van der Does Lisette J M E, Kharbanda Rohit K, Teuwen Christophe P, Knops Paul, Kik Charles, Bogers Ad J J C, de Groot Natasja M S
Department of Cardiology, Erasmus Medical Center Rotterdam, 3015 GD Rotterdam, The Netherlands.
Department of Cardiothoracic Surgery, Erasmus Medical Center Rotterdam, 3015 GD Rotterdam, The Netherlands.
J Clin Med. 2020 Feb 18;9(2):558. doi: 10.3390/jcm9020558.
The predisposition of atrial extrasystoles (AES) to trigger cardiac tachyarrhythmia may arise from intramural conduction disorders causing endo-epicardial asynchrony (EEA). This study aimed to determine whether spontaneous AES disturb endo-epicardial conduction. Simultaneous endo-epicardial mapping of the right atrium was performed in patients during cardiac surgery with two 128-electrode arrays. Sixty spontaneous AES were observed in 23 patients and were analyzed for incidence of conduction delay, conduction block and amount of EEA compared to the previous sinus rhythm beat. Both conduction delay and block occurred more often in AES compared to sinus rhythm. The difference in lines of conduction block between the epicardium and endocardium increased in AES causing a greater imbalance of conduction disorders between the layers. The incidence of EEA with differences ≥10 ms increased significantly in AES. AES caused delays between the epicardium and endocardium up to 130 ms and EEA to increase for up to half (47%) of the mapping area. Conduction disturbances between the epicardial and endocardial layer giving rise to EEA increase during AES. Asynchronous activation of the atrial layers increases during AES which may be a mechanism for triggering cardiac tachyarrhythmia under the right conditions but EEA cannot be recognized by current mapping tools.
房性期前收缩(AES)触发心脏快速性心律失常的易感性可能源于导致心内膜 - 心外膜不同步(EEA)的壁内传导障碍。本研究旨在确定自发性AES是否会干扰心内膜 - 心外膜传导。在心脏手术期间,使用两个128电极阵列对患者的右心房进行同步心内膜 - 心外膜标测。在23例患者中观察到60次自发性AES,并与先前的窦性心律搏动相比,分析传导延迟、传导阻滞的发生率以及EEA的程度。与窦性心律相比,AES中传导延迟和阻滞的发生更为频繁。AES中心外膜和心内膜之间传导阻滞线的差异增加,导致两层之间传导障碍的不平衡更大。差异≥10 ms的EEA发生率在AES中显著增加。AES导致心外膜和心内膜之间的延迟长达130 ms,EEA增加至标测区域的一半(47%)。AES期间心外膜和心内膜层之间导致EEA的传导障碍增加。AES期间心房各层的异步激活增加,这可能是在适当条件下触发心脏快速性心律失常的一种机制,但EEA目前无法被标测工具识别。