Carter Andrew J, Wei Wei, Gibson Lori, Collingwood Robin, Tio Fermin, Dooley John, Kopia Gregory A
Medical Device Research Laboratory, Borgess Medical Center, Kalamazoo, MI 49024, USA.
Cardiovasc Revasc Med. 2005 Apr-Jun;6(2):58-64. doi: 10.1016/j.carrev.2005.05.004.
Low vessel-wall shear stress promotes atherosclerosis and restenosis. We conducted serial analysis of vessel-wall shear stress following placement of metal and sirolimus (SRL) stents to determine the relationship between shear stress and neointima.
Serial quantitative coronary angiography, intracoronary ultrasound (IVUS), and Doppler flow analysis were performed at baseline, immediately poststent, and at 30 and 90 days on 16 stents (metal, n = 8; SRL, n = 8) implanted in the coronary arteries of eight miniswine. Segmental vessel-wall shear stress (dyn/cm2) was calculated at 10 sections within the stent and normalized to the average proximal and distal reference vessel shear stress using IVUS and hyperemic average peak flow velocity. At 90 days, histological analysis was completed to determine vessel-wall morphometry on corresponding sections from each stent.
Stent placement resulted in a similar degree of in-stent stenosis (-5% to 25%) and immediate post-in-stent shear stress. At 30 days, the IVUS neointimal cross-sectional area and percentage of area stenosis were significantly less in SRL (1.2+/-0.8 mm2; 12.7+/-8.5%) versus metal stents (2.3+/-0.4 mm2; 28.2+/-3.4%, P < .003). In-stent normalized shear stress was less for SRL (0.93+/-0.07) versus metal (1.07+/-0.08, P = .002) stents. At 90 days, the mean neointimal area was similar for the SRL (2.50+/-0.47 mm2) and metal stents (2.72+/-1.15 mm2). Linear regression documented a negative correlation between poststent shear stress and neointima for metal stents (r = .61, P < .0001). In the SRL stents, however, the post-in-stent shear stress had a positive correlation with neointima (r = .40, P = .0002).
The placement of oversized stents causes alteration of segmental vessel-wall shear stress, which appears to be an important physiological stimulus for neointimal formation, and may influence the pharmacodynamics of SRL-eluting stent in the porcine coronary model.
低血管壁剪切应力会促进动脉粥样硬化和再狭窄。我们在植入金属和西罗莫司(SRL)支架后对血管壁剪切应力进行了系列分析,以确定剪切应力与新生内膜之间的关系。
对8只小型猪冠状动脉内植入的16枚支架(金属支架,n = 8;SRL支架,n = 8)在基线、支架植入后即刻、30天和90天时进行系列定量冠状动脉造影、血管内超声(IVUS)和多普勒血流分析。使用IVUS和充血平均峰值流速计算支架内10个节段的节段性血管壁剪切应力(dyn/cm2),并将其标准化为近端和远端参考血管平均剪切应力。在90天时,完成组织学分析以确定每个支架相应节段的血管壁形态学。
支架植入导致支架内狭窄程度相似(-5%至25%)以及支架植入后即刻的剪切应力相似。在30天时,与金属支架(2.3±0.4 mm2;28.2±3.4%,P <.003)相比,SRL支架的IVUS新生内膜横截面积和面积狭窄百分比显著更小(1.2±0.8 mm2;12.7±8.5%)。与金属支架(1.07±0.08,P =.002)相比,SRL支架的支架内标准化剪切应力更小(0.93±0.07)。在90天时,SRL支架(2.50±0.47 mm2)和金属支架(2.72±1.15 mm2)的平均新生内膜面积相似。线性回归表明金属支架的支架后剪切应力与新生内膜呈负相关(r =.61,P <.0001)。然而,在SRL支架中,支架内剪切应力与新生内膜呈正相关(r =.40,P =.0002)。
超大尺寸支架的植入会导致节段性血管壁剪切应力改变,这似乎是新生内膜形成的重要生理刺激因素,并且可能影响猪冠状动脉模型中SRL洗脱支架的药效学。