Division of Cardiology, Department of Internal Medicine, McGovern Medical School, The University of Texas Health Science at Houston, 1881 East Road, Houston, TX, 77054, USA.
Boston Children's Hospital, Boston, MA, USA.
Ann Biomed Eng. 2024 Feb;52(2):414-424. doi: 10.1007/s10439-023-03389-6. Epub 2023 Nov 13.
The impact of aortic valve stenosis (AS) extends beyond the vicinity of the narrowed leaflets into the left ventricle (LV) and into the systemic vasculature because of highly unpredictable valve behavior and complex blood flow in the ascending aorta that can be attributed to the strong interaction between the narrowed cusps and the ejected blood. These effects can become exacerbated during exercise and may have implications for disease progression, accurate diagnosis, and timing of intervention. In this 3-D patient-specific study, we employ strongly coupled fluid-structure interaction (FSI) modeling to perform a comprehensive biomechanical evaluation of systolic ejection dynamics in a stenosed aortic valve (AV) during increasing LV contraction. Our model predictions reveal that the heterogeneous ∆P vs. Q relationship that was observed in our previous clinical study can be attributed to a non-linear increase (by ~ 1.5-fold) in aortic valve area as LV heart rate increases from 70 to 115 bpm. Furthermore, our results show that even for a moderately stenotic valve, increased LV contraction during exercise can lead to high-velocity flow turbulence (Re = 11,700) in the aorta similar to that encountered with a severely stenotic valve (Re ~ 10,000), with concomitant greater viscous loss (~3-fold increase) and elevated wall stress in the ascending aorta. Our FSI predictions also reveal that individual valve cusps undergo distinct and highly non-linear increases (>100%) in stress during exercise, potentially contributing to progressive calcification. Such quantitative biomechanical evaluations from realistic FSI workflows provide insights into disease progression and can be integrated with current stress testing for AS patients to comprehensively predict hemodynamics and valve function under both baseline and exercise conditions.
主动脉瓣狭窄 (AS) 的影响不仅局限于瓣叶狭窄部位，还会延伸到左心室 (LV) 和体循环血管，这是由于瓣叶活动不可预测且升主动脉内血流复杂，这归因于狭窄瓣叶与射流血液之间的强相互作用。这些影响在运动期间可能会加剧，并可能对疾病进展、准确诊断和干预时机产生影响。在这项基于患者的 3D 研究中，我们采用强耦合力-结构相互作用 (FSI) 模型，对 LV 收缩逐渐增强时狭窄主动脉瓣 (AV) 收缩期射流动力学进行全面的生物力学评估。我们的模型预测表明，在我们之前的临床研究中观察到的不均匀 ∆P 与 Q 关系可以归因于主动脉瓣面积非线性增加（增加约 1.5 倍），当 LV 心率从 70 增加到 115 bpm。此外，我们的结果表明，即使对于中度狭窄的瓣膜，运动时 LV 收缩增加也会导致主动脉内高速流动湍流（Re = 11,700），类似于严重狭窄瓣膜（Re~10,000），同时伴有更大的粘性损失（增加约 3 倍）和升主动脉壁应力升高。我们的 FSI 预测还表明，在运动过程中，单个瓣叶会经历明显且高度非线性的应力增加（超过 100%），这可能导致进行性钙化。这种来自现实 FSI 工作流程的定量生物力学评估提供了对疾病进展的深入了解，并可与当前的 AS 患者压力测试相结合，全面预测基线和运动条件下的血液动力学和瓣膜功能。
