Stiffness of ascending aorta has a direct impact on left ventricular function: In silico model

Abstract

During systole, longitudinal shortening of the left ventricle (LV) displaces the aortic root toward the apex of the heart and stretches the ascending aorta. Effects of stiffening the ascending aorta (AA) on cardiac function was evaluated with potential implications for heart failure with reduced ejection fraction (HFpEF). Living left heart human model (Dassault Systemes Simulia Corporation) was utilized to simulate LV function in normal and stiff AA model. In a model simulating a normal elastic AA, the ascending aorta was stretched by 11.0mm, baseline computed stroke volume was 92.2ml, and effective stroke work was 8747.5 Joules. Simulations show a typical pressure-volume loop, normal myofiber stress and strain patterns. In a model with a stiffened AA, end-diastolic pressure increased by 8.5%, while end-systolic LV pressure was reduced by 9.1%, stroke volume by 10.8% and effective stroke work by 19.0%. LV shape tended to be more ovalized at end-systole. Average tensile radial strain was reduced by 20.2 ± 2.4% compressive circumferential strain by 6.8 ± 10.9%, and average compressive longitudinal stain by 48.4 ± 36.9%, while septal longitudinal strain was reduced by 94.1%, anterior, lateral and posterior strain by 41.2%, 13.3% and 40.0% respectively. Average myofiber stress increased by 37.0 ± 42.9%, with high-stress areas noted at the LV septum. To restore baseline stroke volume, contractility was doubled, resulting in nearly identical pressure-volume loop, end-diastolic and end-systolic pressures, stroke volume, and effective stroke work as at baseline. Average tensile radial and compressive longitudinal strain remained reduced by 3.7 ± 8.8% and 37.5%±35.0%, respectively, while compressive circumferential strain increased by 13.6 ± 29.1% over baseline. Septal, anterior, lateral, and posterior longitudinal strain remained reduced by 82.3%, 23.5%, 6.7%, and 33.3% respectively. The calculated average myofiber stress was 61.8 ± 88.3% higher compared to baseline, with remarkably increased stress along the LV septum, papillary muscles, and apex. Hypothesis-generating computational study demonstrated deleterious effects of AA stiffening upon longitudinal LV function, indicating that the LV is directly linked to the AA through mechanical coupling. Since a stiff AA and impairment of left ventricular longitudinal strain is common in patients with HFpEF, we hypothesize a direct mechanical pathophysiologic link between reduced aortic stretching and reduced longitudinal left ventricular strain.