Willems Stephan, Hoffmann Boris A, Schaeffer Benjamin, Sultan Arian, Schreiber Doreen, Lüker Jakob, Steven Daniel
Department of Electrophysiology, University Heart Center, University Hospital Eppendorf, Martinistr. 52, 20246, Hamburg, Germany,
J Interv Card Electrophysiol. 2014 Sep;40(3):229-35. doi: 10.1007/s10840-014-9886-y. Epub 2014 Mar 14.
The involvement of the Purkinje system in a subset of patients with idiopathic ventricular fibrillation or polymorphic VT/VF related to structural heart disease was first demonstrated in the pioneering work of Michel Haissaguerre and co-workers (Circulation 106:962-967, 2002 and Lancet 359:677-678, 2002). It is very important to identify these patients with recurrent episodes of ventricular fibrillation and/or ICD shocks with regard to the presence of triggering premature ventricular contractions (PVC), which may be amenable to mapping and catheter ablation by screening Holter and ICD recordings. The practical problem, which is frequently encountered, is the absence of these PVCs when the patients are brought to the EP lab. However, catheter ablation is an important adjunctive tool to antiarrhythmic drug treatment, beta blocker therapy, and general anesthesia in this setting. Local electrogram criteria related to this phenomenon have been identified guiding mapping and ablation (e.g., low amplitude, high-frequency Purkinje potentials preceding a closely coupled ventricular signal (Fig. 1a)). The favorable long-term follow-up after catheter ablation has been demonstrated in the setting of right and left ventricular Purkinje-related PVCs leading to polymorphic VT/VF (Leenhardt et al., Circulation 89:206-215, 1994) and also following myocardial infarction (Baensch et al., Circulation 108:3011-3016, 2003) and right ventricular outflow tract-associated VF (Noda et al., Journal of the American College of Cardiology 46:1288-1294, 2005). Most recently, epicardial ablation strategies leading to suppression of polymorphic VT/VF episodes related to the Brugada syndrome have been described irrespective to the presence of premature ventricular beats (Nademanee et al., Circulation 123:1270-1279, 2011).
米歇尔·海萨热尔及其同事的开创性研究(《循环》第106卷:962 - 967页,2002年;《柳叶刀》第359卷:677 - 678页,2002年)首次证明了浦肯野系统参与了一部分特发性室颤或与结构性心脏病相关的多形性室性心动过速/室颤患者的发病过程。对于存在触发室性早搏(PVC)的反复发生室颤和/或植入式心律转复除颤器(ICD)电击的患者,识别这些患者非常重要,通过筛查动态心电图和ICD记录,这些触发早搏可能适合进行标测和导管消融。实际中经常遇到的问题是,当患者被带到心脏电生理(EP)实验室时,这些PVC不存在。然而,在这种情况下,导管消融是抗心律失常药物治疗、β受体阻滞剂治疗和全身麻醉的重要辅助工具。已经确定了与这种现象相关的局部电图标准,以指导标测和消融(例如,紧跟紧密耦联的心室信号之前的低振幅、高频浦肯野电位(图1a))。在导致多形性室性心动过速/室颤的右心室和左心室浦肯野相关PVC的情况下(勒恩哈特等人,《循环》第89卷:206 - 215页,1994年),以及在心肌梗死后(本施等人,《循环》第108卷:3011 - 3016页,2003年)和右心室流出道相关室颤(野田等人,《美国心脏病学会杂志》第46卷:1288 - 1294页,2005年),导管消融后的长期随访结果良好。最近,已经描述了无论是否存在室性早搏,导致与布加综合征相关的多形性室性心动过速/室颤发作得到抑制的心外膜消融策略(纳迪曼尼等人,《循环》第123卷:1270 - 1279页),。