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. 2013 Sep 5;8(9):e73485.
doi: 10.1371/journal.pone.0073485. eCollection 2013.

Stroke propensity is increased under atrial fibrillation hemodynamics: a simulation study

Affiliations

Stroke propensity is increased under atrial fibrillation hemodynamics: a simulation study

Hyo Won Choi et al. PLoS One. .

Abstract

Atrial fibrillation (AF) is the most common sustained dysfunction in heart rhythm clinically and has been identified as an independent risk factor for stroke through formation and embolization of thrombi. AF is associated with reduced cardiac output and short and irregular cardiac cycle length. Although the effect of AF on cardiac hemodynamic parameters has been reported, it remains unclear how the hemodynamic perturbations affect the potential embolization of blood clots to the brain that can cause stroke. To understand stroke propensity in AF, we performed computer simulations to describe trajectories of blood clots subject to the aortic flow conditions that represent normal heart rhythm and AF. Quantitative assessment of stroke propensity by blood clot embolism was carried out for a range of clot properties (e.g., 2-6 mm in diameter and 0-0.8 m/s ejection speed) under normal and AF flow conditions. The simulations demonstrate that the trajectory of clot is significantly affected by clot properties as well as hemodynamic waveforms which lead to significant variations in stroke propensity. The predicted maximum difference in stroke propensity in the left common carotid artery was shown to be about 60% between the normal and AF flow conditions examined. The results suggest that the reduced cardiac output and cycle length induced by AF can significantly increase the incidence of carotid embolism. The present simulations motivate further studies on patient-specific risk assessment of stroke in AF.

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Conflict of interest statement

Competing Interests: 3DT Holdings, Inc. (Indianapolis, IN) provided funding to this project. There are no patents, products in development or marketed products to declare. This does not alter the authors’ adherence to all the PLOS ONE policies on sharing data and materials.

Figures

Figure 1
Figure 1. Computational domain and flow conditions for simulations.
(A) Aortic arch model used for simulations and clot release positions at the aortic inlet. The initial positions of a clot were assumed to be circumferentially distributed at a radial distance of 0–40% of aortic radius (position 1 to 17). (B) Normal and AF flow velocity profiles specified at the aortic inlet. Solid and dashed lines represent normal and AF aortic flow conditions, respectively. The velocity profiles reflect the reduction in cardiac output and cycle length. The cardiac output and cycle length corresponding to the normal and AF conditions were 5.5 vs. 3.8 L/min and 1 vs. 0.6s. The black, gray, and white circle symbols denote three different clot ejection moments assumed which correspond to a beginning of systolic, accelerating, and peak stage of the cardiac cycle, respectively.
Figure 2
Figure 2. Instantaneous streamlines and WSS contour at (A) accelerating, (B) peak systole, and (C) decelerating stage of a cardiac cycle for the normal (left panels) and AF (right panels) conditions.
Figure 3
Figure 3. Trajectory of clots ranging from 2 to 6(A) normal and (B) AF condition, respectively.
Figure 4
Figure 4. Stroke propensity for the clots of 2–6 mm diameter released at the (A) moderate and (B) high ejection speeds for the normal and AF flow conditions.
The gray and black bars represent the normal and AF flow condition, respectively. Definition of stroke propensity is the percent ratio of clots whose trajectories ended up in carotid to all the clots released at the aortic inlet or 17 clots depicted in Fig. 1A.
Figure 5
Figure 5. Stroke propensity for the clots of 2–6 mm diameter released at a range of clot ejection speeds (i.e., 0.1–0.7 m/s) under the (A) normal and (B) AF flow conditions.
The black, dark gray, light gray, white, and blue bars represent 2, 3, 4, 5, and 6–6 mm diameter with a range of clot ejection speeds of 0–0.7 m/s released at three different ejection times indicated in Fig. 1B under the (C) normal and (D) AF flow conditions. The white, gray, and black bars denote the clot ejection moment corresponding to the beginning of systolic, accelerating, and peak stage of the cardiac cycle, respectively.
Figure 6
Figure 6. Modulation of stroke propensity for two aortic arch models under the (A) normal and (B) AF flow condition at the high ejection speed.
Overall stroke propensity for the clots of 2–6 mm diameter with a range of clot ejection speeds of 0–0.7 m/s released at three different ejection points indicated in Fig. 1B under the (C) normal and (D) AF flow conditions. Case I and II indicate upper and lower ranges of carotid diameters observed in the previous study (23), respectively. Also, they represent two different branch sizes and locations relative to aorta.
Figure 7
Figure 7. Variation of stroke propensity among three different flow modeling approaches (i.e., no turbulence model, LES, and k-ω SST model) at the high ejection speed for the normal (A) and AF (B) flow conditions.
The white, gray, and black bars represent no turbulence model, LES and k-ω SST model, respectively.

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