Structural and Biomechanical Adaptations of Right Ventricular Remodeling-In Pulmonary Arterial Hypertension-Reduces Left Ventricular Rotation During Contraction: A Computational Study

被引:12
作者
Kheyfets, Vitaly O. [1 ]
Uyen Truong [1 ]
Ivy, Dunbar [1 ]
Shandas, Robin [1 ]
机构
[1] Univ Colorado, Childrens Hosp Colorado, Anschutz Med Campus, Aurora, CO 80045 USA
来源
JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME | 2019年 / 141卷 / 05期
关键词
MYOSIN HEAVY-CHAIN; HUMAN HEART; MECHANICS; PRESSURE; MYOCARDIUM; STRAIN; GENE; HYPERTROPHY; EXPRESSION; PHYSIOLOGY;
D O I
10.1115/1.4042682
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
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.
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收藏
页数:10
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