A parametric study of the effect of 3D plaque shape on local hemodynamics and implications for plaque instability

• Published in: Biomechanics and modeling in mechanobiology Vol. 23; no. 4; pp. 1209 - 1227
• Main Authors: Hossain, Shaolie S., Johnson, Michael J., Hughes, Thomas J. R.
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01-08-2024; Springer Nature B.V
• Subjects: Biological and Medical Physics; Biomedical Engineering and Bioengineering; Biophysics; Blood flow; Computer applications; Coronary artery; Coronary vessels; Engineering; Finite element method; Flow stability; Hemodynamics; Instability; Lipids; Original Paper; Plaques; Rupture; Shape effects; Shear stress; Software; Theoretical and Applied Mechanics; Thrombosis; Vascular cell adhesion molecule 1; Wall shear stresses; Workflow; Isogeometric analysis; Vulnerable plaque; Patient-specific modeling; Inflammation; Wall shear stress gradient; Atherosclerosis
• ISSN: 1617-7959; 1617-7940; 1617-7940
• DOI: 10.1007/s10237-024-01834-6

The vast majority of heart attacks occur when vulnerable plaques rupture, releasing their lipid content into the blood stream leading to thrombus formation and blockage of a coronary artery. Detection of these unstable plaques before they rupture remains a challenge. Hemodynamic features including wall shear stress (WSS) and wall shear stress gradient (WSSG) near the vulnerable plaque and local inflammation are known to affect plaque instability. In this work, a computational workflow has been developed to enable a comprehensive parametric study detailing the effects of 3D plaque shape on local hemodynamics and their implications for plaque instability. Parameterized geometric 3D plaque models are created within a patient-specific coronary artery tree using a NURBS (non-uniform rational B-splines)-based vascular modeling pipeline. Realistic blood flow features are simulated by using a Navier–Stokes solver within an isogeometric finite-element analysis framework. Near wall hemodynamic quantities such as WSS and WSSG are quantified, and vascular distribution of an inflammatory marker (VCAM-1) is estimated. Results show that proximally skewed eccentric plaques have the most vulnerable combination of high WSS and high positive spatial WSSG, and the presence of multiple lesions increases risk of rupture. The computational tool developed in this work, in conjunction with clinical data, -could help identify surrogate markers of plaque instability, potentially leading to a noninvasive clinical procedure for the detection of vulnerable plaques before rupture.