Why the study?
LV internal structures may reduce blood flow velocity and promote LV thrombus formation in healthy hearts or atrial fibrillation, but their specific hemodynamic effects require numerical clarification.
Does the presence of trabeculae carneae and atrial fibrillation affect blood flow stagnation in the left ventricle?
Does the presence of trabeculae carneae and atrial fibrillation affect blood flow stagnation in the left ventricle?
Computational modeling suggests that trabeculae carneae and atrial fibrillation contribute to blood flow stagnation in the left ventricle, potentially increasing the risk of thrombus formation.
Internal structures of the inner wall of the left ventricle (LV), such as trabeculae carneae (TC) and papillary muscles, may reduce the blood flow velocity, resulting in thrombus formation in the LV of a healthy heart or a heart with atrial fibrillation. The purpose of the present study was to numerically clarify the effects of simplified TC models around the LV wall and atrial fibrillation on the blood flow field as a fundamental study. The LV model was constructed from magnetic resonance images, and the model considering atrial fibrillation was constructed based on the volume change data of a healthy subject from which volume increase with atrial contraction was removed. Numerical analysis was performed considering eight simplified TC models around the LV wall. The numerical results revealed that the oscillatory shear index and relative residence time (RRT) at the apex in the LV model with internal structures were larger than those in the LV model without internal structures, which indicates that the blood flow tends to stagnate. On the other hand, as a result of the LV model considering the atrial fibrillation, the time-averaged wall shear stress decreases and the RRT increases at valley points of the internal structures.
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MIYAUCHI et al. (2019) studied this question.
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