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

Progressive Calcification in Bicuspid Valves: A Coupled Hemodynamics and Multiscale Structural Computations.
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DOI:
10.1007/s10439-021-02877-x
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发表时间:
2021-12
影响因子:
3.8
通讯作者:
Haj-Ali R
Haj-Ali R
中科院分区:
工程技术2区
文献类型:
--
作者:
Lavon K;Morany A;Halevi R;Hamdan A;Raanani E;Bluestein D;Haj-Ali R

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二叶式主动脉瓣(BAV)是最常见的先天性心脏病。钙化性主动脉瓣疾病(CAVD)占主动脉瓣狭窄(AS)病例的大多数。被诊断为AS的患者中有一半患有BAV,其进展速度加快。本研究旨在开发一种计算建模方法,用于BAV中的钙化进展及其在疾病进展期间结合流体-结构相互作用(FSI)模拟的生物力学响应。根据切除的钙化BAV瓣叶的Micro-CT图像对钙化进行患者特定重建,并使用新型反向钙化技术进行处理,该技术使用基于密度的标准预测CAVD的先前状态,从而产生多层钙化结构。生成了4个渐进性多层钙化BAV模型:健康、轻度、中度和重度,并在整个心动周期内通过FSI模拟进行建模。在体外脉冲复制器中测试由切除的钙化BAV瓣叶组成的瓣膜装置模型,以验证严重模型。对超声心动图扫描的健康模型进行了验证。进行性AS的特征是较高的收缩期射流速度(2.08、2.3、3.37和3.85 m s-1),这在射流周围诱导了强烈的涡流,加上不规则的再循环回流模式,提高了瓣叶上的粘性剪切应力。本研究阐明了驱动BAV患者CAVD进展的流体-结构机制。
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.
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