Risk Factor For Aortic Regurgitation Research Articles

Aortic Regurgitation Requiring Unplanned Surgery following Transcatheter Closure of Ventricular Septal Defect in Children: Incidence and Risk Factors

Introduction: Our aim was to investigate the incidence and risk factors for aortic regurgitation (AR) requiring unplanned surgery after transcatheter closure of ventricular septal defect (VSD) in children. Methods: Medical records of 876 children with VSD who underwent transcatheter closure from July 2009 to September 2018 in our hospital were retrospectively reviewed. Groups with and without new-onset or increasing AR requiring unplanned surgery were compared. Univariate and multivariate analyses were used to identify the possible risk factors. Smoothing plot and threshold effect analysis were carried out to find the relationship between possible factors and risk of new-onset or increasing AR. Results: A total of 29 children (3.3%) underwent unplanned surgery after transcatheter closure owing to new-onset or increasing AR, including 6 children with new-onset AR and 23 children with increasing AR. Multivariate regression analysis revealed that preoperative mild AR (OR: 60.39, 95% CI: 11.53–316.30, p < 0.001), larger ratio between diameter to body surface area (OR: 1.25, 95% CI: 1.01–1.55, p = 0.039), intracristal VSD (OR: 34.09, 95% CI: 4.07–285.65, p < 0.001), and shorter distance from the upper edge of defect to the aortic valve (or the sub-aortic rim) (OR: 0.12, 95% CI: 0.05–0.27, p < 0.001) were risk factors for new-onset or increasing AR requiring unplanned surgery. And, low risk of AR after muscular VSD transcatheter closure was found. An L-shaped nonlinear relationship between the sub-aortic rim and the risk of new-onset or increasing AR was observed, and the risk of new-onset or increasing AR with the sub-aortic rim up to the turning point (2 mm) (adjusted OR: 0.00, 95% CI: 0.00–0.08; p =0.001). With a median time of 7.3 years’ follow-up, no new-onset or increasing AR has been found for children who initially did not have unplanned surgery. Conclusion: Preoperative mild AR, larger ratio between diameter to body surface area, intracristal VSD, and shorter distance of the sub-aortic rim (especially <2 mm) could increase the risk of new-onset or increasing AR requiring unplanned surgery after transcatheter closure of VSD.

Parametric Computational Assessment of Valvular Dysfunction in Discrete Subaortic Stenosis and Aortoseptal Angle Abnormalities

Objective: Discrete subaortic stenosis (DSS) is a left-ventricular outflow tract (LVOT) obstruction caused by a membranous lesion. DSS is commonly associated with steep aortoseptal angles (AoSAs) and is a major risk factor for aortic regurgitation (AR). However, the etiology of AR secondary to DSS remains poorly understood. This study aimed at quantifying computationally the mechanistic impact of AoSA steepening and DSS on aortic valve (AV) hemodynamics and AR development. Methods: A 2D LV geometry reconstructed from cine-MRI data was connected to an AV geometry to generate a unified 2D LV-AV model (Figure 1A). Six geometrical variants were considered: unobstructed (CTRL) and DSS-obstructed LVOT (DSS), each reflecting three AoSA variations (110°, 120°, 130°). (Figure 1B). Fluid-structure interaction simulations were run to compute LV blood flow, AV leaflet dynamics, and regurgitant fraction (RF). Results: AoSA steepening and DSS generated vortex dynamics alterations and stenotic flow conditions (Figure 1D). While the CTRL-110° generated the highest degree of leaflet opening asymmetry, DSS preferentially altered superior leaflet kinematics, and caused leaflet-dependent alterations in systolic fluttering. LVOT steepening and DSS subjected the leaflets to increasing WSS overloads (up to 94% increase in temporal shear magnitude), while DSS also increased WSS bidirectionality on the inferior leaflet belly (+0.30-point in oscillatory shear index) (Figure 1E). Although AoSA steepening and DSS increased diastolic transvalvular backflow, regurgitant fractions (RF<7%) remained below the threshold defining clinical mild AR. Conclusions: The mechanical interactions between AV leaflets and LVOT steepening/DSS hemodynamic derangements do not cause AR. However, the leaflet WSS abnormalities predicted in those anatomies provide new support to a mechanobiological etiology of AR secondary to DSS. Figure 1. Unified 2D LV-AV FSI simulations in unobstructed (CTRL) and obstructed (DSS) LVOT anatomies: A) schematic showing the LV-AV assembly, B) LVOT geometries in considered in this study, C) AV geometry with WSS characterization sites, D) snapshots of velocity vector and vorticity contour fields taken at peak systole, E) 3D surface plots regional showing time-averaged WSS characteristics for all models

Computational Assessment of Valvular Dysfunction in Discrete Subaortic Stenosis: A Parametric Study.

Discrete subaortic stenosis (DSS) is a left-ventricular outflow tract (LVOT) obstruction caused by a membranous lesion. DSS is associated with steep aortoseptal angles (AoSAs) and is a risk factor for aortic regurgitation (AR). However, the etiology of AR secondary to DSS remains unknown. This study aimed at quantifying computationally the impact of AoSA steepening and DSS on aortic valve (AV) hemodynamics and AR. An LV geometry reconstructed from cine-MRI data was connected to an AV geometry to generate a unified 2D LV-AV model. Six geometrical variants were considered: unobstructed (CTRL) and DSS-obstructed LVOT (DSS), each reflecting three AoSA variations (110°, 120°, 130°). Fluid-structure interaction simulations were run to compute LVOT flow, AV leaflet dynamics, and regurgitant fraction (RF). AoSA steepening and DSS generated vortex dynamics alterations and stenotic flow conditions. While the CTRL-110° model generated the highest degree of leaflet opening asymmetry, DSS preferentially altered superior leaflet kinematics, and caused leaflet-dependent alterations in systolic fluttering. LVOT steepening and DSS subjected the leaflets to increasing WSS overloads (up to 94% increase in temporal shear magnitude), while DSS also increased WSS bidirectionality on the inferior leaflet belly (+ 0.30-point in oscillatory shear index). Although AoSA steepening and DSS increased diastolic transvalvular backflow, regurgitant fractions (RF < 7%) remained below the threshold defining clinical mild AR. The mechanical interactions between AV leaflets and LVOT steepening/DSS hemodynamic derangements do not cause AR. However, the leaflet WSS abnormalities predicted in those anatomies provide new support to a mechanobiological etiology of AR secondary to DSS.

Impact of Aortoseptal Angle Abnormalities and Discrete Subaortic Stenosis on Left-Ventricular Outflow Tract Hemodynamics: Preliminary Computational Assessment.

Discrete subaortic stenosis (DSS) is an obstruction of the left ventricular outflow tract (LVOT) due to the formation of a fibromuscular membrane upstream of the aortic valve. DSS is a major risk factor for aortic regurgitation (AR), which often persists after surgical resection of the membrane. While the etiology of DSS and secondary AR is largely unknown, the frequent association between DSS and aortoseptal angle (AoSA) abnormalities has supported the emergence of a mechanobiological pathway by which hemodynamic stress alterations on the septal wall could trigger a biological cascade leading to fibrosis and membrane formation. The resulting LVOT flow disturbances could activate the valve endothelium and contribute to AR. In an effort to assess this hypothetical mechano-etiology, this study aimed at isolating computationally the effects of AoSA abnormalities on septal wall shear stress (WSS), and the impact of DSS on LVOT hemodynamics. Two-dimensional computational fluid dynamics models featuring a normal AoSA (N-LV), a steep AoSA (S-LV), and a steep AoSA with a DSS lesion (DSS-LV) were designed to compute the flow in patient-specific left ventricles (LVs). Boundary conditions consisted of transient velocity profiles at the mitral inlet and LVOT outlet, and patient-specific LV wall motion. The deformation of the DSS lesion was computed using a two-way fluid-structure interaction modeling strategy. Turbulence was accounted for via implementation of the k-ω turbulence model. While the N-LV and S-LV models generated similar LVOT flow characteristics, the DSS-LV model resulted in an asymmetric LVOT jet-like structure, subaortic stenotic conditions (up to 2.4-fold increase in peak velocity, 45% reduction in effective jet diameter vs. N-LV/S-LV), increased vorticity (2.8-fold increase) and turbulence (5- and 3-order-of-magnitude increase in turbulent kinetic energy and Reynolds shear stress, respectively). The steep AoSA subjected the septal wall to a 23% and 69% overload in temporal shear magnitude and gradient, respectively, without any substantial change in oscillatory shear index. This study reveals the existence of WSS overloads on septal wall regions prone to DSS lesion formation in steep LVOTs, and the development of highly turbulent, stenotic and asymmetric flow in DSS LVOTs, which support a possible mechano etiology for DSS and secondary AR.

Long-term outcomes and risk factors for aortic regurgitation after discrete subvalvular aortic stenosis resection in children

ObjectivesTo characterise long-term outcomes after discrete subaortic stenosis (DSS) resection and to identify risk factors for reoperation and aortic regurgitation (AR) requiring repair or replacement.MethodsAll patients who underwent DSS resection...

Eisenmenger Ventricular Septal Defect: Classification, Morphology, and Indications for Surgery

This study aimed to examine the definition and indications for surgery, to elucidate the morphologic substrate of aortic regurgitation, and to extrapolate the pathologic mechanisms of subpulmonary stenosis in Eisenmenger ventricular septal defect (EVSD). The study enrolled 160 patients. Preoperative respiratory symptoms and poor growth were present in 41 patients (26%), and 21 patients (13%) required mechanical ventilation. Perimembranous ventricular septal defect (pVSD) had been diagnosed previously for 136 of the patients (85%) at other institutions. Of the 160 patients, 51 (32%) had muscular posteroinferior rims. Aortic regurgitation was experienced by 36 patients (23%), found to be mild in 31 cases (19%) and moderate in 5 cases (3%). None of the patients had severe regurgitation. No aortic valvuloplasty was performed. The significant risk factors for aortic regurgitation were subpulmonary stenosis (p=0.001) and a muscular posteroinferior rim (p=0.000). Subpulmonary stenosis was seen in 57 patients (35%), found to be mild to moderate in 42 cases (26%) and severe in 15 cases (9%). Adequacy of the stenosis band was repaired through the tricuspid valve for 57 of these patients. The definition of EVSD should identify it as a subgroup different from pVSD, and it should be closed as soon as it is identified in developing countries. Aortic regurgitation occurs rarely, and aortic valvoplasty should be performed if it exceeds a moderate level. The subpulmonary stenosis can be repaired through the tricuspid valve.

Aortic root replacement with the pulmonary autograft: an invariably competent aortic valve?

Background. Pulmonary autograft aortic root replacement was used in adults. Risk factors for aortic regurgitation (AR), and for pulmonary allograft valve stenosis are identified. Methods. From February 1991 through April 1998, 80 adults (mean age 34.4 years) underwent pulmonary autograft aortic root replacement. Primary diagnosis was AR in 43 (53.7%) patients, aortic stenosis in 13 (16.3%) and mixed disease in 24 (30%) patients. A root reinforcement ring was used in 32 (40%) patients. Results. There was no hospital mortality. Estimated patient survival is 100% at 7 years. A total of 3 patients underwent reoperation: 2 on the autograft for severe AR, 1 for pulmonary allograft stenosis. Freedom from reoperation on the autograft is 96.7 ± 2.4% at 7 years. Multivariate analysis indicated bicuspid aortic valve disease as an incremental risk factor for AR at discharge ( p = 0.036, odds 3.5). Univariate analysis identified operation for pure AR as risk factor for AR during follow-up ( p = 0.041). Mild AR or more increased from 2.5% at discharge to 11.3% during follow-up ( p = 0.008). Progression of AR was limited by the use of a reinforcement root ring ( p = 0.031). Freedom from mild AR or more in patients with and without a reinforcement root ring was 100% and 72.9 ± 9.3% respectively, at 5 years ( p = 0.119). Pulmonary allograft stenosis occurred in 15 (22.5%) patients. Multivariate analysis revealed that large sized pulmonary allografts were less prone to stenosis ( p = 0.048, odds 0.13). Conclusions. Pulmonary autograft root replacement can be performed with few complications. During follow-up, a significant increase in mild AR or more is observed. The use of a reinforcement root ring is effective in preventing progression of AR.