Key result
Trabeculae carneae decrease wall shear stress and increase apical blood stagnation time in LV models.
Why the study?
It was unclear whether complex internal structures such as trabeculae carneae and papillary muscles, alongside torsional motion, cause blood stagnation and potential thrombus formation in the left ventricle.
Computational fluid dynamics modeling reveals that left ventricular internal structures like trabeculae carneae and torsional motion can induce blood stagnation at the apex, providing a mechanistic basis for potential thrombus formation.
Answers are grounded in this paper and cite their sources.
TC may increase apical blood residence time in LV CFD models; leaves open their contribution to clinical thrombus risk.
It is generally believed that thrombus formation does not occur in the left ventricle (LV) because of the high speed of blood flow. However, the LV has complex internal structures such as trabeculae carneae (TC) and papillary muscles (PM) on its inner wall, which may cause blood stagnation resulting in thrombus formation. In this study, the effects of the TC, PM, and torsional motion on the hemodynamics in the LV were investigated by computational fluid dynamics (CFD) analyses. An LV model was reconstructed from magnetic resonance imaging, and the shape was modified to mimic TC and PM. Then, the CFD analyses of blood flow were performed using several different combinations of TC, PM, and torsional motion. As the results, the presence of TC decreased the time-averaged wall shear stress and increased the relative residence time (RRT) of a blood stagnation index at the apex of the LV model. The TC-induced blood stagnation was also confirmed by a transportation analysis of the passive scalar. These hemodynamic changes were attributed to the fact that TC blocked the large vortex structures generated during the diastole, thus preventing them from reaching the apex. Moreover, the PM only affected the hemodynamics in its immediate vicinity, and torsional motion caused irregular changes to the RRT level and distribution at the apex. Therefore, the complex internal structures and torsional motion of the LV could cause blood stagnation.
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MIYAUCHI et al. (2023) studied Left ventricle hemodynamics and blood stagnation. Trabeculae carneae, papillary muscles, and torsional motion vs. Models without these structures or motions was evaluated on Hemodynamics (time-averaged wall shear stress and relative residence time). The presence of trabeculae carneae decreased time-averaged wall shear stress and increased the relative residence time of blood stagnation at the apex of the left ventricle model.
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