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全景心内膜光学标测显示胆碱能性心房颤动发作时,转子的连续加速和活动复杂性增加。

Panoramic Endocardial Optical Mapping Demonstrates Serial Rotors Acceleration and Increasing Complexity of Activity During Onset of Cholinergic Atrial Fibrillation.

机构信息

Center for Arrhythmia Research Department of Internal Medicine - Cardiology University of Michigan Ann Arbor MI.

Facultad de Medicina Universidad Francisco de Vitoria, Pozuelo de Alarcon Mardid Spain.

出版信息

J Am Heart Assoc. 2021 Nov 16;10(22):e022300. doi: 10.1161/JAHA.121.022300. Epub 2021 Nov 2.

DOI:10.1161/JAHA.121.022300
PMID:34726079
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8751940/
Abstract

Background Activation during onset of atrial fibrillation is poorly understood. We aimed at developing a panoramic optical mapping system for the atria and test the hypothesis that sequential rotors underlie acceleration of atrial fibrillation during onset. Methods and Results Five sheep hearts were Langendorff perfused in the presence of 0.25 µmol/L carbachol. Novel optical system recorded activations simultaneously from the entire left and right atrial endocardial surfaces. Twenty sustained (>40 s) atrial fibrillation episodes were induced by a train and premature stimuli protocol. Movies obtained immediately (Initiation stage) and 30 s (Early Stabilization stage) after premature stimulus were analyzed. Serial rotor formation was observed in all sustained inductions and none in nonsustained inductions. In sustained episodes maximal dominant frequency increased from (mean±SD) 11.5±1.74 Hz during Initiation to 14.79±1.30 Hz at Early Stabilization (<0.0001) and stabilized thereafter. At rotor sites, mean cycle length (CL) during 10 prerotor activations increased every cycle by 0.53% (=0.0303) during Initiation and 0.34% (=0.0003) during Early Stabilization. In contrast, CLs at rotor sites showed abrupt decreases after the rotors appearances by a mean of 9.65% (<0.0001) during both stages. At Initiation, atria-wide accelerations and decelerations during rotors showed a net acceleration result whereby post-rotors atria-wide minimal CL (CLmin) were 95.5±6.8% of the prerotor CLmin (=0.0042). In contrast, during Early Stabilization, there was no net acceleration in CLmin during accelerating rotors (prerotor=84.9±11.0% versus postrotor=85.8±10.8% of Initiation, =0.4029). Levels of rotor drift distance and velocity correlated with atria-wide acceleration. Nonrotor phase singularity points did not accelerate atria-wide activation but multiplied during Initiation until Early Stabilization. Increasing number of singularity points, indicating increased complexity, correlated with atria-wide CLmin reduction (<0.0001). Conclusions Novel panoramic optical mapping of the atria demonstrates shortening CL at rotor sites during cholinergic atrial fibrillation onset. Atrial fibrillation acceleration toward Early Stabilization correlates with the net result of atria-wide accelerations during drifting rotors activity.

摘要

背景

心房颤动发作时的激活机制尚不清楚。我们旨在开发一种用于心房的全景光学映射系统,并测试以下假说:在发作过程中,连续的转子是加速心房颤动的基础。

方法和结果

5 只羊心在 0.25μmol/L 卡巴胆碱存在的情况下进行 Langendorff 灌流。新型光学系统同时记录整个左、右心耳心内膜表面的激活情况。采用刺激程序诱发 20 次持续(>40 s)心房颤动发作。分析刺激后即刻(起始阶段)和 30 s(早期稳定阶段)获得的电影。在所有持续诱发的病例中均观察到连续转子的形成,而在非持续诱发的病例中则没有。在持续发作中,最大主导频率从起始阶段的(平均值±标准差)11.5±1.74 Hz 增加到早期稳定阶段的 14.79±1.30 Hz(<0.0001),此后稳定。在转子部位,在起始阶段,10 次转子前激活的平均周期长度(CL)每周期增加 0.53%(=0.0303),而在早期稳定阶段增加 0.34%(=0.0003)。相比之下,在转子部位的 CLs 在转子出现后突然下降,在两个阶段的平均下降幅度为 9.65%(<0.0001)。在起始阶段,转子处心房的加速和减速表现出净加速的结果,即在转子后的心房最小 CL(CLmin)为转子前 CLmin 的 95.5±6.8%(=0.0042)。相比之下,在早期稳定阶段,加速转子的 CLmin 没有净加速(转子前=84.9±11.0%,转子后=85.8±10.8%,与起始阶段相比,=0.4029)。转子漂移距离和速度的水平与心房的整体加速相关。非转子相的奇点点不会加速心房的激活,但在起始阶段会增加,直到早期稳定阶段。奇点点数量的增加,表明复杂性的增加,与心房最小 CL 的减少相关(<0.0001)。

结论

新型全景光学映射心房的研究表明,在胆碱能性心房颤动发作时,转子部位的 CL 缩短。向早期稳定阶段的心房颤动加速与漂移转子活动时心房整体加速的净结果相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/a136bb31bc8b/JAH3-10-e022300-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/8df5b49d7aca/JAH3-10-e022300-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/4b51d5855ec4/JAH3-10-e022300-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/5ff130d2778e/JAH3-10-e022300-g002.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/8510070c82c9/JAH3-10-e022300-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/7f1f971abf9c/JAH3-10-e022300-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/a136bb31bc8b/JAH3-10-e022300-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/8df5b49d7aca/JAH3-10-e022300-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/4b51d5855ec4/JAH3-10-e022300-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/5ff130d2778e/JAH3-10-e022300-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/901421116788/JAH3-10-e022300-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/8510070c82c9/JAH3-10-e022300-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/7f1f971abf9c/JAH3-10-e022300-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fad/8751940/a136bb31bc8b/JAH3-10-e022300-g006.jpg

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