Georgina Palau-Caballero1, John Walmsley2, John Gorcsan3, Joost Lumens2, Tammo Delhaas2. 1. Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. Electronic address: g.palaucaballero@maastrichtuniversity.nl. 2. Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands. 3. University of Pittsburgh, Pittsburgh, Pennsylvania.
Abstract
BACKGROUND: Assessment of aortic regurgitation (AR) severity is often based on Doppler echocardiographic imaging. Hemodynamic responses to AR are influenced by the interplay among cardiovascular properties, including left ventricular (LV) and aortic tissue properties, that cannot be measured directly. The aim of this study was to investigate how both echocardiographic measures of AR severity and the hemodynamic consequences of AR are influenced by LV and aortic stiffness. METHODS: AR was simulated using the CircAdapt computational model of the human cardiovascular system. Simulations were performed with normal LV and aortic stiffness, high LV stiffness, high aortic stiffness, and high LV and aortic stiffness. For each configuration of levels of stiffness, four AR severity grades were simulated by setting the effective regurgitant orifice area (ROA) of the aortic valve at 0, 0.05, 0.25, and 0.6 cm2, representing no, mild, moderate, and severe AR, respectively. The regurgitant volume, regurgitant fraction (RF), and pressure half-time (PHT) were computed for each simulation giving an AR severity score (mild, moderate, or severe). Mean left atrial pressure was also calculated. RESULTS: Increasing ROA resulted in faster decay of diastolic flow velocity and larger regurgitant blood flow across the aortic valve. This caused shorter PHT and larger regurgitant volume and RF, all indicating higher AR severity. Increasing aortic stiffness resulted in a larger decline in diastolic aortic pressure, whereas increasing LV stiffness resulted in a larger rise in diastolic LV pressure. Hence, increasing LV and/or aortic stiffness led to faster decay of the transvalvular pressure gradient and, therefore, to faster decay of diastolic flow velocity across the aortic valve compared with normal stiffness with the same ROA. This faster decay led, on one hand, to a shorter PHT, indicating higher severity scores, and, on the other hand, to a lower RF, as less regurgitant blood volume traveled into the left ventricle, indicating lower severity scores. AR severity scores reflected mean left atrial pressure poorly when variations in tissue properties were present. CONCLUSIONS: Simulating altered AR hemodynamics caused by variations in cardiovascular tissue properties led to inconsistent severity scores when evaluating the severity using RF, regurgitant volume, and PHT. In this situation, pulmonary congestion is poorly reflected by AR severity as quantified by ROA, RF, and PHT. Cardiac and aortic tissue properties should therefore be taken into account to improve clinical assessment of AR severity.
BACKGROUND: Assessment of aortic regurgitation (AR) severity is often based on Doppler echocardiographic imaging. Hemodynamic responses to AR are influenced by the interplay among cardiovascular properties, including left ventricular (LV) and aortic tissue properties, that cannot be measured directly. The aim of this study was to investigate how both echocardiographic measures of AR severity and the hemodynamic consequences of AR are influenced by LV and aortic stiffness. METHODS: AR was simulated using the CircAdapt computational model of the human cardiovascular system. Simulations were performed with normal LV and aortic stiffness, high LV stiffness, high aortic stiffness, and high LV and aortic stiffness. For each configuration of levels of stiffness, four AR severity grades were simulated by setting the effective regurgitant orifice area (ROA) of the aortic valve at 0, 0.05, 0.25, and 0.6 cm2, representing no, mild, moderate, and severe AR, respectively. The regurgitant volume, regurgitant fraction (RF), and pressure half-time (PHT) were computed for each simulation giving an AR severity score (mild, moderate, or severe). Mean left atrial pressure was also calculated. RESULTS: Increasing ROA resulted in faster decay of diastolic flow velocity and larger regurgitant blood flow across the aortic valve. This caused shorter PHT and larger regurgitant volume and RF, all indicating higher AR severity. Increasing aortic stiffness resulted in a larger decline in diastolic aortic pressure, whereas increasing LV stiffness resulted in a larger rise in diastolic LV pressure. Hence, increasing LV and/or aortic stiffness led to faster decay of the transvalvular pressure gradient and, therefore, to faster decay of diastolic flow velocity across the aortic valve compared with normal stiffness with the same ROA. This faster decay led, on one hand, to a shorter PHT, indicating higher severity scores, and, on the other hand, to a lower RF, as less regurgitant blood volume traveled into the left ventricle, indicating lower severity scores. AR severity scores reflected mean left atrial pressure poorly when variations in tissue properties were present. CONCLUSIONS: Simulating altered AR hemodynamics caused by variations in cardiovascular tissue properties led to inconsistent severity scores when evaluating the severity using RF, regurgitant volume, and PHT. In this situation, pulmonary congestion is poorly reflected by AR severity as quantified by ROA, RF, and PHT. Cardiac and aortic tissue properties should therefore be taken into account to improve clinical assessment of AR severity.
Authors: Sjoerd Bouwmeester; Tim van Loon; Meike Ploeg; Thomas P Mast; Nienke J Verzaal; Lars B van Middendorp; Marc Strik; Frans A van Nieuwenhoven; Lukas R Dekker; Frits W Prinzen; Joost Lumens; Patrick Houthuizen Journal: PLoS One Date: 2022-07-15 Impact factor: 3.752