Automated finite element approach to generate anatomical patient-specific biomechanical models of atherosclerotic arteries from virtual histology-intravascular ultrasound.

Abstract

Despite advancements in early detection and treatment, atherosclerosis remains the leading cause of death across all cardiovascular diseases (CVD). Biomechanical analysis of atherosclerotic lesions has the potential to reveal biomechanically instable or rupture-prone regions. Treatment decisions rarely consider the biomechanics of the stenosed lesion due in-part to difficulties in obtaining this information in a clinical setting. Previous 3D FEA approaches have incompletely incorporated the complex curvature of arterial geometry, material heterogeneity, and use of patient-specific data. To address these limitations and clinical need, herein we present a user-friendly fully automated program to reconstruct and simulate the wall mechanics of patient-specific atherosclerotic coronary arteries. The program enables 3D reconstruction from patient-specific data with heterogenous tissue assignment and complex arterial curvature. Eleven arteries with coronary artery disease (CAD) underwent baseline and 6-month follow-up angiographic and virtual histology-intravascular ultrasound (VH-IVUS) imaging. VH-IVUS images were processed to remove background noise, extract VH plaque material data, and luminal and outer contours. Angiography data was used to orient the artery profiles along the 3D centerlines. The resulting surface mesh is then resampled for uniformity and tetrahedralized to generate the volumetric mesh using TetGen. A mesh convergence study revealed edge lengths between 0.04 mm and 0.2 mm produced constituent volumes that were largely unchanged, hence, to save computational resources, a value of 0.2 mm was used throughout. Materials are assigned and finite element analysis (FEA) is then performed to determine stresses and strains across the artery wall. In a representative artery, the highest average effective stress was in calcium elements with 235 kPa while necrotic elements had the lowest average stress, reaching as low as 0.79 kPa. After applying nodal smoothening, the maximum effective stress across 11 arteries remained below 288 kPa, implying biomechanically stable plaques. Indeed, all atherosclerotic plaques remained unruptured at the 6-month longitudinal follow up diagnosis. These results suggest our automated analysis may facilitate assessment of atherosclerotic plaque stability.