Structural and Biomechanical Adaptations of Right Ventricular Remodeling-In Pulmonary Arterial Hypertension-Reduces Left Ventricular Rotation During Contraction: A Computational Study
Structural and Biomechanical Adaptations of Right Ventricular Remodeling-In Pulmonary Arterial Hypertension-Reduces Left Ventricular Rotation During Contraction: A Computational Study
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DOI：
10.1115/1.4042682
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发表时间：
2019-05-01
影响因子：
1.7
通讯作者：
Shandas, Robin
中科院分区：
文献类型：
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作者：
Kheyfets, Vitaly O.;Uyen Truong;Shandas, Robin
肺动脉高压（PH）是一种退行性疾病，其特征是右心室负荷逐渐增加，最终导致功能下降。最近的观察性研究表明，在儿童和成人PH患者中，左室（LV）射血时扭转减少，左室射血分数（EF）保持不变。本研究的目的是建立一个双心室心脏的计算模型，并利用它来评估左室扭转力学的变化，以响应右室自由壁的力学、结构和血流动力学的变化。心脏模型显示，左室机械刚度增加和右室心肌纤维重新定向时，左室扭转和心尖旋转减少，这在ph中得到了证实。此外，右室结构的改变对右室EF有显著影响，但对左室EF的影响不大。左室压力过载使左室心肌应激呈指数增加。本研究的计算结果与成人和儿童PH患者的临床观察结果一致，显示左室扭转减少并保留左室EF。此外，发现的左室扭转减少的原因与PH啮齿动物研究中发现的左室结构适应一致，这也可能解释了左室心肌基因和蛋白表达的疑似应激诱导变化。
Pulmonary hypertension (PH) is a degenerative disease characterized by progressively increased right ventricular (RV) afterload that leads to ultimate functional decline. Recent observational studies have documented a decrease in left ventricular (LV) torsion during ejection, with preserved LV ejection fraction (EF) in pediatric and adult PH patients. The objective of this study was to develop a computational model of the biventricular heart and use it to evaluate changes in LV torsion mechanics in response to mechanical, structural, and hemodynamic changes in the RV free wall. The heart model revealed that LV torsion and apical rotation were decreased when increasing RV mechanical rigidity and during re-orientation of RV myocardial fibers, both of which have been demonstrated in PH. Furthermore, structural changes to the RV appear to have a notable impact on RV EF, but little influence on LV EF. Finally, RV pressure overload exponentially increased LV myocardial stress. The computational results found in this study are consistent with clinical observations in adult and pediatric PH patients, which reveal a decrease in LV torsion with preserved LV EF. Furthermore, discovered causes of decreased LV torsion are consistent with RV structural adaptations seen in PH rodent studies, which might also explain suspected stress-induced changes in LV myocardial gene and protein expression.