IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac-Bordeaux, France; University of Bordeaux, Institut de Mathématiques de Bordeaux, UMR 5251, 33400, Talence, France.
IHU Liryc, Electrophysiology and Heart Modeling Institute, fondation Bordeaux Université, 33600, Pessac-Bordeaux, France; University of Bordeaux, Institut de Mathématiques de Bordeaux, UMR 5251, 33400, Talence, France.
Comput Methods Programs Biomed. 2024 Aug;253:108239. doi: 10.1016/j.cmpb.2024.108239. Epub 2024 May 23.
The excitable gap (EG), defined as the excitable tissue between two subsequent wavefronts of depolarization, is critical for maintaining reentry that underlies deadly ventricular arrhythmias. EG in the His-Purkinje Network (HPN) plays an important role in the maintenance of electrical wave reentry that underlies these arrhythmias.
To determine if rapid His bundle pacing (HBP) during reentry reduces the amount of EG in the HPN and ventricular myocardium to suppress reentry maintenance and/or improve defibrillation efficacy.
In a virtual human biventricular model, reentry was initiated with rapid line pacing followed by HBP delivered for 3, 6, or 9 s at pacing cycle lengths (PCLs) ranging from 10 to 300 ms (n=30). EG was calculated independently for the HPN and myocardium over each PCL. Defibrillation efficacy was assessed for each PCL by stimulating myocardial surface EG with delays ranging from 0.25 to 9 s (increments of 0.25 s, n=36) after the start of HBP. Defibrillation was successful if reentry terminated within 1 s after EG stimulation. This defibrillation protocol was repeated without HBP. To test the approach under different pathological conditions, all protocols were repeated in the model with right (RBBB) or left (LBBB) bundle branch block.
Compared to without pacing, HBP for >3 seconds reduced average EG in the HPN and myocardium across a broad range of PCLs for the default, RBBB, and LBBB models. HBP >6 seconds terminated reentrant arrhythmia by converting HPN activation to a sinus rhythm behavior in the default (6/30 PCLs) and RBBB (7/30 PCLs) models. Myocardial EG stimulation during HBP increased the number of successful defibrillation attempts by 3%-19% for 30/30 PCLs in the default model, 3%-6% for 14/30 PCLs in the RBBB model, and 3%-11% for 27/30 PCLs in the LBBB model.
HBP can reduce the amount of excitable gap and suppress reentry maintenance in the HPN and myocardium. HBP can also improve the efficacy of low-energy defibrillation approaches targeting excitable myocardium. HBP during reentrant arrhythmias is a promising anti-arrhythmic and defibrillation strategy.
兴奋间隙（EG）定义为两个去极化波阵面之间的可兴奋组织，对于维持折返激动至关重要，折返激动是引发致命性室性心律失常的基础。希氏束浦肯野网络（HPN）中的 EG 在维持折返激动中起着重要作用，而折返激动是引发这些心律失常的基础。
确定折返激动时快速希氏束起搏（HBP）是否减少 HPN 和心室心肌中的 EG 量，以抑制折返激动的维持和/或提高除颤效果。
在虚拟人心室双腔模型中，通过快速线路起搏引发折返激动，然后在起搏周期长度（PCL）为 10 至 300 毫秒（n=30）的情况下进行 3、6 或 9 秒的 HBP。在每个 PCL 上，分别计算 HPN 和心肌的 EG。通过在 HBP 开始后 0.25 至 9 秒（递增 0.25 秒，n=36）的延迟刺激心肌表面 EG，评估每个 PCL 的除颤效果。如果在 EG 刺激后 1 秒内终止折返激动，则除颤成功。在没有 HBP 的情况下重复该除颤方案。为了在不同的病理条件下测试该方法，在具有右束支（RBBB）或左束支（LBBB）阻滞的模型中重复所有方案。
与无起搏相比，HBP 持续 >3 秒会降低默认、RBBB 和 LBBB 模型在广泛 PCL 范围内的 HPN 和心肌中的平均 EG。在默认（6/30 PCL）和 RBBB（7/30 PCL）模型中，HBP >6 秒可将 HPN 激活转换为窦性节律行为，从而终止折返性心律失常。在默认模型中，30/30 PCL 的 HBP 期间的心肌 EG 刺激使成功除颤尝试的次数增加了 3%-19%，在 RBBB 模型中增加了 3%-6%，在 LBBB 模型中增加了 3%-11%。
HBP 可以减少 HPN 和心肌中的 EG 量并抑制折返激动的维持。HBP 还可以提高针对可兴奋心肌的低能量除颤方法的效果。折返激动时的 HBP 是一种有前途的抗心律失常和除颤策略。
