Left Ventricular Outflow Tract Flow Research Articles

Examining temporal changes in model-optimized parameters using longitudinal hemodynamic measurements

BackgroundWe previously applied hemodynamic data to personalize a mathematical model of the circulation expressed as physically interpretable parameters. The aim of this study was to identify patterns in the data that could potentially explain the estimated parameter changes. This included investigating whether the parameters could be used to track the effect of physical activity on high blood pressure. Clinical trials have repeatedly detected beneficial changes in blood pressure after physical activity and uncovered changes in lower level phenotypes (such as stiffened or high-resistance blood vessels). These phenotypes can be characterized by parameters describing the mechanical properties of the circulatory system. These parameters can be incorporated in and contextualized by physics-based cardiovascular models of the circulation, which in combination can become tools for monitoring cardiovascular disease progression and management in the future.MethodsClosed-loop and open-loop models of the left ventricle and systemic circulation were previously optimized to data from a pilot study with a 12-week exercise intervention period. Basal characteristics and hemodynamic data such as blood pressure in the carotid, brachial and finger arteries, as well as left-ventricular outflow tract flow traces were collected in the trial. Model parameters estimated for measurements made on separate days during the trial were used to compute parameter changes for total peripheral resistance, systemic arterial compliance, and maximal left-ventricular elastance. We compared the changes in these cardiovascular model-based estimates to changes from more conventional estimates made without the use of physics-based models by correlation analysis. Additionally, ordinary linear regression and linear mixed-effects models were applied to determine the most informative measurements for the selected parameters. We applied maximal aerobic capacity (measured as VO2max\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\ ext{VO2max}$$\\end{document}) data to examine if exercise had any impact on parameters through regression analysis and case studies.Results and conclusionsParameter changes in arterial parameters estimated using the cardiovascular models correlated moderately well with conventional estimates. Estimates based on carotid pressure waveforms gave higher correlations (0.59 and above when p<0.05\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$<0.05$$\\end{document}) than those for finger arterial pressure. Parameter changes over the 12-week study duration were of similar magnitude when compared to short-term changes after a bout of intensive exercise in the same parameters. The short-term changes were computed from measurements made immediately before and 24 h after a cardiopulmonary exercise test used to measure VO2max\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\ ext{VO2max}$$\\end{document}. Regression analysis indicated that changes in VO2max\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\ ext{VO2max}$$\\end{document} did not account for any substantial amount of variability in total peripheral resistance, systemic arterial compliance, or maximal left-ventricular elastance. On the contrary, changes in stroke volume contributed to far more explained variability. The results suggest that more research is required to be able to accurately track exercise-induced changes in the vasculature for people with pre-hypertension and hypertension using lumped-parameter models.

Flow pattern analysis of right ventricular outflow tract in repaired tetralogy of Fallot through 4D flow MRI.

Cardiac magnetic resonance imaging (CMR) often shows discrepancies between right ventricular outflow tract (RVOT) flow and left ventricular outflow tract flow in patients with late-stage repaired tetralogy of Fallot (rTOF), leading to potential errors in pulmonary regurgitation fraction (PRF) assessment. This study aimed to identify the conditions under which RVOT flow can be acutely evaluated using four-dimensional (4D) flow CMR. Twenty-seven consecutive patients with rTOF underwent both two-dimensional phase-contrast (2D PC) and 4D flow CMR between 2016 and 2018, excluding those with peripheral pulmonary artery stenosis, RVOT conduit replacement, unknown surgical method, and an aortic valve regurgitation greater than 20%. Seven healthy controls also underwent only 4D Flow CMR. All healthy controls and fifteen patients with rTOF showed laminar RVOT flow, while seven patients exhibited helical, and four patients exhibited vortical RVOT flow in 4D flow CMR visualization. Flow-volume concordance between the pulmonary artery and aortic flow was significantly lower in patients with rTOF and PRF > 40% in 2D PC CMR. This concordance rate in the suprapulmonary valve was high in both the TOF and control groups, comparing at five RVOT locations in 4D flow CMR. Regarding RVOT flow regurgitation in 4D flow, the whole bulk evaluation exhibited greater variation depending on the flow type compared to the whole pixel-wise evaluation. The study confirmed the flow volume at the upper section of the pulmonary valve as the most accurate correlate of aortic flow volume. Furthermore, the 4D flow CMR using the pixel-wise method demonstrated superior accuracy compared to the traditional bulk flow method.

First description and validation of a new method for estimating aortic stenosis burden and predicting the functional response to TAVI.

Up to one-fifth of patients continue to have poor quality of life after transcatheter aortic valve implantation (TAVI), with an additional similar proportion not surviving 1 year after the procedure. We aimed to assess the value of a new method based on an integrated analysis of left ventricular outflow tract flow velocity and aortic pressure to predict objective functional improvement and prognosis after TAVI. In a cohort of consecutive patients undergoing TAVI, flow velocity-pressure integrated analysis was obtained from simultaneous pressure recordings in the ascending aorta and flow velocity recordings in the left ventricular outflow tract by echocardiography. Objective functional improvement 6 months after TAVI was assessed through changes in a 6-min walk test and NT-proBNP levels. A clinical follow-up was conducted at 2 years. Of the 102 patients studied, 82 (80.4%) showed objective functional improvement. The 2-year mortality of these patients was significantly lower (9% vs. 44%, p = 0.001). In multivariate analysis, parameter "(Pressure at Vmax - Pressure at Vo)/Vmax" was found to be an independent predictor for objective improvement. The C-statistic was 0.70 in the overall population and 0.78 in the low-gradient subgroup. All echocardiographic parameters and the valvuloarterial impedance showed a C-statistic of <0.6 for the overall and low-gradient patients. In a validation cohort of 119 patients, the C-statistic was 0.67 for the total cohort and 0.76 for the low-gradient subgroup. This new method allows predicting objective functional improvement after TAVI more precisely than the conventional parameters used to assess the severity of aortic stenosis, particularly in low-gradient patients.

Impact of Premature Ventricular Complex (PVC) Burden on the Left Ventricle in the Structurally Normal Heart: Hemodynamic Alterations of Idiopathic PVC on Echocardiography.

Premature ventricular complex (PVC) without structural heart disease is mostly viewed as a benign arrhythmia. However, the high burden of PVC causes cardiomyopathy due to intraventricular dyssynchrony. The effects of ectopic contraction on left ventricular (LV) hemodynamics in the structurally normal heart are unclear. To examine the effect of PVC burden on LV dimension, LV systolic function, and intraventricular blood flow, and to determine whether ectopic ventricular contraction affects LV hemodynamics. Patients aged ≥ 18 years with PVC ≥ 5% on Holter recording were enrolled and divided into groups G1 (5-10%), G2 (10-20%), and G3 (≥ 20%). We excluded patients with structural heart diseases, pacemakers, and LV systolic dysfunction [LV ejection fraction (LVEF) < 50%]. Clinical characteristics and routine transthoracic echocardiography parameters were compared. The end-systolic LV internal dimension increased according to the PVC burden from G1 to G3 (p = 0.001). LVEF was inversely associated with PVC burden from G1 to G3 (p = 0.002). The same pattern was seen for LV outflow tract (LVOT) maximal velocity (p = 0.005) and maximal pressure gradient (PG) (p = 0.005), LVOT velocity time integral (VTI) (p = 0.03) and LV stroke volume index (LVSI) (p = 0.008). Systolic function and LV end-systolic dimension were inversely associated with PVC burden. Decreased LVOT flow velocity and PG were related to increased PVC burden. LVOT VTI and LVSI were smaller when the PVC burden exceeded 20%. These negative hemodynamic manifestations of idiopathic PVC were considerable even in structure normal hearts, hence the early elimination of PVC is strongly advised.

Fluid structure computational model of simulating mitral valve motion in a contracting left ventricle

Background:Fluid structure interaction simulations h hold promise in studying normal and abnormal cardiac function, including the effect of fluid dynamics on mitral valve (MV) leaflet motion. The goal of this study was to develop a 3D fluid structure interaction computational model to simulate bileaflet MV when interacting with blood motion in left ventricle (LV). Methods:The model consists of ideal geometric-shaped MV leaflets and the LV, with MV dimensions based on human anatomical measurements. An experimentally-based hyperelastic isotropic material was used to model the mechanical behaviour of the MV leaflets, with chordae tendineae and papillary muscle tips also incorporated. LV myocardial tissue was prescribed using a transverse isotropic hyperelastic formulation. Incompressible Navier–Stokes fluid formulations were used to govern the blood motion, and the Arbitrary Lagrangian Eulerian (ALE) method was employed to determine the mesh deformation of the fluid and solid domains due to trans-valvular pressure on MV boundaries and the resulting leaflet movement. Results:The LV–MV generic model was able to reproduce physiological MV leaflet opening and closing profiles resulting from the time-varying atrial and ventricular pressures, as well as simulating normal and prolapsed MV states. Additionally, the model was able to simulate blood flow patterns after insertion of a prosthetic MV with and without left ventricular outflow tract flow obstruction. In the MV–LV normal model, the regurgitant blood flow fraction was 10.1 %, with no abnormality in cardiac function according to the mitral regurgitation severity grades reported by the American Society of Echocardiography. Conclusion:Our simulation approach provides insights into intraventricular fluid dynamics in a contracting LV with normal and prolapsed MV function, as well as aiding in the understanding of possible complications after transcatheter MV implantation prior to clinical trials.

Significance of aortoseptal angle anomalies to left ventricular hemodynamics and subaortic stenosis: A numerical study

Discrete subaortic stenosis (DSS) is an obstructive cardiac disease caused by a membranous lesion in the left ventricular (LV) outflow tract (LVOT). Although its etiology is unknown, the higher prevalence of DSS in LVOT anatomies featuring a steep aortoseptal angle (AoSA) suggests a potential role for hemodynamics. Therefore, the objective of this study was to quantify the impact of AoSA steepening on the LV three-dimensional (3D) hemodynamic stress environment. A 3D LV model reconstructed from cardiac cine-magnetic resonance imaging was connected to four LVOT geometrical variations spanning the clinical AoSA range (115°-160°). LV hemodynamic stresses were characterized in terms of cycle-averaged pressure, temporal shear magnitude (TSM), and oscillatory shear index. The wall shear stress (WSS) topological skeleton was further analyzed by computing the scaled divergence of the WSS vector field. AoSA steepening caused an increasingly perturbed subaortic flow marked by LVOT flow skewness and complex 3D secondary flow patterns. These disturbances generated WSS overloads (>45% increase in TSM vs. 160° model) on the inferior LVOT wall, and increased WSS contraction (>66% decrease in WSS divergence vs. 160° model) in regions prone to DSS membrane formation. AoSA steepening generated substantial hemodynamic stress abnormalities in LVOT regions prone to DSS formation. Further studies are needed to assess the possible impact of such mechanical abnormalities on the tissue and cellular responses.

Application of the proximal isovelocity surface area method for estimation of the effective orifice area in aortic stenosis

Although the echocardiographic effective orifice area (EOA) calculated using the continuity equation is widely used for the assessment of severity in aortic stenosis (AS), the existence of high flow velocity at the left ventricular outflow tract (LVOT) potentially causes its overestimation. The proximal isovelocity surface area (PISA) method could be an alternative tool for the estimation of EOA that limits the influence of upstream flow velocity. EOA was calculated using the continuity equation (EOACont) and PISA method (EOAPISA), respectively, in 114 patients with at least moderate AS. The geometric orifice area (GOA) was also measured using the planimetry method in 51 patients who also underwent three-dimensional transesophageal echocardiography. Patients were divided into two groups according to the median LVOT flow velocity. EOAPISA could be obtained in 108 of the 114 patients (95%). Although there was a strong correlation between EOACont and EOAPISA (r = 0.78, P < 0.001), EOACont was statistically significantly larger than EOAPISA (0.86 ± 0.33 vs 0.75 ± 0.29 cm2, P < 0.001). Both EOACont and EOAPISA similarly correlated with GOA (r = 0.70, P < 0.001 and r = 0.77, P < 0.001, respectively). However, a fixed bias, which is hydrodynamically supposed to exist between EOA and GOA, was not observed between EOACont and GOA. In contrast, there was a negative fixed bias between EOAPISA and GOA with smaller EOAPISA than GOA. The difference between EOACont and GOA was significantly greater with a larger EOACont relative to GOA in patients with high LVOT flow velocity than in those without (0.16 ± 0.25 vs - 0.07 ± 0.10 cm2, P < 0.001). In contrast, the difference between EOAPISA and GOA was consistent regardless of the LVOT flow velocity (- 0.07 ± 0.12 vs - 0.07 ± 0.15 cm2, P = 0.936). The PISA method was applied to estimate EOA in patients with AS. EOAPISA could be an alternative parameter for AS severity grading in patients with high LVOT flow velocity in whom EOACont would potentially overestimate the orifice area.

Dynamic nature of the LVOT following transcatheter mitral valve replacement with LAMPOON: new insights from post-procedure imaging.

To characterize the dynamic nature of the left ventricular outflow tract (LVOT) geometry and flow rate in patients following transcatheter mitral valve replacement (TMVR) with anterior leaflet laceration (LAMPOON) and derive insights to help guide future patient selection. Time-resolved LVOT geometry and haemodynamics were analysed with post-procedure computed tomography and echocardiography in subjects (N = 19) from the LAMPOON investigational device exemption trial. A novel post hoc definition for LVOT obstruction was employed to account for systolic flow rate and quality of life improvement [obstruction was defined as LVOT gradient >30 mmHg or LVOT effective orifice area (EOA) ≤1.15 cm2]. The neo-LVOT and skirt neo-LVOT were observed to vary substantially in area throughout systole (64 ± 27% and 25 ± 14% change in area, respectively). The peak systolic flow rate occurred most commonly just prior to mid-systole, while minimum neo-LVOT (and skirt neo-LVOT) area occurred most commonly in early-diastole. Subjects with LVOT obstruction (n = 5) had smaller skirt neo-LVOT values across systole. Optimal thresholds for skirt neo-LVOT area were phase-specific (260, 210, 200, and 180 mm2 for early-systole, peak flow, mid-systole, and end-systole, respectively). The LVOT geometry and flow rate exhibit dynamic characteristics following TMVR with LAMPOON. Subjects with LVOT obstruction had smaller skirt neo-LVOT areas across systole. The authors recommend the use of phase-specific threshold values for skirt neo-LVOT area to guide future patient selection for this procedure. LVOT EOA is a 'flow-independent' metric which has the potential to aid in characterizing LVOT obstruction severity.

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.

Factors contributing to energy loss in left ventricle during diastolic and systolic phases in elderly patients.

The change of left ventricular function deteriorated with age because of gradual increases of blood pressure may result in increased energy loss (EL) in left ventricle (LV). The present study investigated EL in LV among hypertensive elderly patients and examined factors contributing to EL. A single-center retrospective study was performed on elderly hypertensive outpatients (≥65 years) who underwent echocardiography (N = 105). EL in the LV was measured using a vector flow mapping system, and factors affecting peak EL during the early-diastolic phase (ED-EL), late-diastolic phase (LD-EL), and systolic phase (Sys-EL) were evaluated. Mean age was 79.9 ± 6.4 years (male 43%). Mean ED-EL, LD-EL, and Sys-EL were 42.1 ± 46.7, 75.6 ± 60.2, and 40.4 ± 40.2 mJ/N/s. In a stepwise regression analysis, the E/e'(lateral) (unstandardized B = 0.005, 95%CI -0.03 to 0.007, standardized β = 0.434, P < .001) was identified as factors affecting ED-EL. The factors affecting LD-EL were E/A ratio (B = -0.122, 95%CI -0.176 to -0.068, β = -0.470, P < .001) and time velocity integral (TVI) in LVOT (unstandardized B = 0.002, 95%CI 0.000 to 0.004, β = 0.247, P = .021). The factors influencing Sys-EL were TVI in LVOT (B = 0.002, 95%CI 0.001 to 0.004, β = 0.390, P < .001), E/A ratio (B = -0.054, 95%CI -0.093 to -0.015, β = -0.258, P = .008), left ventricular outflow tract (LVOT) diameter (B = -0.006, 95%CI -0.010 to -0.002, β = -0.307, P = .006), and left ventricular mass index (B = 0.000, 95%CI 0.000 to 0.001, β = 0.208, P = .039). Peak EL in the LV was higher during diastolic phase than systolic phase among elderly hypertensive patients. Peak EL both during late-diastolic phase and systolic phase was affected by systolic blood flow in LVOT and LV transmitral flow pattern.

Abstract 12586: Assessing Valvuloarterial Impedance in Aortic Stenosis: A Comparison of Echocardiographic- and Cardiac Magnetic Resonance-derived Methods

Introduction: Valvuloarterial impedance (Z VA ) represents the valvular and arterial factors that oppose Left Ventricular (LV) ejection and is recognised as an important index to assess global LV load in patients with Aortic Stenosis (AS). Z VA is traditionally determined by Transthoracic Echocardiogram (TTE) and brachial cuff pressure. Hypothesis: Our study sought to compare Z VA-TTE with Z VA calculated using a simultaneous Cardiac Magnetic Resonance (CMR) and Applanation Tonometry (AT) (Z VA-CMR ) technique to determine whether TTE measurement of aortic flow velocity resulted in an underestimation of Z VA. Methods: Twenty AS patients underwent a protocol of CMR/AT followed by TTE. Z VA-CMR was determined as the relationship of derived aortic pressure (radial) to CMR aortic flow velocity in the frequency domain. Z VA-TTE was determined from digitised flow velocity within the left ventricular outflow tract (LVOT) on pulsed-wave Doppler and derived central pressure waveforms. Systemic vascular resistance (SVR) was calculated from mean pressure and flow. Values from both methods were compared. Results: Our study found that Z VA-TTE values (mean±SD, 638±381 dyne.s.cm -3 ) were consistently lower (p=0.07) than Z VA-CMR values (946±318 dyne.s.cm -3 ), and attribute this to an overestimation of LVOT flow velocity on TTE. SVR calculated by CMR/AT (2215±616 dyne.s.cm -5 ) was almost four times higher than TTE (618±245 dyne.s.cm -5 ) (p&lt;0.001). This is due to more robust axi-symmetrical sampling of aortic flow across the entire cross-section of the ascending aorta (well above the stenotic jet) during CMR, than using operator-dependent TTE. Conclusions: Whilst Z VA -TTE is commonly performed in patients with AS to assess global LV load, newer methods to assess Z VA using simultaneous CMR/AT likely represent a more accurate non-invasive assessment.

Left-ventricular outflow tract acceleration time is associated with symptoms in patients with obstructive hypertrophic cardiomyopathy

AimsNot all obstructive hypertrophic cardiomyopathy (HCM) patients are symptomatic. The relation between obstructive HCM and symptoms is not well understood. The hypothesis of this study is that left-ventricular outflow tract (LVOT) acceleration time (AT) is associated with symptoms.MethodsWe included 187 patients (61% men, mean age 55 ± 14 years) with obstructive HCM, defined as a maximal wall thickness ≥ 15 mm and a resting or provoked LVOT peak gradient ≥ 30 mmHg. Peak velocity (PV), left-ventricular (LV) ejection time (ET), and AT (the time between LVOT flow onset and the moment of PV) were measured on continuous-wave (CW) Doppler tracings. Logistic and Cox proportional hazard regression analyses were used to evaluate the relation between symptoms [New York Heart Association (NYHA) class ≥ II] and echocardiographic measurements, including AT. Reproducibility was assessed using the intraclass correlation coefficient (ICC).ResultsSymptomatic patients were more often female and had higher mean AT values. Logistic regression demonstrated a significant association between AT and symptomatic status (odds ratio 1.31 per 10 ms, p < 0.01) after adjustment for sex, negative inotropes, PV, LVOT diameter, and diastolic dysfunction. AT was independently associated with symptoms and septal reduction during follow-up (hazard ratio 1.09 per 10 ms, p < 0.05). The ICC was 0.98 with a mean difference of 0.28 ± 8.4 ms.ConclusionIn obstructive HCM patients, increased AT is significantly related to symptoms after adjustment for sex, negative inotropes, PV, LVOT diameter, and diastolic dysfunction, and is associated with the symptomatic status during follow-up. AT represents an easily measured echocardiographic variable with excellent inter-reader reproducibility.

Feasibility of Estimation of Aortic Wave Intensity Using Non-invasive Pressure Recordings in the Absence of Flow Velocity in Man.

BackgroundWave intensity analysis provides valuable information on ventriculo-arterial function, hemodynamics, and energy transfer in the arterial circulation. Widespread use of wave intensity analysis is limited by the need for concurrent measurement of pressure and flow waveforms. We describe a method that can estimate wave intensity patterns using only non-invasive pressure waveforms (pWIA).MethodsRadial artery pressure and left ventricular outflow tract (LVOT) flow velocity waveforms were recorded in 12 participants in the Southall and Brent Revisited (SABRE) study. Pressure waveforms were analyzed using custom-written software to derive the excess pressure (Pxs) which was scaled to peak LVOT velocity and used to calculate wave intensity. These data were compared with wave intensity calculated using the measured LVOT flow velocity waveform. In a separate study, repeat measures of pWIA were performed on 34 individuals who attended two clinic visits at an interval of ≈1 month to assess reproducibility and reliability of the method.ResultsPxs waveforms were similar in shape to aortic flow velocity waveforms and the time of peak Pxs and peak aortic velocity agreed closely. Wave intensity estimated using pWIA showed acceptable agreement with estimates using LVOT velocity tracings and estimates of wave intensity were similar to values reported previously in the literature. The method showed fair to good reproducibility for most parameters.ConclusionThe Pxs is a surrogate of LVOT flow velocity which, when appropriately scaled, allows estimation of aortic wave intensity with acceptable reproducibility. This may enable wider application of wave intensity analysis to large studies.

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.

291 Assessing Valvuloarterial Impedance in Aortic Stenosis: A Comparison of Echocardiographic- and Cardiac Magnetic Resonance-derived Methods

Valvuloarterial impedance (ZVA) represents the valvular and arterial factors that oppose Left Ventricular (LV) ejection and is recognised as an important index to assess global LV load in patients with Aortic Stenosis (AS). ZVA is traditionally determined by Transthoracic Echocardiogram (TTE) and brachial cuff pressure. Our study sought to compare ZVA-TTE with ZVA calculated using a simultaneous Cardiac Magnetic Resonance (CMR) and Applanation Tonometry (AT) (ZVA-CMR) technique. Twenty AS patients underwent a protocol of CMR/AT followed by TTE. ZVA-CMR was determined as the relationship of derived aortic pressure (radial) to CMR aortic flow velocity in the frequency domain. ZVA-TTE was determined from digitised flow velocity within the left ventricular outflow tract (LVOT) on pulsed-wave Doppler and derived central pressure waveforms. Systemic vascular resistance (SVR) was calculated from mean pressure and flow. Values from both methods were compared. Our study found that ZVA-TTE values (mean±SD, 638±381 dyne.s.cm-3) were consistently lower (p=0.07) than ZVA-CMR values (946±318 dyne.s.cm-3), and attribute this to an overestimation of LVOT flow velocity on TTE. SVR calculated by CMR/AT (2215±616 dyne.s.cm-5) was almost four times higher than TTE (618±245 dyne.s.cm-5) (p<0.001). This is due to more robust axi-symmetrical sampling of aortic flow across the entire cross-section of the ascending aorta (well above the stenotic jet) during CMR, than using operator-dependent TTE. Whilst ZVA -TTE is commonly performed in patients with AS to assess global LV load, newer methods to assess ZVA using simultaneous CMR/AT likely represent a more accurate non-invasive assessment.

P802 Delayed time to peak left ventricular outflow tract velocity is associated with symptomatic status in patients with hypertrophic obstructive cardiomyopathy

Abstract Funding Acknowledgements None. The presence and magnitude of left ventricular outflow tract (LVOT) obstruction in hypertrophic obstructive cardiomyopathy (HOCM) patients is weakly associated with presence of symptoms. The factors underlying this are not well understood. We hypothesize that time to peak velocity (TPV) of LVOT flow is associated with symptomatic status. We included 136 HOCM patients (58% men, mean age 55 ± 14 years) with peak gradients ≥30 mmHg at rest or during Valsalva without aortic valve stenosis. At rest and during Valsalva, continuous wave Doppler tracings from 3 consecutive beats were used to assess peak velocity (PV), left ventricular ejection time (LVET) and TPV, which was defined as the time interval between the onset of flow over the LVOT and the moment of PV. Differences were compared between asymptomatic and symptomatic patients (defined as New York Heart Association class I vs. II-IV). The relation between symptom status and TPV was investigated using logistic regression models. A random sample of 20 patients was examined by 2 observers and reproducibility was assessed using the intraclass correlation coefficient (ICC). Symptomatic patients were more often female (table) and had significantly higher mean TPV values (figure). In multivariable logistic regression models, TPV was an independent predictor of symptomatic status after correction for PV, LVOT diameter, heart rate and age (odds ratio 1.02 per 1 ms, p &amp;lt; 0.001). The ICC was 0.99 with a mean difference of 0.28 ± 8.5 ms. Delayed TPV is associated with symptomatic status in HOCM patients, after adjustment for heart rate, peak velocity, LVOT diameter and age, and is an easily measured echocardiographic variable with excellent inter-reader reproducibility. The clinical implications of delayed TPV, particularly in the context risk prediction and clinical decision making, remain to be determined. Characteristics per group Asymptomatic HOCM patients n = 47 Symptomatic HOCM patients n = 89 p value Age, y 55 ± 14 55 ± 14 0.99 Male gender 34 (72%) 45 (51%) 0.01 Body mass index, kg/m&amp;sup2; 27 ± 5 28 ± 5 0.08 Left atrial diameter, mm 46 ± 7 47 ± 7 0.64 Septal wall thickness, mm 18 ± 4 19 ± 5 0.58 LV outflow tract diameter, mm 22 ± 3 21 ± 3 0.001 Peak velocity, cm/s 403 ± 86 434 ± 79 0.03 LV ejection time, ms 316 ± 44 340 ± 42 0.002 Time to peak velocity, ms 157 ± 32 178 ± 32 &amp;lt;0.001 HOCM = hypertrophic obstructive cardiomyopathy, LV = left ventricular. Abstract P802 Figure. Time to peak velocity per NYHA class

Impact of left ventricular outflow tract flow acceleration on aortic valve area calculation in patients with aortic stenosis

Objective: Due to its circular shape, the area of the proximal left ventricular tract (PLVOT) adjacent to aortic valve can be derived from a single linear diameter. This is also the location of flow acceleration (FA) during systole, and pulse wave Doppler (PWD) sample volume in the PLVOT can lead to overestimation of velocity (V1) and the aortic valve area (AVA). Therefore, it is recommended to derive V1 from a region of laminar flow in the elliptical shaped distal LVOT (away from the annulus). Besides being inconsistent with the assumptions of continuity equation (CE), spatial difference in the location of flow and area measurement can result in inaccurate AVA calculation. We evaluated the impact of FA in the PLVOT on the accuracy of AVA by continuity equation (CE) in patients with aortic stenosis (AS).Methods: CE-based AVA calculations were performed in patients with AS once with PWD-derived velocity time integral (VTI) in the distal LVOT (VTILVOT) and then in the PLVOT to obtain a FA velocity profile (FA-VTILVOT) for each patient. A paired sample t-test (P < 0.05) was conducted to compare the impact of FA-VTILVOT and VTILVOT on the calculation of AVA.Result: There were 46 patients in the study. There was a 30.3% increase in the peak FA-VTILVOT as compared to the peak VTILVOT and AVA obtained by FA-VTILVOT was 29.1% higher than obtained by VTILVOT. p]Conclusion: Accuracy of AVA can be significantly impacted by FA in the PLVOT. LVOT area should be measured with 3D imaging in the distal LVOT.

Inconsistency in aortic stenosis severity between CT and echocardiography: prevalence and insights into mechanistic differences using computational fluid dynamics

ObjectivesThe aims of this study were to evaluate the inconsistency of aortic stenosis (AS) severity between CT aortic valve area (CT-AVA) and echocardiographic Doppler parameters, and to investigate potential underlying...

Preoperative apical 5-chamber view transthoracic echocardiogram—the protruding mass is causing left ventricular outflow tract flow acceleration

Preoperative apical 5-chamber view transthoracic echocardiogram—the protruding mass is causing left ventricular outflow tract flow acceleration

4D flow MRI and T1 -Mapping: Assessment of altered cardiac hemodynamics and extracellular volume fraction in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy (HCM) is associated with altered hemodynamics in the left ventricular outflow tract (LVOT) and myocardial tissue abnormalities such as fibrosis. The aim of this study was to quantify changes in LVOT 3D hemodynamics and myocardial extracellular volume fraction (ECV, measure of fibrosis) and to investigate relationships between elevated flow metrics and left ventricular (LV) tissue abnormalities. Cardiac magnetic resonance imaging (MRI) including 4D flow (field strength = 1.5T, resolution = 2.1-4.0 × 2.1-4.0 × 2.5-3.2 mm(3) ; venc = 150-250 cm/s; TE/TR/FA = 2.2-2.5msec/4.6-4.9msec/15°) for the in vivo assessment of 3D blood flow velocities with full coverage of the LVOT was applied in 35 patients with HCM (54 ± 15 years) and 10 age-matched healthy controls (45 ± 14 years). In addition, pre- and postcontrast myocardial T1 -mapping (resolution = 2.3 × 1.8 mm, slice thickness = 8 mm, TE/TR-FA = 1.0-1.1msec/2.0-2.2msec/35°) of the LV (basal, mid-ventricular, apical short axis) was performed in a subgroup of 23 HCM patients. Analysis included the segmentation of the LVOT and quantification of peak systolic LVOT pressure gradients and rate of viscous energy loss EL ' as well as left ventricular ECV. HCM patients demonstrated significantly elevated peak systolic LVOT pressure gradients (21 ± 16 mmHg vs. 9 ± 2 mmHg) and energy loss EL ' (3.8 ± 2.5 mW vs. 1.5 ± 0.7 mW, P < 0.005) compared to controls. There was a significant relationship between increased LV fibrosis (ECV) with both elevated pressure gradients (R(2) = 0.44, P < 0.001) and energy loss EL ' (R(2) = 0.46, P < 0.001). The integration of 4D-flow and T1 -mapping-MRI allowed for the evaluation of tissue and flow abnormalities in HCM patients. Our findings suggest a mechanistic link between abnormal LVOT flow, increased LV loading, and adverse myocardial remodeling in HCM.