Biomechanical behavior of human left ventricle with aortic stenosis considering hypertrophy

Abstract

Aortic stenosis (AS) and mitral regurgitation (MR) are the two most prevalent diseases in aged individuals. Studying AS and MR in clinical settings is expensive and time-consuming. Instead, we used a finite element model of the human left ventricle (LV) coupled with a closed-loop circulatory model to simulate different AS and MR severity levels. We find that aortic stenosis increases peak LV systolic pressure and reduces stroke volume. Ejection fraction (EF) falls as low as 51.8% in severe cases. Higher degrees of afterload cause LV to develop higher contractile force increasing the myofiber stress. Peak myofiber stress increases by 6%, 14%, and 34.6% as the disease progresses from mild to severe. Myocardial deformation in circumferential, radial and longitudinal directions reduces. In severe AS, the peak strain value drops by up to 22% in the circumferential direction. MR causes a maximum 27% reduction of LV peak systolic pressure in severe cases. It increases ejection fraction up to 68.1%. Decreased LV cavity pressure requires the myofiber to generate lower contractile force, and thus there is a 9%, 16%, and 27% reduction in peak myofiber stress in mild, moderate, and severe MR. The increased extent of contraction during systole raises the peak circumferential strain value to 32.8%. The left ventricle undergoes remodeling to offset the imbalances caused by these diseases. Concentric hypertrophy tries to restore the ejection fraction and increase aortic pressure in AS. In severe AS, EF increases from 51.8% to 58.4% due to hypertrophy. Remodeling also counteracts the increased fiber stress and elevates circumferential shortening. But peak longitudinal strain value decreases by as high as 20% in severe cases due to increased myofiber wall stiffness. However, in MR, eccentric hypertrophy restores the LV and aortic pressure. It causes around a 32% increase in myofiber stress but reduces deformation in circumferential and radial directions. MR poses a compensatory effect on LV biomechanics when combined with AS. With maximum LV pressure, myofiber stress, and minimum ejection fraction, concurrent severe AS with moderate MR seems the deadliest combination. Hypertrophy increases LV pressure, aortic blood pressure, and end-diastolic and end-systolic volume in all combinations of AS and MR, but the stroke volume and ejection fraction are reduced in an attempt to restore normal LV systolic function. It also increases peak systolic fiber stress and reduces peak strain values in all three directions. Different biomechanical data found in our study are consistent with the available literature, and the trend of effects of various parameters on LV biomechanics is comparable.