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Updated: Apr 7, 2026

Lumped-Parameter and Finite Element Modeling of Heart Failure with Preserved Ejection Fraction
Published on: February 13, 2021
Hydraulic forces assist left ventricular filling in aortic stenosis at baseline and after valve replacement
Bryce Watson1, Jonathan Bennett2, Nikoo Aziminia2
1Institute of Cardiovascular Science, University College London, London, United Kingdom; St George Physician Training Network, Sydney, Australia.
Background:
Diastolic dysfunction in the setting of aortic valve replacement (AVR) for aortic stenosis (AS) is incompletely understood. This study aims to assess the net hydraulic force of left ventricular (LV) filling in participants with severe symptomatic AS undergoing AVR.
Methods:
This single-centre prospective observational cohort study evaluated patients with severe, symptomatic AS undergoing AVR between 2012 and 2015. Clinical assessment and cardiovascular magnetic resonance were completed prior to AVR and 1-year post-operatively. Atrioventricular area difference (AVAD) was used as a surrogate for the hydraulic force of LV filling. AVAD at mid-diastole was measured as the difference between LV short-axis area and left atrial short-axis area.
Results:
In patients with AS (n = 110, 54% [59/110] male, age 71 [64-77] years, aortic valve area 0.74 ± 0.25 cm2), AVAD was positive at baseline (2.8 ± 6.5 cm2), consistent with a net hydraulic force assisting LV filling. While AVAD did not change post-operatively on a group level (p = 0.70), an improvement in AVAD was associated univariably with increasing baseline LV ejection fraction, and decreasing baseline AVAD, LV volume, mass, myocardial extracellular volume, and infarct size (p<0.05 for all), and multivariably with baseline decreasing AVAD, LV mass, and age (model adjusted R2 = 0.49, p<0.001).
Conclusion:
In severe AS, hydraulic force contributes to LV filling prior to and following AVR. The greatest improvement in hydraulic force following AVR occurred in those with the lowest baseline hydraulic force, but also with lower age and the absence of otherwise deleterious LV myocardial remodelling.
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