冠状动脉血流速度和干扰血流预测冠状动脉成形术后的不良临床结果

S. Kinlay, J. Grewal, Deborah Manuelin, J. Fang, A. Selwyn, J. Bittl, P. Ganz
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引用次数: 19

摘要

目的:层流在高速下受到干扰,减少剪切应力,增加血管炎症和增殖,这是再狭窄和动脉粥样硬化的关键过程。我们假设冠状动脉血管成形术后血流紊乱与不良的长期临床结果有关。方法与结果对97例行激光辅助冠状动脉成形术患者的影像学资料进行分析。采用帧计数技术和定量冠状动脉造影测量冠状动脉血流速度、残余病变尺寸和雷诺数(紊乱血流指标)。Cox比例风险用于评估指标手术后平均2.5年内不良事件(靶血管重建术、心肌梗死或死亡)的相对风险。在245例患者年的随访期间,有41例不良事件(每年随访17%)。高血流速度(>250 mm/s;相对危险度为2.5,95% CI为1.3 ~ 4.7)或在手术结束时狭窄入口的高雷诺数(>200)(相对危险度为2.1,95% CI为1.1 ~ 4.1)。对其他因素进行调整并没有改变这些结果。结论:高雷诺数表明冠状动脉成形术后血流紊乱,可能通过剪切应力相关的分子机制促进再狭窄和动脉粥样硬化,从而增加不良临床事件的风险。
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Coronary Flow Velocity and Disturbed Flow Predict Adverse Clinical Outcome After Coronary Angioplasty
Objective—Laminar flow becomes disturbed at high velocities, reducing shear stress and augmenting vascular inflammation and proliferation, processes that are pivotal in restenosis and atherogenesis. We hypothesized that disturbed blood flow after coronary angioplasty is associated with adverse long-term clinical outcome. Methods and Results—The cineangiograms from 97 patients undergoing laser-assisted coronary angioplasty were analyzed. Coronary blood flow velocity, the residual lesion dimensions, and the Reynolds number (an index of disturbed flow) were measured by using a frame-counting technique and quantitative coronary angiography. Cox proportional hazards were used to assess the relative risk of adverse events (target-vessel revascularization, myocardial infarction, or death) over a mean 2.5 years after the index procedure. There were 41 adverse events during 245 patient years of follow-up (17% per year of follow-up). The risk of an adverse event was increased for patients with a high flow velocity (>250 mm/s; relative risk 2.5, 95% CI 1.3 to 4.7) or a high Reynolds number (>200) at the stenosis inlet (relative risk 2.1, 95% CI 1.1 to 4.1) at the end of the procedure. Adjustment for other factors did not alter these results. Conclusions—High Reynolds numbers, indicating disturbed blood flow after coronary angioplasty, increase the risk of adverse clinical events, potentially through shear-stress–related molecular mechanisms that promote restenosis and atherogenesis.
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