Computational Fluid Dynamics Analysis of the Effect of Plaques in the Left Coronary Artery

Thanapong Chaichana,Zhonghua Sun,James Jewkes

doi:10.1155/2012/504367

Abstract

This study was to investigate the hemodynamic effect of simulated plaques in left coronary artery models, which were generated from a sample patient's data. Plaques were simulated and placed at the left main stem and the left anterior descending (LAD) to produce at least 60% coronary stenosis. Computational fluid dynamics analysis was performed to simulate realistic physiological conditions that reflect the in vivo cardiac hemodynamics, and comparison of wall shear stress (WSS) between Newtonian and non-Newtonian fluid models was performed. The pressure gradient (PSG) and flow velocities in the left coronary artery were measured and compared in the left coronary models with and without presence of plaques during cardiac cycle. Our results showed that the highest PSG was observed in stenotic regions caused by the plaques. Low flow velocity areas were found at postplaque locations in the left circumflex, LAD, and bifurcation. WSS at the stenotic locations was similar between the non-Newtonian and Newtonian models although some more details were observed with non-Newtonian model. There is a direct correlation between coronary plaques and subsequent hemodynamic changes, based on the simulation of plaques in the realistic coronary models.

Highlights

Coronary artery disease (CAD) is the leading cause of death in advanced countries
The analysis demonstrates a strong relationship between hemodynamic change and plaques at the left coronary artery
This study shows that coronary plaques produce a significant impact on the subsequent flow changes in the coronary artery, in addition to the local hemodynamic interference due to the presence of plaques

Summary

Introduction

Coronary artery disease (CAD) is the leading cause of death in advanced countries. The most common cause of CAD is atherosclerosis which is caused by the presence of plaques on the artery wall, resulting in the lumen stenosis. Plaques have been associated with blood clots and compromise blood flow to the myocardium. This occurs when the coronary plaques suddenly rupture; if a clot cannot be treated in time, the heart muscle will be impaired due to ischemic changes, leading to myocardial ischemia or infarction or, more severely, necrosis [1]. If the local wall shear stress is low, a proliferative plaque will form. Since the progression and development of vulnerable plaque is associated with low wall shear stress and the presence of expansive remodelling, measurement of these characteristics in vivo will enable risk stratification for the entire coronary circulation [2]

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