Langeveld Bas, Roks Anton J M, Tio Rene A, Voors Adriaan A, Zijlstra Felix, van Gilst Wiek H
Department of Clinical Pharmacology, University Hospital Groningen, Groningen, the Netherlands.
J Cardiovasc Pharmacol. 2005 Jan;45(1):88-98. doi: 10.1097/00005344-200501000-00015.
The occurrence of in-stent restenosis is a major drawback of percutaneous transluminal coronary angioplasty with stent placement. Target vessel revascularization is necessary in 15% of patients who receive a stent. Recent advances in the development of drug-eluting stents have reduced these numbers tremendously. However refinement of antirestenotic therapies remains obligatory. The emerging interest in more physiological antirestenotic therapies might unchain an interest in the well-known inhibitors of the rennin-angiotensin system (RAS), the angiotensin-converting enzyme inhibitors, and the angiotensin II type I receptor blockers. Contradictory results overshadow the discussion of whether intervention in the RAS could prevent in-stent restenosis. This review discusses the pathophysiology of in-stent restenosis, the role of the RAS in in-stent restenosis, and the possible role of RAS intervention in the prevention of in-stent restenosis.
支架内再狭窄的发生是冠状动脉支架置入术的主要缺点。在接受支架置入的患者中，15%需要进行靶血管血运重建。药物洗脱支架的最新进展已大幅降低了这一比例。然而，抗再狭窄治疗的优化仍必不可少。对更具生理性抗再狭窄疗法的新兴趣可能会引发对熟知的肾素-血管紧张素系统（RAS）抑制剂、血管紧张素转换酶抑制剂及血管紧张素II 1型受体阻滞剂的兴趣。关于干预RAS是否可预防支架内再狭窄的讨论因相互矛盾的结果而蒙上阴影。本综述讨论了支架内再狭窄的病理生理学、RAS在支架内再狭窄中的作用以及RAS干预在预防支架内再狭窄中的可能作用。
