Department of Cardiology, Chonnam National University Hospital, Gwangju, Republic of Korea (N.Y.).
Masonic Medical Research Laboratory, Utica, NY (N.Y., B.P., C.A.).
Circ Arrhythm Electrophysiol. 2018 Sep;11(9):e006511. doi: 10.1161/CIRCEP.118.006511.
Early repolarization syndrome (ERS) is an inherited cardiac arrhythmia syndrome associated with sudden cardiac death. Approaches to therapy are currently very limited. This study probes the mechanisms underlying the electrocardiographic and arrhythmic manifestation of experimental models of ERS and of the ameliorative effect of radiofrequency ablation.
Action potentials, bipolar electrograms, and transmural pseudo-ECGs were simultaneously recorded from coronary-perfused canine left ventricular wedge preparations (n=11). The I agonist NS5806 (7-10 μmol/L), calcium channel blocker verapamil (3 μmol/L), and acetylcholine (1-3 μmol/L) were used to pharmacologically mimic the effects of genetic defects associated with ERS.
The provocative agents induced prominent J waves in the ECG secondary to accentuation of the action potential notch in epicardium but not endocardium. Bipolar recordings displayed low-voltage fractionated potentials in epicardium because of temporal and spatial variability in appearance of the action potential dome. Concealed phase 2 reentry developed when action potential dome was lost at some epicardial sites but not others, appearing in the bipolar electrogram as discrete high-frequency spikes. Successful propagation of the phase 2 reentrant beat precipitated ventricular tachycardia/ventricular fibrillation. Radiofrequency ablation of the epicardium destroyed the cells displaying abnormal repolarization and thus suppressed the J waves and the development of ventricular tachycardia/ventricular fibrillation in 6/6 preparations.
Our findings suggest that low-voltage fractionated electrical activity and high-frequency late potentials recorded from the epicardial surface of the left ventricle can identify regions of abnormal repolarization responsible for ventricular tachycardia/ventricular fibrillation in ERS and that radiofrequency ablation of these regions in left ventricular epicardium can suppress ventricular tachycardia/ventricular fibrillation by destroying regions of ER.
早期复极综合征（ERS）是一种与心源性猝死相关的遗传性心律失常综合征。目前治疗方法非常有限。本研究探讨了ERS 实验模型中心电图和心律失常表现的机制以及射频消融的改善作用。
从冠状灌注的犬左心室楔形标本（n=11）同时记录动作电位、双极电图和跨壁假性 ECG。I 型激动剂 NS5806（7-10 μmol/L）、钙通道阻滞剂维拉帕米（3 μmol/L）和乙酰胆碱（1-3 μmol/L）用于模拟与 ERS 相关的遗传缺陷的作用。
刺激剂在心电图中引起明显的 J 波，这是由于心外膜动作电位切迹的加重。双极记录显示心外膜的低电压碎裂电位，因为动作电位穹顶的出现具有时间和空间变异性。当某些心外膜部位的动作电位穹顶丢失而其他部位没有丢失时，会出现隐蔽的 2 相折返，在双极电图中表现为离散的高频尖峰。2 相折返的成功传播引发室性心动过速/心室颤动。心外膜射频消融破坏了显示异常复极的细胞，从而抑制了 J 波和 6/6 标本中室性心动过速/心室颤动的发展。
我们的发现表明，从左心室心外膜表面记录的低电压碎裂电活动和高频晚电位可以识别出导致 ERS 室性心动过速/心室颤动的异常复极区域，并且左心室心外膜这些区域的射频消融可以通过破坏 ER 区域来抑制室性心动过速/心室颤动。
