4.5 Article

Progressive Calcification in Bicuspid Valves: A Coupled Hemodynamics and Multiscale Structural Computations

期刊

ANNALS OF BIOMEDICAL ENGINEERING
卷 49, 期 12, 页码 3310-3322

出版社

SPRINGER
DOI: 10.1007/s10439-021-02877-x

关键词

Bicuspid aortic valve; Calcific aortic valve disease; Fluid-structure interaction

资金

  1. NIH-NIBIB [BRP U03EB026414]
  2. Planning and Budgeting Committee -Israeli Council for Higher Education

向作者/读者索取更多资源

This study develops a computational modeling approach to simulate the calcification progression in bicuspid aortic valve (BAV) and its biomechanical response during disease progression. The study sheds light on the fluid-structure mechanism that drives calcific aortic valve disease (CAVD) progression in BAV patients, by analyzing flow patterns and shear stresses on the leaflets during the full cardiac cycle.
Bicuspid aortic valve (BAV) is the most common congenital heart disease. Calcific aortic valve disease (CAVD) accounts for the majority of aortic stenosis (AS) cases. Half of the patients diagnosed with AS have a BAV, which has an accelerated progression rate. This study aims to develop a computational modeling approach of both the calcification progression in BAV, and its biomechanical response incorporating fluid-structure interaction (FSI) simulations during the disease progression. The calcification is patient-specifically reconstructed from Micro-CT images of excised calcified BAV leaflets, and processed with a novel reverse calcification technique that predicts prior states of CAVD using a density-based criterion, resulting in a multilayered calcified structure. Four progressive multilayered calcified BAV models were generated: healthy, mild, moderate, and severe, and were modeled by FSI simulations during the full cardiac cycle. A valve apparatus model, composed of the excised calcified BAV leaflets, was tested in an in-vitro pulse duplicator, to validate the severe model. The healthy model was validated against echocardiography scans. Progressive AS was characterized by higher systolic jet flow velocities (2.08, 2.3, 3.37, and 3.85 m s(-1)), which induced intense vortices surrounding the jet, coupled with irregular recirculation backflow patterns that elevated viscous shear stresses on the leaflets. This study shed light on the fluid-structure mechanism that drives CAVD progression in BAV patients.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.5
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据