Multifactorial assessment of hemodynamic thresholds in a three-layered elastic stenosed coronary artery

Abstract

Hemodynamics controls the pathogenesis of atherosclerosis in coronary arteries having stenoses, but the joint effect of stenosis degree, blood viscosity, heart rate, and Reynolds number (Re) on coronary artery dynamics has not been explored using a fluid–structure interaction model. A two-dimensional fluid–structure interaction model of the left anterior descending coronary artery having a hyperelastic three-layered arterial wall was established; wall shear stress (WSS), luminal pressure, radial arterial displacement, and velocity field were calculated at the peak systole, mid-diastole, and late diastole for different stenosis degree (25%–35%), blood viscosity (0.003 65–0.0045 Pa-s), heart rate (60–100 bpm), and Re (50–200). An increase in stenosis degree from 25% to 35% resulted in an increase in peak wall deformation by 7.7% (0.65–0.70 mm) under hemodynamically significant trans-stenotic pressure gradients. A 23% increase in viscosity resulted in a 36% increase in peak wall deformation and a 43% increase in peak WSS, resulting in decreased coronary flow reserve of 25%–30%, which is consistent with the hemodynamic challenge due to polycythemia and diabetic microangiopathy. Heart rate variation exhibited an inverse relationship with wall deformation, governed by the Frank–Starling mechanism: bradycardia (60 bpm) provided a deformation nearly eightfold greater compared to tachycardia (100 bpm) (0.95 mm vs 0.12 mm) while giving 67% more diastolic perfusion time. A Re range of 50–200 encompasses conditions ranging from inward wall displacement at Re = 50 to a peak WSS of 23 Pa at Re = 200. Model-defined parameters for critical stenosis are greater than 30% diameter reduction, hematocrit of more than 45%, and heart rates of 65–80 bpm.