Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure
Epicardial and intramural excitation during ventricular pacing: effect of myocardial structure
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DOI：
10.1152/ajpheart.01400.2007
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发表时间：
2008-04-01
影响因子：
4.8
通讯作者：
Ershler, Philip R.
中科院分区：
文献类型：
--
作者：
Taccardi, Bruno;Punske, Bonnie B.;Ershler, Philip R.
已发表的研究表明，犬心脏的心室起搏产生三种不同的心外膜兴奋模式：靠近心外膜起搏部位的椭圆等时线，具有不对称的凸起;具有高传播速度的区域，高达2或3 m/s和许多突破部位;以及低速区域（< 1 m/s），其中兴奋穿过隔膜的心外膜投影。随着起搏深度的增加，心外膜电位最大值的幅度变得不对称。产生不同模式的电生理机制尚未完全阐明。在这项研究中，我们对这些机制进行了实验研究。在戊巴比妥麻醉下，通过心外膜电极阵列和透壁插入电极记录了22只暴露或离体犬心脏的心外膜和壁内兴奋等时线和电位图。在五项实验中，用稀释的卢戈溶液灌注心室腔。心外膜隆起是由波前的螺旋形心外膜下部分的电紧张吸引引起的。高速模式和相关的多个突破是由于浦肯野网络的参与。中隔通过处的低速是由于该区域浦肯野受累缺失所致。心外膜电位最大值的不对称幅度和由深部刺激引起的突破部位的移位是壁内纤维的外膜-内膜扩张的结果。这些结果提高了我们对室性期前收缩和起搏搏动期间壁内和心外膜传播的理解。这可用于解释手术时记录的心外膜标测图或从体表ECG反向计算的心外膜标测图。
Published studies show that ventricular pacing in canine hearts produces three distinct patterns of epicardial excitation: elliptical isochrones near an epicardial pacing site, with asymmetric bulges; areas with high propagation velocity, up to 2 or 3 m/s and numerous breakthrough sites; and lower velocity areas (< 1 m/s), where excitation moves across the epicardial projection of the septum. With increasing pacing depth, the magnitude of epicardial potential maxima becomes asymmetric. The electrophysiological mechanisms that generate the distinct patterns have not been fully elucidated. In this study, we investigated those mechanisms experimentally. Under pentobarbital anesthesia, epicardial and intramural excitation isochrone and potential maps have been recorded from 22 exposed or isolated dog hearts, by means of epicardial electrode arrays and transmural plunge electrodes. In five experiments, a ventricular cavity was perfused with diluted Lugol solution. The epicardial bulges result from electrotonic attraction from the helically shaped subepicardial portions of the wave front. The high-velocity patterns and the associated multiple breakthroughs are due to involvement of the Purkinje network. The low velocity at the septum crossing is due to the missing Purkinje involvement in that area. The asymmetric magnitude of the epicardial potential maxima and the shift of the breakthrough sites provoked by deep stimulation are a consequence of the epi-endocardial obliqueness of the intramural fibers. These results improve our understanding of intramural and epicardial propagation during premature ventricular contractions and paced beats. This can be useful for interpreting epicardial maps recorded at surgery or inversely computed from body surface ECGs.