Vigmond Edward, Pashaei Ali, Amraoui Sana, Cochet Hubert, Hassaguerre Michel
L'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Fondation Université de Bordeaux, Hôpital Xavier-Arnozan, Pessac, France; Institut de Mathématiques de Bordeaux, Université de Bordeaux, Talence, France.
L'Institut de Rythmologie et Modélisation Cardiaque LIRYC, Fondation Université de Bordeaux, Hôpital Xavier-Arnozan, Pessac, France; Institut de Mathématiques de Bordeaux, Université de Bordeaux, Talence, France.
Heart Rhythm. 2016 Jul;13(7):1536-43. doi: 10.1016/j.hrthm.2016.03.019. Epub 2016 Mar 11.
Complex fractionated atrial electrograms (CFAEs) have long been associated with proarrhythmic alterations in atrial structure or electrophysiology. Structural alterations disrupt and slow smoothly propagating wavefronts, leading to wavebreaks and electrogram (EGM) fractionation, but the exact nature and characteristics for arrhythmia remain unknown. Clinically, in atrial fibrillation (AF) patients, increases in frequency, whether by pacing or fibrillation, increase EGM fractionation and duration, and reentry can occur in relation with the conduction disturbance. Recently, percolation has been proposed as an arrhythmogenic mechanism, but its role in AF has not been investigated.
We sought to determine if percolation can explain reentry formation and EGM behavior observed in AF patients.
Computer models of fibrotic tissue with different densities were generated based on late gadolinium-enhanced magnetic resonance images, using pixel intensity as a fibrosis probability to avoid an arbitrary binary threshold. Clinical pacing protocols were followed to induce AF, and EGMs were computed.
Reentry could be elicited, with a biphasic behavior dependent on fibrotic density. CFAEs were recorded above fibrotic regions, and consistent with clinical data, EGM duration and fractionation increased with more rapid pacing.
These findings confirm percolation as a potential mechanism to explain AF in humans and give new insights into dynamics underlying conduction distortions and fractionated signals in excitable media, which correlate well with the experimental findings in fibrotic regions. The greater understanding of the different patterns of conduction changes and related EGMs could lead to more individualized and effective approaches to AF ablation therapy.
复杂碎裂心房电图(CFAEs)长期以来一直与心房结构或电生理的致心律失常改变相关。结构改变会破坏并减慢平滑传播的波前,导致波破碎和电图(EGM)碎裂,但心律失常的确切性质和特征仍不清楚。临床上,在心房颤动(AF)患者中,无论是通过起搏还是颤动,频率增加都会增加EGM碎裂和持续时间,并且折返可能与传导障碍有关。最近,渗流被提出作为一种致心律失常机制,但其在AF中的作用尚未得到研究。
我们试图确定渗流是否可以解释AF患者中观察到的折返形成和EGM行为。
基于钆增强磁共振延迟成像生成具有不同密度的纤维化组织计算机模型,使用像素强度作为纤维化概率以避免任意二进制阈值。遵循临床起搏方案诱发AF,并计算EGM。
可以诱发折返,其具有依赖于纤维化密度的双相行为。在纤维化区域上方记录到CFAEs,并且与临床数据一致,随着起搏速度加快,EGM持续时间和碎裂增加。
这些发现证实渗流是解释人类AF的一种潜在机制,并为可兴奋介质中传导畸变和碎裂信号的潜在动力学提供了新的见解,这与纤维化区域的实验结果密切相关。对传导变化和相关EGM的不同模式有更深入的了解可能会导致更个性化和有效的AF消融治疗方法。