological mediators have not been defined, and pharmacological therapy has not been effective in preventing restenosis. Restenosis is a multifactorial and sequential process, which is initiated by mechanical injury of the vessel wall, and involves neointima formation caused by the local proliferation of smooth muscle cells and production of an extracellular matrix, followed by vascular remodelling. Numerous mediators are involved in these processes, e.g., protooncogenes, growth factors, cytokines and nitric oxide. This review discusses the pathobiological mechanisms underlying coronary restenosis, and outlines the prospects for future therapy.
经皮腔内冠状动脉成形术（PTCA）后，约30%-40%的患者会出现症状性再狭窄。尽管进行了深入研究，但主要的病理生理介质尚未明确，药物治疗在预防再狭窄方面也未取得成效。再狭窄是一个多因素的连续过程，由血管壁的机械损伤引发，涉及平滑肌细胞局部增殖和细胞外基质产生导致的新生内膜形成，随后是血管重塑。许多介质参与这些过程，如原癌基因、生长因子、细胞因子和一氧化氮。本文综述了冠状动脉再狭窄的病理生物学机制，并概述了未来治疗的前景。
