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Systolic anterior motion in hypertrophic cardiomyopathy: a fluid–structure interaction computational model
Theoretical and Computational Fluid Dynamics ( IF 2.2 ) Pub Date : 2021-03-03 , DOI: 10.1007/s00162-021-00564-0
Valentina Meschini , Rajat Mittal , Roberto Verzicco

We present direct numerical simulations for the pathophysiology of hypertrophic cardiomyopathy of the left ventricle of the human heart. This cardiovascular disorder manifests itself through systolic anterior motion (SAM), a drift of the mitral leaflets towards the aortic subvalvular region, sometimes causing ventricular obstruction during systole. This pathology is induced by a combination of factors, including a thickening of the interventricular septum and an elongation of the mitral valve leaflets: we perform a full parametric study to assess their effect on the disease. From our results we observe that SAM occurs when elongated leaflets, hypertrophic ventricles and strong ejection fraction are present at the same time. In contrast, a physiological ventricle with elongated leaflets, an hypertrophic ventricle with physiological leaflets or diseased ventricle and leaflets with a weak ejection fraction do not produce SAM. After verifying that the numerical results are consistent and in agreement with the clinical data from the literature, we virtually test the two standard surgical procedures, leaflet plication and septal myectomy, adopted for the surgical treatment of SAM. For all the considered cases we obtain quantitative confirmation for the reliability of the intraventricular subvalvular pressure drop (or subvalvular pressure gradient for the medical community) as diagnostic indicator of the systolic anterior motion: when this quantity attains the value of 30 mmHg, SAM of the mitral leaflets is observed, while when this threshold is exceeded the SAM becomes obstructive. On the other hand, in all cases for which SAM is not observed the above pressure drop is always below the threshold.



中文翻译:

肥厚型心肌病的收缩前运动:流固耦合计算模型

我们提出了人类心脏左心室肥厚型心肌病的病理生理学的直接数值模拟。这种心血管疾病通过收缩前运动(SAM)表现出来,即二尖瓣小叶向主动脉瓣下区域的漂移,有时在收缩期引起心室阻塞。这种病理是由多种因素引起的,包括室间隔增厚和二尖瓣小叶延长:我们进行了一项完整的参数研究,以评估其对疾病的影响。从我们的结果中我们观察到,当同时存在细长的小叶,肥厚的心室和强射血分数时,就会发生SAM。相比之下,生理室的小叶细长,具有生理性小叶或患病的心室的肥厚型心室以及射血分数较弱的小叶不会产生SAM。在验证了数值结果的一致性并与文献中的临床数据相符之后,我们实际上测试了用于SAM外科手术的两种标准手术程序,即小叶折皱和间隔肌切开术。对于所有考虑到的情况,我们都获得了定量的心室内瓣膜下压降(或医学界的瓣膜下压力梯度)作为收缩前运动的诊断指标的可靠性的确认:当该量达到30 mmHg时,SAM的观察到二尖瓣小叶,而当超过此阈值时,SAM变得阻塞。另一方面,

更新日期:2021-03-03
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