PoliToBIOMed Lab, Department of Mechanical and Aerospace Engineering, Politecnico di Torino, Corso Duca degli Abruzzi, 24, 10129, Turin, Italy.
Department of Cardiology, Biomedical Engineering, Erasmus MC, 3000 CA, Rotterdam, The Netherlands.
Ann Biomed Eng. 2021 Sep;49(9):2606-2621. doi: 10.1007/s10439-021-02829-5.
Although unphysiological wall shear stress (WSS) has become the consensus hemodynamic mechanism for coronary atherosclerosis, the complex biomechanical stimulus affecting atherosclerosis evolution is still undetermined. This has motivated the interest on the contraction/expansion action exerted by WSS on the endothelium, obtained through the WSS topological skeleton analysis. This study tests the ability of this WSS feature, alone or combined with WSS magnitude, to predict coronary wall thickness (WT) longitudinal changes. Nine coronary arteries of hypercholesterolemic minipigs underwent imaging with local WT measurement at three time points: baseline (T1), after 5.6 ± 0.9 (T2), and 7.6 ± 2.5 (T3) months. Individualized computational hemodynamic simulations were performed at T1 and T2. The variability of the WSS contraction/expansion action along the cardiac cycle was quantified using the WSS topological shear variation index (TSVI). Alone or combined, high TSVI and low WSS significantly co-localized with high WT at the same time points and were significant predictors of thickening at later time points. TSVI and WSS magnitude values in a physiological range appeared to play an atheroprotective role. Both the variability of the WSS contraction/expansion action and WSS magnitude, accounting for different hemodynamic effects on the endothelium, (1) are linked to WT changes and (2) concur to identify WSS features leading to coronary atherosclerosis.
虽然非生理性壁面切应力 (WSS) 已成为冠状动脉粥样硬化的共识血流动力学机制,但影响动脉粥样硬化演变的复杂生物力学刺激仍未确定。这激发了人们对 WSS 通过 WSS 拓扑骨架分析对内皮细胞产生的收缩/扩张作用的兴趣。本研究测试了该 WSS 特征(单独或与 WSS 幅度结合使用)预测冠状动脉壁厚度 (WT) 纵向变化的能力。9 只患有高胆固醇血症的小型猪的 9 条冠状动脉在三个时间点进行了成像,同时进行局部 WT 测量:基线 (T1)、5.6±0.9 个月后 (T2) 和 7.6±2.5 个月后 (T3)。在 T1 和 T2 进行个体化计算血流动力学模拟。使用 WSS 拓扑剪切变化指数 (TSVI) 量化了整个心动周期中 WSS 收缩/扩张作用的可变性。单独或联合使用时,高 TSVI 和低 WSS 与同一时间点的高 WT 高度重合,是后期 WT 增厚的显著预测因子。处于生理范围内的 TSVI 和 WSS 幅度值似乎起到了抗动脉粥样硬化的作用。WSS 收缩/扩张作用的可变性和 WSS 幅度都反映了对内皮的不同血流动力学影响,(1) 与 WT 变化相关,(2) 共同确定导致冠状动脉粥样硬化的 WSS 特征。