Van Den Abeele Robin, Hendrickx Sander, Van Nieuwenhuyse Enid, Dunnink Albert, Panfilov Alexander V, Vos Marc A, Wülfers Eike M, Vandersickel Nele
Biophysics Group, Department of Physics and Astronomy, Faculty of Sciences, Ghent University, Ghent, Belgium.
Department of Medical Physiology, University Medical Center Utrecht, Utrecht, Netherlands.
Front Physiol. 2023 Jul 26;14:1201260. doi: 10.3389/fphys.2023.1201260. eCollection 2023.
Torsade de Pointes is a polymorphic ventricular tachycardia which is as yet incompletely understood. While the onset of a TdP episode is generally accepted to be caused by triggered activity, the mechanisms for the perpetuation is still under debate. In this study, we analysed data from 54 TdP episodes divided over 5 dogs (4 female, 1 male) with chronic atrioventricular block. Previous research on this dataset showed both reentry and triggered activity to perpetuate the arrhythmia. 13 of those TdP episodes showed reentry as part of the driving mechanism of perpetuating the episode. The remaining 41 episodes were purely ectopic. Reentry was the main mechanism in long-lasting episodes (>14 beats), while focal sources were responsible for maintaining shorter episodes. Building on these results, we re-analysed the data using directed graph mapping This program uses principles from network theory and a combination of positional data and local activation times to identify reentry loops and focal sources within the data. The results of this study are twofold. First, concerning reentry loops, we found that on average non-terminating (NT) episodes (≥10 s) show significantly more simultaneous reentry loops than self-terminating (ST) TdP (<10 s). Non-terminating episodes have on average 2.72 ± 1.48 simultaneous loops, compared to an average of 1.33 ± 0.66 for self-terminating episodes. In addition, each NT episode showed a presence of (bi-)ventricular loops between 10.10% and 69.62% of their total reentry duration. Compared to the ST episodes, only 1 in 4 episodes (25%) showed (bi-)ventricular reentry, lasting only 7.12% of its total reentry duration. This suggests that while focal beats trigger TdP, macro-reentry and multiple simultaneous localized reentries are the major drivers of long-lasting episodes. Second, using heatmaps, we found focal sources to occur in preferred locations, instead of being distributed randomly. This may have implications on treatment if such focal origins can be disabled reliably.
尖端扭转型室性心动过速是一种尚未被完全理解的多形性室性心动过速。虽然一般认为尖端扭转型室性心动过速发作的起始是由触发活动引起的,但其持续存在的机制仍在争论中。在本研究中,我们分析了来自5只患有慢性房室传导阻滞的犬(4只雌性,1只雄性)的54次尖端扭转型室性心动过速发作的数据。此前对该数据集的研究表明,折返和触发活动均可使心律失常持续存在。其中13次尖端扭转型室性心动过速发作显示折返是使发作持续的驱动机制的一部分。其余41次发作纯粹是异位性的。折返是持续时间较长的发作(>14次搏动)的主要机制,而局灶性起源则负责维持较短的发作。基于这些结果,我们使用有向图映射重新分析了数据。该程序运用网络理论的原理以及位置数据和局部激活时间的组合来识别数据中的折返环和局灶性起源。本研究的结果有两方面。首先,关于折返环,我们发现平均而言,非终止性(NT)发作(≥10秒)比自终止性(ST)尖端扭转型室性心动过速(<10秒)显示出明显更多的同时折返环。非终止性发作平均有2.72±1.48个同时环,相比之下,自终止性发作平均为1.33±0.66个。此外,每次NT发作在其总折返持续时间的10.10%至69.62%之间显示存在(双)心室环。与ST发作相比,每4次发作中只有1次(25%)显示(双)心室折返,仅持续其总折返持续时间的7.12%。这表明虽然局灶性搏动触发了尖端扭转型室性心动过速,但大折返和多个同时的局部折返是持续时间较长发作的主要驱动因素。其次,使用热图,我们发现局灶性起源出现在偏好位置,而非随机分布。如果能够可靠地消除此类局灶性起源,这可能对治疗有影响。