Subject-specific factors affecting particle residence time distribution of left atrial appendage in atrial fibrillation: A computational model-based study

Front Cardiovasc Med. 2023 Mar 13:10:1070498. doi: 10.3389/fcvm.2023.1070498. eCollection 2023.

Abstract

Background: Atrial fibrillation (AF) is a prevalent arrhythmia, that causes thrombus formation, ordinarily in the left atrial appendage (LAA). The conventional metric of stroke risk stratification, CHA2DS2-VASc score, does not account for LAA morphology or hemodynamics. We showed in our previous study that residence time distribution (RTD) of blood-borne particles in the LAA and its associated calculated variables (i.e., mean residence time, tm , and asymptotic concentration, C ) have the potential to improve CHA2DS2-VASc score. The purpose of this research was to investigate the effects of the following potential confounding factors on LAA tm and C : (1) pulmonary vein flow waveform pulsatility, (2) non-Newtonian blood rheology and hematocrit level, and (3) length of the simulation.

Methods: Subject-Specific data including left atrial (LA) and LAA cardiac computed tomography, cardiac output (CO), heart rate, and hematocrit level were gathered from 25 AF subjects. We calculated LAA tm and C based on series of computational fluid dynamics (CFD) analyses.

Results: Both LAA tm and C are significantly affected by the CO, but not by temporal pattern of the inlet flow. Both LAA tm and C increase with increasing hematocrit level and both calculated indices are higher for non-Newtonian blood rheology for a given hematocrit level. Further, at least 20,000 s of CFD simulation is needed to calculate LAA tm and C values reliably.

Conclusions: Subject-specific LA and LAA geometries, CO, and hematocrit level are essential to quantify the subject-specific proclivity of blood cell tarrying inside LAA in terms of the RTD function.

Keywords: computational fluid dynamics; confounding variables; hematocrit; mean residence time; pulmonary vein flow; pulsatility; simulation length.

Grants and funding

This study was supported by Gerald E. McGinnis Endowed Chair Funds (SGS), American Heart Association grant [#20PRE35210594] (SS), and Leonard H. Berenfield Graduate Fellowship in Cardiovascular Bioengineering (SS).