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心房颤动维持机制的“药理学”分析:折返、小波还是局灶性?

"Pharmacological" analysis of atrial fibrillation maintenance mechanism: reentry, wavelets, or focal?

作者信息

Burashnikov Alexander

机构信息

Lankenau Institute for Medical Research, Wynnewood, PA, United States.

出版信息

Front Cardiovasc Med. 2025 Jan 24;12:1447542. doi: 10.3389/fcvm.2025.1447542. eCollection 2025.

DOI:10.3389/fcvm.2025.1447542
PMID:39925977
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11802512/
Abstract

The primary electrophysiological mechanism of atrial fibrillation (AF) maintenance is poorly defined. AF mapping studies readily record focal activations (defining them as focal sources or breakthroughs) and "incomplete reentries" (defining them as reentries or would-be-reentries) but do not or rarely detect complete circular activations. Electrophysiological alterations induced by anti-AF drugs before AF cardioversion may help delineate the mechanism of AF maintenance. Cardioversion of AF by antiarrhythmic drugs is associated with prolongation of the AF cycle length and temporal excitable gap (t-EG), resulting in improvement in AF organization (AF-org), and with or without alterations in the refractory period, conduction velocity and wavelength. Such electrophysiological pattern is conceivable with termination of a single focal source but not a single reentry (Class III agents do not increase reentrant t-EG). Yet, a single focal source and multiple focal sources are plausible as the primary mechanism of AF maintenance prior drug administration. Improvement in AF-org caused by anti-AF agents before AF cardioversion is coherent with simultaneous multiple random reentries and wavelets. However, simultaneous multiple reentries are unlikely to occur regularly (most of the contemporary AF mapping studies report either a single reentry at a time or no reentry at all), and the ability of random wavelets to maintain AF is speculative. The conducted analysis inclines toward the focal source as the primary mechanism of AF maintenance.

摘要

心房颤动(AF)维持的主要电生理机制尚不清楚。房颤标测研究很容易记录到局灶性激动(将其定义为局灶性起源或突破点)和“不完全折返”(将其定义为折返或潜在折返),但未检测到或很少检测到完整的环形激动。房颤复律前抗房颤药物引起的电生理改变可能有助于阐明房颤维持的机制。抗心律失常药物使房颤复律与房颤周期长度和瞬时可兴奋间隙(t-EG)延长有关,导致房颤组织化(AF-org)改善,且伴有或不伴有不应期、传导速度和波长的改变。这种电生理模式在单个局灶性起源终止时是可以想象的,但在单个折返时则不然(Ⅲ类药物不会增加折返性t-EG)。然而,在给药前,单个局灶性起源和多个局灶性起源作为房颤维持的主要机制是合理的。房颤复律前抗房颤药物引起的AF-org改善与同时存在的多个随机折返和小波相一致。然而,多个折返同时发生不太可能是规律的(大多数当代房颤标测研究报告一次只有一个折返或根本没有折返),并且随机小波维持房颤的能力是推测性的。所进行的分析倾向于局灶性起源作为房颤维持的主要机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb10/11802512/8d9efe2f5269/fcvm-12-1447542-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb10/11802512/7d66501c9b4b/fcvm-12-1447542-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb10/11802512/8d9efe2f5269/fcvm-12-1447542-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb10/11802512/7d66501c9b4b/fcvm-12-1447542-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bb10/11802512/8d9efe2f5269/fcvm-12-1447542-g005.jpg

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Spatial and temporal relationship between focal and rotational activations and their relationship to structural remodeling in patients with persistent atrial fibrillation.
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