Effects of hematocrit levels on hemodynamics and atherosclerosis risk in the left main coronary artery: a comparative computational mechanobiological study

Abstract

Coronary artery disease is the leading cause of cardiovascular mortality worldwide, yet the role of altered hematocrit (Hct) in atherosclerotic plaque formation remains unclear. This study uses a mechanobiological model to computationally investigate the effect of non-Newtonian blood behavior and varying Hct on plaque formation in a three-dimensional left main coronary artery. Hct levels of 25 % (low), 45 % (normal), and 65 % (high) are investigated. The Navier–Stokes and Darcy equations are solved to model fluid flow. Coupled convection–diffusion–reaction equations for low-density lipoprotein (LDL), oxidized LDL, monocytes, macrophages, and foam cells (FC) are solved to simulate a 10-year inflammatory evolution within the arterial wall. The results reveal that as Hct increases in the non-Newtonian model, peak FC concentration within the wall decreases. After 5 years, low Hct leads to a maximum concentration that is 1.6- and 4.7-fold higher than normal and high Hct concentration respectively, and 1.2-fold higher than that in the Newtonian model. Therefore, low Hct results in maximal plaque growth. Additionally, low Hct expands the areas of high FC concentration, thereby increasing plaque burden. Moreover, in the non-Newtonian model, the ratio of peak FC concentration at 10 years to that at 5 years rises with Hct. High Hct shows a ratio that is 1.17- and 1.43-fold greater than normal and low Hct, respectively, and 1.24-fold higher than that in the Newtonian model. Therefore, high Hct accelerates plaque formation during the second half of the 10-year inflammatory process. In addition, with increasing Hct, regions of high FC concentration in the left anterior descending artery (LAD) shift from the myocardial side to the carina. These findings deepen our understanding of atherosclerosis.