Numerical analysis of hemodynamic changes in the left atrium due to atrial fibrillation
Introduction
The left atrium (LA) is located at the upper dorsal part of the heart and has a characteristic part called the left atrial appendage (LAA), which bulges in the inner forward direction (Al-Saady et al., 1999). It pumps arterial blood from the four bilateral pulmonary veins (PVs) and ejects the blood toward the left ventricle (LV) through the mitral valve (MV) by both passive and active motions synchronized with ventricular expansion and contraction (Pagel et al., 2003). Atrial fibrillation (AF) is the most common arrhythmia which disrupts the movement of the LA (Iwasaki et al., 2011). The important characteristics of AF can be summarized as a lack of an active contraction of the LA (atrial kick) in late diastole and the occurrence of high-frequency fibrillation (>400 bpm) of the atrial wall. AF may cause no symptoms but is often associated with heart palpitation. Except for patients with severe underlying disease or hypofunction of LV contraction, aggressive treatments are not performed. However, it has been reported that thromboembolism derived from AF worsened the vital prognosis (Benjamin et al., 1998). An increase in the incidence of AF due to aging has also been suggested to be a cause of severe cerebral infarction (Wolf et al., 1991, Yamanouchi et al., 1989). Therefore, diagnosis, treatment, and management of AF are clinically important issues.
AF is diagnosed mainly by electrocardiogram (ECG). In order to diagnose the causes and complications of AF, morphological approach for entire heart, including LA and LAA, is conducted by means of computed tomography or ultrasound imaging, in addition to a blood test. On the other hand, there have been trials to utilize hemodynamic information on the LA obtained by phase-contrast magnetic resonance imaging (PC MRI) (Fluckiger et al., 2013, Fyrenius et al., 2001, Kilner et al., 2000) and ultrasonic measurement (Nakai et al., 2007, Nishimura et al., 1990, Park et al., 2013) for development of therapeutic strategy. Computational fluid dynamics (CFD) (Zhang and Gay, 2008) and particle image velocimetry (PIV) (Mouret et al., 2004) have also revealed morphological changes of vortices in the LV due to AF and stagnation of blood flow in the LAA leading to formation of thrombosis. However, though hemodynamics in LA during sinus rhythm and AF were qualitatively compared, no quantitative evaluations were conducted. Moreover, effects of each phenomenon caused by AF, i.e., the lack of an atrial kick and the occurrence of high-frequency fibrillation, on the blood flow field and hemodynamic stresses have not been completely understood.
In this study, effects of the above-mentioned two characteristics of AF on blood flow and hemodynamic parameters were quantitatively investigated. Hemodynamic analyses were performed using healthy and diseased LA models, and their computational results were compared.
Section snippets
Magnetic resonance imaging
This study was approved by the local ethics committees, and informed consent was obtained from the participating volunteer. First, for measurement of variation of the LA morphology, the heart of the 23-year-old healthy male volunteer was measured using a 1.5 T MRI scanner system (Achieva 1.5T, Philips Electronics, Holland) with a SENSE cardiac coil and a two-dimensional balanced turbo field echo at Miyagi Cardiovascular and Respiratory Center. Four chamber T1 weighted images were acquired on 12
Results
Variations of blood flow volume at the MV and PV4 are compared in Fig. 4. In Fig. 4(a), the waveform at the MV in the HA model has two peaks: one is the E wave due to relaxation of LV in the early diastole, and the other one is the A wave due to the atrial kick in late diastole. On the other hand, the A wave is not observed in the AF0 and AF1 models, and a fluctuation by high-frequency fibrillation is observed in the AF1 model. The E/A peak velocity ratio and the mean blood flow volume at the
Discussion
The results demonstrated that each characteristic phenomenon of AF, i.e., the lack of an atrial kick and the occurrence of high-frequency fibrillation, influenced the blood flow field and hemodynamic stresses. Especially, AF caused a local stagnation of blood flow in the LAA. As clearly indicated by streamlines in Fig. 6, the LAA is a thrombosis-prone site because it is located at a distal site of the mainstream of blood from PVs to the MV, resulting in that blood entering into the LAA is
Conclusion
The effects of a lack of atrial kick and the occurrence of high-frequency fibrillation caused by AF on blood flow and hemodynamic stresses were quantitatively investigated by hemodynamic analyses using healthy and diseased LA models constructed based on MRI of a healthy volunteer heart. The results revealed that each characteristic phenomenon of AF influenced hemodynamics. Especially, the atrial wall movement by the high-frequency fibrillation has a large impact on stagnation of blood flow,
Conflict of interest statement
None of the authors have any financial and personal relationships with other people or organizations that could inappropriately influence (bias) their work.
Acknowledgments
Part of this work was carried out under the Collaborative Research Project of the Institute of Fluid Science, Tohoku University. All computations were performed using the supercomputer system at the Advanced Fluid Information Research Center, Institute of Fluid Science, Tohoku University.
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