Demonstration of Patient-Specific Simulations to Assess Left Atrial Appendage Thrombogenesis Risk.

Demonstration of Patient-Specific Simulations to Assess Left Atrial Appendage Thrombogenesis Risk.
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证明患者特异性模拟评估左心房破裂血栓形成风险。

DOI:
10.3389/fphys.2021.596596
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发表时间:
2021
影响因子:
4
通讯作者:
Del Álamo JC
Del Álamo JC
中科院分区:
医学2区
文献类型:
--
作者:
García-Villalba M;Rossini L;Gonzalo A;Vigneault D;Martinez-Legazpi P;Durán E;Flores O;Bermejo J;McVeigh E;Kahn AM;Del Álamo JC

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房颤(AF)改变左心房(LA)血流动力学,可导致左心耳(LAA)血栓形成、全身性栓塞和卒中。房颤患者卒中的个性化风险分层将改善预防性抗凝治疗与出血风险的平衡。我们研究了LA解剖结构和功能如何影响LA和LAA血流动力学,并探讨了通过计算流体动力学(CFD)进行的患者特异性分析是否可以预测LAA血栓形成的风险。我们使用内部浸入边界CFD求解器分析了LA室壁运动的4D-CT采集。我们考虑了6名具有不同心房功能的患者,其中3名患者有左心耳血栓(在运行模拟前进行数字切除)或短暂性脑缺血发作史(LAAT/TIA-pos),3名患者无左心耳血栓或TIA(LAAT/TIA-neg)。我们发现,与LAAT/TIA-neg患者相比,LAAT/TIA-pos患者左心耳内的血液在停留时间和动能方面有显着变化。此外,我们还显示了左心房导管、储血器和升压器功能如何明显影响左心房和左心耳血流动力学。最后,固定壁和移动壁模拟产生不同的左心房血流动力学和停留时间预测为每个病人。因此,固定壁模拟对我们的小队列进行的左心耳血栓形成风险分层比移动壁模拟更差,特别是左心耳驻留时间居中的患者。总体而言,这些结果表明,壁动力学和LAA形态都有助于LAA血液淤滞和血栓形成。
Atrial fibrillation (AF) alters left atrial (LA) hemodynamics, which can lead to thrombosis in the left atrial appendage (LAA), systemic embolism and stroke. A personalized risk-stratification of AF patients for stroke would permit improved balancing of preventive anticoagulation therapies against bleeding risk. We investigated how LA anatomy and function impact LA and LAA hemodynamics, and explored whether patient-specific analysis by computational fluid dynamics (CFD) can predict the risk of LAA thrombosis. We analyzed 4D-CT acquisitions of LA wall motion with an in-house immersed-boundary CFD solver. We considered six patients with diverse atrial function, three with either a LAA thrombus (removed digitally before running the simulations) or a history of transient ischemic attacks (LAAT/TIA-pos), and three without a LAA thrombus or TIA (LAAT/TIA-neg). We found that blood inside the left atrial appendage of LAAT/TIA-pos patients had marked alterations in residence time and kinetic energy when compared with LAAT/TIA-neg patients. In addition, we showed how the LA conduit, reservoir and booster functions distinctly affect LA and LAA hemodynamics. Finally, fixed-wall and moving-wall simulations produced different LA hemodynamics and residence time predictions for each patient. Consequently, fixed-wall simulations risk-stratified our small cohort for LAA thrombosis worse than moving-wall simulations, particularly patients with intermediate LAA residence time. Overall, these results suggest that both wall kinetics and LAA morphology contribute to LAA blood stasis and thrombosis.
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