冠状动脉空洞化作为动脉粥样硬化斑块进展的触发因素：简化的数值和计算流体动力学演示。

Coronary artery cavitation as a trigger for atherosclerotic plaque progression: a simplified numerical and computational fluid dynamic demonstration.

机构信息

Division of Cardiology, Department of Specialistic Medicine, Rovigo General Hospital, 45100 Rovigo, Italy.

Department of Translational Medicine, University of Ferrara, 44121 Ferrara, Italy.

出版信息

Rev Cardiovasc Med. 2022 Feb 12;23(2):58. doi: 10.31083/j.rcm2302058.

DOI:10.31083/j.rcm2302058

PMID:35229549

Abstract

BACKGROUNDS

Coronary cavitation is supposed to be generated by both concentric and eccentric coronary artery stenosis which propagates downstream the vessel, creating microbubbles which exploded when the fluid pressure was lower than the vapor pressure at a local thermodynamic state.

OBJECTIVE

To assess, using numerical and computational fluid dynamic analysis (CFD), the potential of cavitation to both induce damage to coronary artery endothelium and to promote atherosclerotic plaque progression.

METHODS

We retrospectively reviewed the data 12 consecutive patients evaluated between 1st January 2013 and 1st January 2014 with an isolated hemodynamically significant Left Main (LM) disease. The patient specific geometries have been reconstructed. Bubble velocity has been calculated in accordance with Newton's second law. Both the forces arising from the bubbles' interaction with the continuous phase and impact with the endothelium have been evaluated. The impact of turbulence on the motion of bubbles have been modelled with a dispersion model.

RESULTS

Among the 12 patients retrospectively analysed [8 males, mean age 68.2 ± 12.8 years old], the mean LM stenosis was 72.3 ± 3.6%. As expected, in all subjects, LM stenoses induced cavitation which propagates downstream the vessel creating microbubbles. The higher concentration of vapor region was detected before the carina (within 0.8 to 1.3 cm from the stenosis). Due to the pressure gradient generated by the stenosis, formation of a re-entry jet which penetrates each bubble generated a shock wave. Before the carina, the mean bubbles radius observed was 4.2 ± 1.4 μm, which generated a mean peak pressure of 3.9 ± 0.5 MPa when they explode.

CONCLUSION

The cavitation phenomenon is effectively generated in a model of LM bifurcation and instantaneous pressure-peaks due to collapses of vapor bubbles resulted in a measurable dynamic load on vessel wall potentially able to induce endothelial damage.

摘要

背景

冠状动脉气穴现象据推测是由同心性和偏心性冠状动脉狭窄产生的，这些狭窄会沿着血管向下游传播，产生微泡，当局部热力学状态下的流体压力低于蒸汽压力时，这些微泡会爆炸。

目的

使用数值和计算流体动力学分析（CFD）评估气穴现象对内皮细胞的潜在损伤和促进动脉粥样硬化斑块进展的能力。

方法

我们回顾性分析了 2013 年 1 月 1 日至 2014 年 1 月 1 日期间连续评估的 12 例孤立性左主干（LM）疾病患者的数据。患者的特定几何形状已被重建。根据牛顿第二定律计算了气泡的速度。评估了气泡与连续相相互作用产生的力和与内皮相互作用的冲击力。使用弥散模型模拟了湍流对气泡运动的影响。

结果

在回顾性分析的 12 例患者中[8 例男性，平均年龄 68.2 ± 12.8 岁]，LM 狭窄的平均程度为 72.3 ± 3.6%。如预期的那样，在所有患者中，LM 狭窄都诱发了气穴现象，这些气穴现象沿着血管向下游传播，产生微泡。在隆嵴（狭窄处前 0.8 至 1.3 厘米范围内）之前检测到了更高浓度的蒸汽区域。由于狭窄产生的压力梯度，形成穿透每个气泡的再进入射流，产生了冲击波。在隆嵴之前，观察到的平均气泡半径为 4.2 ± 1.4 μm，当它们爆炸时，产生的平均峰值压力为 3.9 ± 0.5 MPa。