Key result
Altering mitral inflow shifts LV vorticity by ~23%, impacting vortices more than endocardial contractility.
Why the study?
Despite the recognized significance of left ventricular vortices in cardiac efficiency and disease progression, a comprehensive understanding of the mechanisms underlying their formation remains lacking.
How do endocardial wall motion and mitral inflow rate influence left ventricular vortices in a patient-specific fluid-structure interaction model?
How do endocardial wall motion and mitral inflow rate influence left ventricular vortices in a patient-specific fluid-structure interaction model?
Mitral inflow rate has a more pronounced impact on left ventricular vorticity magnitude than endocardial contractility in computational fluid-structure interaction models.
Mitral inflow may outweigh contractility in LV vorticity; hypothesis-generating in models, clinical translation remains open.
Recent studies have underscored the importance of evaluating the vortical structure of blood flow in the left ventricle (LV) as a promising approach for assessing LV efficiency and understanding the flow mechanisms that drive cardiac disease progression. LV vortices, characterized by swirling flows of particles around a central axis, play a crucial role in maintaining the momentum and kinetic energy of diastolic flow and in guiding blood flow toward the aortic outflow tract during systole. Despite the recognized significance of these vortices, a comprehensive understanding of the mechanisms underlying their formation remains lacking. In this study, we utilized a patient-specific fluid-structure interaction (FSI) modeling framework, leveraging phase-contrast magnetic resonance imaging (PC-MRI) data, to investigate the influence of endocardial wall motion and mitral inflow rate on LV vortices. Five FSI models were developed to capture LV hemodynamics, explicitly focusing on LV vortices. These models included one with patient-specific boundaries, two with synthetically modified mitral inflow rates, and two with artificially altered endocardial contractility. Our results demonstrated that alterations in mitral flow had a more pronounced impact on the LV vorticity magnitude averaged over the cardiac cycle compared to changes in endocardial contractility. Enhancing and attenuating mitral inflow by 20% resulted in volumetric vorticity magnitude variations of +22.45% and -23.68%, respectively, while similar artificial modifications to endocardial contractility led to comparatively smaller changes of +3.68% and -3.85%, respectively. Furthermore, changes in wall motion had a more significant impact on systolic vortices than diastolic vortices. These findings highlight the need for further studies incorporating more physiological and pathological boundary conditions to fully understand the interplay between endocardial wall motion, mitral inflow, and intraventricular vortex dynamics.
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Peighambari et al. (2025) studied Left ventricular vortices. Synthetically modified mitral inflow rates and endocardial contractility vs. Patient-specific boundaries was evaluated on LV vorticity magnitude averaged over the cardiac cycle. Altering mitral inflow by ±20% resulted in volumetric vorticity magnitude variations of +22.45% and -23.68%, demonstrating a more pronounced impact on LV vortices than changes in endocardial contractility.
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