Involvement of Rho-Kinase Activation in the Pathogenesis of Coronary Hyperconstricting Responses Induced by Drug-Eluting Stents in Patients With Coronary Artery Disease
Involvement of Rho-Kinase Activation in the Pathogenesis of Coronary Hyperconstricting Responses Induced by Drug-Eluting Stents in Patients With Coronary Artery Disease
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DOI：
10.1253/circj.cj-12-0662
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发表时间：
2012-11-01
影响因子：
3.3
通讯作者：
Shimokawa, Hiroaki
中科院分区：
文献类型：
--
作者：
Aizawa, Kentaro;Yasuda, Satoshi;Shimokawa, Hiroaki
背景：Rho 激酶的激活在猪体内药物洗脱支架 (DES) 诱导的冠状动脉过度收缩反应的发病机制中发挥着核心作用，这一点已被证实。在本研究中，对冠状动脉疾病 (CAD) 患者这些反应中涉及的 Rho 激酶激活进行了检查。 方法和结果：在 24 名接受 DES 或裸金属支架 (BMS) 冠状动脉介入治疗的 CAD 患者中，检查了在使用 Rho 激酶抑制剂、法舒地尔进行冠状动脉内预处理之前和之后冠状动脉血管舒缩反应对冠状动脉内乙酰胆碱 (ACh) 的反应。通过定量冠状动脉造影（QCA）评估冠状血管舒缩反应，并通过光学相干断层扫描（OCT）评估冠状血管结构。 ()CA显示，与BMS组相比，DES组在支架附近的近端和远端节段对ACh的冠状血管收缩反应均显着增强（近端：BMS -13.0 +/- 10.7% vs. DES -25.4 +/- 14.3%，P=0.036；远端：BMS -24.4 +/- 12.2% vs. DES -43.8 +/- 14.7%，P=0.003）。重要的是，法舒地尔显着减弱了 DES 组中对 ACh 的增强血管收缩反应（与法舒地尔之前相比，近端 10.2 +/- 11.7%，远端 14.4 +/- 10.5%，均 P
Background: Activation of Rho-kinase plays a central role in the pathogenesis of drug-eluting stents (DES)-induced coronary hyperconstricting responses in pigs in vivo has been previously demonstrated. In the present study, Rho-kinase activation involved in those responses in patients with coronary artery disease (CAD) is examined.Methods and Results: In 24 patients with CAD who underwent coronary intervention with either DES or bare-metal stents (BMS), coronary vasomotor responses to intracoronary acetylcholine (ACh) before and after intracoronary pre-treatment with a Rho-kinase inhibitor, fasudil was examined. Coronary vasomotor responses by quantitative coronary angiography (QCA) and coronary vascular structure by optical coherence tomography (OCT) was evaluated. ()CA showed that the coronary vasoconstricting responses to ACh were significantly enhanced in the DES group compared with the BMS group both at the proximal and the distal segments adjacent to the stents (proximal: BMS -13.0 +/- 10.7% vs. DES -25.4 +/- 14.3%, P=0.036; distal: BMS -24.4 +/- 12.2% vs. DES -43.8 +/- 14.7%, P=0.003). Importantly, fasudil markedly attenuated the enhanced vasoconstricting responses to ACh in the DES group (proximal 10.2 +/- 11.7%, distal 14.4 +/- 10.5% vs. before fasudil, both P