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在对浦肯野纤维网络进行建模时,是否重新连接远端浦肯野纤维是个问题。

To reconnect or not reconnect distal Purkinje fibers, that is the question when modeling the Purkinje fiber network.

作者信息

Bayer Jason D, Gillette Karli, Coronel Ruben, Plank Gernot, Vigmond Edward J

机构信息

Electrophysiology and Heart Modeling Institute, IHU Liryc, Fondation Bordeaux Université, Pessac-Bordeaux, France.

Institut de Mathématiques de Bordeaux, UMR5251, University of Bordeaux, Bordeaux, France.

出版信息

Front Physiol. 2025 Sep 1;16:1657611. doi: 10.3389/fphys.2025.1657611. eCollection 2025.

Abstract

BACKGROUND AND AIMS

Multiple rule-based approaches exist to model the structure of the His-Purkinje system (HPS). While some approaches reconnect Purkinje fibers in the Purkinje fiber network, others do not. The aim of this study was to determine the impact of distal Purkinje fiber reconnections on anterograde activation, retrograde activation, and reentrant arrhythmias.

METHODS

In a human biventricular model with or without distal Purkinje fiber reconnections, normal sinus rhythm was simulated by His bundle pacing (anterograde activation), followed by an S1S2 protocol applied to the right ventricular apex (retrograde activation). Activation times in the myocardium and HPS were compared for both anterograde and retrograde HPS activation. Arrhythmia vulnerability windows and duration were determined by identifying the S1S2 coupling intervals that induced a reentry of at least two full rotations. Arrhythmia maintenance was further studied by inducing reentry with 4 Hz line pacing applied to the left ventricular epicardial surface. Reentry duration for each protocol was determined over a 20 s window. The S1S2 and line pacing protocols were repeated in the biventricular model without an HPS.

RESULTS

Anterograde activation times and arrhythmia initiation vulnerability windows were mostly unaltered when removing distal Purkinje fiber reconnections. However, retrograde activation times were 18% longer in the HPS and 8% longer in the myocardium when removing distal Purkinje fiber reconnections. Reentrant arrhythmias from the S1S2 protocol and rapid line pacing lasted longer for the model with (11.2 and >20 s) versus without (3.2 and 8.2 s) distal Purkinje fiber reconnections. The S1S2 protocol did not induce reentrant arrhythmias in the human ventricles model without an HPS, and reentry induced with 4 Hz line pacing lasted only 3.6 s.

CONCLUSION

Retrograde activation times increased and the duration of reentrant arrhythmias shortened in the absence of Purkinje fiber reconnections in the Purkinje fiber network. This could be an important structural HPS property to incorporate into computational heart models when investigating retrograde activation and/or reentrant arrhythmias. Modifying the structure of the Purkinje fiber network to remove Purkinje fiber reconnections in patients with life threatening ventricular arrhythmia might be antiarrhythmic.

摘要

背景与目的

存在多种基于规则的方法来模拟希氏-浦肯野系统(HPS)的结构。虽然一些方法在浦肯野纤维网络中重新连接浦肯野纤维,但其他方法则不然。本研究的目的是确定远端浦肯野纤维重新连接对顺行激活、逆行激活和折返性心律失常的影响。

方法

在有或无远端浦肯野纤维重新连接的人体双心室模型中,通过希氏束起搏模拟正常窦性心律(顺行激活),随后在右心室心尖应用S1S2方案(逆行激活)。比较了顺行和逆行HPS激活时心肌和HPS中的激活时间。通过确定诱导至少两个完整旋转折返的S1S2耦合间期来确定心律失常易损窗口和持续时间。通过在左心室心外膜表面应用4Hz线性起搏诱导折返来进一步研究心律失常的维持。在每个方案的20秒窗口内确定折返持续时间。在没有HPS的双心室模型中重复S1S2和线性起搏方案。

结果

去除远端浦肯野纤维重新连接时,顺行激活时间和心律失常起始易损窗口大多未改变。然而,去除远端浦肯野纤维重新连接时,HPS中的逆行激活时间延长了18%,心肌中的逆行激活时间延长了8%。与没有远端浦肯野纤维重新连接的模型(3.2秒和8.2秒)相比,有远端浦肯野纤维重新连接的模型中,S1S2方案和快速线性起搏引起的折返性心律失常持续时间更长(11.2秒和>20秒)。S1S2方案在没有HPS的人体心室模型中未诱发折返性心律失常,4Hz线性起搏诱发的折返仅持续3.6秒。

结论

在浦肯野纤维网络中没有浦肯野纤维重新连接的情况下,逆行激活时间增加,折返性心律失常的持续时间缩短。在研究逆行激活和/或折返性心律失常时,这可能是一个重要的HPS结构特性,可纳入计算心脏模型中。在患有危及生命的室性心律失常的患者中,修改浦肯野纤维网络的结构以去除浦肯野纤维重新连接可能具有抗心律失常作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8591/12433980/ba4ea44a3088/fphys-16-1657611-g001.jpg

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