Left Ventricular Trabeculations Decrease the Wall Shear Stress and Increase the Intra-Ventricular Pressure Drop in CFD Simulations

The aim of the present study is to characterize the hemodynamics of left ventricular (LV) geometries to examine the impact of trabeculae and papillary muscles (PMs) on blood flow using high performance computing (HPC). Five pairs of detailed and smoothed LV endocardium models were reconstructed from high-resolution magnetic resonance images (MRI) of ex-vivo human hearts. The detailed model of one LV pair is characterized only by the PMs and few big trabeculae, to represent state of art level of endocardial detail. The other four detailed models obtained include instead endocardial structures measuring ≥1 mm2 in cross-sectional area. The geometrical characterizations were done using computational fluid dynamics (CFD) simulations with rigid walls and both constant and transient flow inputs on the detailed and smoothed models for comparison. These simulations do not represent a clinical or physiological scenario, but a characterization of the interaction of endocardial structures with blood flow. Steady flow simulations were employed to quantify the pressure drop between the inlet and the outlet of the LVs and the wall shear stress (WSS). Coherent structures were analyzed using the Q-criterion for both constant and transient flow inputs. Our results show that trabeculae and PMs increase the intra-ventricular pressure drop, reduce the WSS and disrupt the dominant single vortex, usually present in the smoothed-endocardium models, generating secondary small vortices. Given that obtaining high resolution anatomical detail is challenging in-vivo, we propose that the effect of trabeculations can be incorporated into smoothed ventricular geometries by adding a porous layer along the LV endocardial wall. Results show that a porous layer of a thickness of 1.2·10−2 m with a porosity of 20 kg/m2 on the smoothed-endocardium ventricle models approximates the pressure drops, vorticities and WSS observed in the detailed models.This paper has been partially funded by CompBioMed project, under H2020-EU.1.4.1.3 European Union’s Horizon 2020 research and innovation programme, grant agreement n◦ 675451. FS is supported by a grant from Severo Ochoa (n◦ SEV-2015-0493-16-4), Spain. CB is supported by a grant from the Fundació LaMarató de TV3 (n◦ 20154031), Spain. TI and PI are supported by the Institute of Engineering in Medicine, USA, and the Lillehei Heart Institute, USA.Peer ReviewedPostprint (published version

Fractal analysis of right ventricular trabeculae in pulmonary hypertension

Purpose: To measure right ventricular (RV) trabecular complexity by its fractal dimension (FD) in healthy subjects and patients with pulmonary hypertension (PH) and assess its relationship to hemodynamic and functional parameters, and future cardiovascular events. Materials and methods: This retrospective study used data acquired from May 2004 to October 2013 for 256 patients with newly-diagnosed PH that underwent cardiac magnetic resonance (CMR) imaging, right heart catheterization and six-minute walk distance testing with a median follow-up of 4.0 years. 256 healthy controls underwent CMR only. Biventricular FD, volumes and function were assessed on short-axis cine images. Reproducibility was assessed by intraclass correlation coefficient, correlation between variables was assessed by Pearson’s correlation test, and mortality prediction compared by univariable and multivariable Cox regression analysis. Results: RV-FD reproducibility had an intraclass correlation coefficient of 0.97 (95% confidence interval [CI]: 0.96, 0.98). RV-FD was higher in PH patients than healthy subjects (median 1.310, inter-quartile range [IQR] 1.281-1.341 vs 1.264, 1.242-1.295, P <.001) with the greatest difference near the apex. RV-FD was associated with pulmonary vascular resistance (r=0.30, P <.001). In univariable Cox regression analysis, RV-FD was a significant predictor of death (hazards ratio [HR]: 1.256, CI: 1.011, 1.560, P =.04), but in a multivariable analysis did not predict survival independently of conventional parameters of RV remodeling (HR: 1.179, CI: 0.871, 1.596, P =0.29). Conclusion: Fractal analysis of RV trabecular complexity is a highly reproducible measure of remodeling in PH associated with afterload, although the gain in survival prediction over traditional markers is not significant

Evaluating the roles of detailed endocardial structures on right ventricular haemodynamics by means of CFD simulations

Computational modelling plays an important role in right ventricular (RV) haemodynamic analysis. However, current approaches use smoothed ventricular anatomies. The aim of this study is to characterise RV haemodynamics including detailed endocardial structures like trabeculae, moderator band, and papillary muscles. Four paired detailed and smoothed RV endocardium models (2 male and 2 female) were reconstructed from ex vivo human hearts high‐resolution magnetic resonance images. Detailed models include structures with ≥1 mm2 cross‐sectional area. Haemodynamic characterisation was done by computational fluid dynamics simulations with steady and transient inflows, using high‐performance computing. The differences between the flows in smoothed and detailed models were assessed using Q‐criterion for vorticity quantification, the pressure drop between inlet and outlet, and the wall shear stress. Results demonstrated that detailed endocardial structures increase the degree of intra‐ventricular pressure drop, decrease the wall shear stress, and disrupt the dominant vortex creating secondary small vortices. Increasingly turbulent blood flow was observed in the detailed RVs. Female RVs were less trabeculated and presented lower pressure drops than the males. In conclusion, neglecting endocardial structures in RV haemodynamic models may lead to inaccurate conclusions about the pressures, stresses, and blood flow behaviour in the cavity.The DICOMdatasetswere provided by the Visible Heart R Laboratory, obtained byMRI scanning of perfusion fixed hearts that were graciously donated by the organ donors and their families through LifeSource. Part of the simulation hours were provided by the CompBioMed project in the Archer supercomputer, EPCC, UK.Peer ReviewedPostprint (author's final draft

Using high resolution cardiac CT data to model and visualize patient-specific interactions between trabeculae and blood flow

Abstract. In this paper, we present a method to simulate and visualize blood flow through the human heart, using the reconstructed 4D motion of the endocardial surface of the left ventricle as boundary conditions. The reconstruction captures the motion of the full 3D surfaces of the complex features, such as the papillary muscles and the ventricular trabeculae. We use visualizations of the flow field to view the interactions between the blood and the trabeculae in far more detail than has been achieved previously, which promises to give a better understanding of cardiac flow. Finally, we use our simulation results to compare the blood flow within one healthy heart and two diseased hearts.

Image based computational modeling of intracardiac flows

With continuous advancements in four-dimensional medical imaging technologies, increasing computational speeds, and widespread availability of high performance computing facilities, computational modeling of intracardiac flows is becoming increasingly viable and has the potential to become a powerful non-invasive diagnostic tool for the diagnosis and treatment of cardiovascular disease. The motive of the current study is to develop a modeling framework that facilitates image-based analysis of intracardiac flows in health as well as disease and to use this framework to gain fundamental insights into intracardiac hemodynamics. A procedure is developed for constructing computational fluid dynamics (CFD) – ready models from in vivo imaging data. The key components of this procedure are the registration and segmentation of the 4D data for several (~20) key frames, template based mapping to ensure surface grid conformality and high-fidelity simulations using a sharp-interface immersed boundary solver. A physiologically representative, kinematic model of the mitral valve is also developed for use in these simulations. As a precursor, a comprehensive quantitative validation of the flow solver is performed using experimental data in a simple model of the left ventricle. A quantitative comparison of the phase-averaged velocity and vorticity fields between the simulation and the experiment shows a reasonable agreement. The detailed assessment of this comparison is used to identify and discuss the key challenges and uncertainties associated in conducting such a validation study. The vast majority of computational investigations of intracardiac flows have focused either on the left or the right ventricles while the corresponding atria were modeled in highly simplistic ways. However, the impact of this simplification on the hemodynamics of the ventricular filling has not been clearly understood. Additionally, the surface of the ventricle has been assumed to be smooth although it is well known that the left ventricle is highly corrugated with surface protrusions or trabeculae and papillary muscles extending deep into the ventricular cavity. Hence, separate studies were conducted to understand the effect of complex atrial flows on the intraventricular flow development and also to understand and quantify the impact of the trabeculae and papillary muscles on ventricular hemodynamics Results indicate that the trabeculae and papillary muscles significantly impact ventricular flow resulting in a deeper penetration of the mitral jet into the ventricle during filling. These anatomical features are also found to produce a “squeezing” effect that enhances apical washout. It is also demonstrated that the complex flow dynamics developed inside the left atrium have minimal influence on the flow inside the left ventricle, which is primarily governed by the mitral valve leaflets configuration. The complex vortical structures inside the left atrium are rapidly dissipated due to the complex interaction of multiple vortex rings leading to breakup, annihilation and enhanced viscous dissipation so that the flow is smoothly streamlined as it enters the mitral orifice and produces a near-uniform velocity profile at the level of the mitral annulus. The implications of these findings on the modeling of the intra-ventricular flows are also discussed