Singh Prabhpreet, Noheria Amit
Tulane Heart and Vascular Institute, Tulane University, 1430 Tulane Avenue, #8548, New Orleans, LA, 70112, USA.
Cardiac Electrophysiology Section, Cardiovascular Division, Washington University School of Medicine, 660 S. Euclid Ave., #8086, St. Louis, MO, 63110, USA.
Curr Treat Options Cardiovasc Med. 2018 Mar 6;20(3):21. doi: 10.1007/s11936-018-0612-4.
Invasive electrophysiology (EP) mapping and catheter ablation has increasingly become the standard of care for many cardiac arrhythmias like supraventricular tachycardias, atrial fibrillation, premature ventricular complexes (PVC), and monomorphic ventricular tachycardia. In this review, we discuss the recent progress made in the mapping and ablation of ventricular fibrillation (VF). Ventricular activation during VF is apparently disorganized, making mapping and interpretation difficult. Prolonged mapping during VF would require mechanical circulatory support as VF causes complete hemodynamic collapse. These limitations have been addressed by the realization that there is often a reliable trigger arrhythmia that initiates the clinical VF episodes, and an approach to map and ablate this trigger can be successful. Such triggers can be PVCs localizing to the Purkinje/fascicular system, and in other cases can be ectopy from outflow tracts or intracavitary structures like papillary muscles, false tendons or moderator band, or can be monomorphic VT or preexcited atrial fibrillation that degenerate into VF. More recently, approaches beyond trigger elimination directly targeting the VF substrate have been devised. This includes elimination of the arrhythmogenic substrate localizing to the epicardial right ventricular outflow tract in patients with Brugada syndrome, akin to elimination of the arrhythmogenic substrate harbored by regions within scar in ischemic and non-ischemic cardiomyopathies. Further, recent attempts have been made to try to identify and ablate rotors during VF that may be important in perpetuating the VF episode. Such exciting advances in "curing" VF are proving to be life saving for resuscitated survivors of arrhythmic death.
有创电生理(EP)标测和导管消融已日益成为许多心律失常(如室上性心动过速、心房颤动、室性早搏(PVC)和单形性室性心动过速)的标准治疗方法。在本综述中,我们讨论了心室颤动(VF)标测和消融方面的最新进展。VF期间的心室激活明显紊乱,使得标测和解读变得困难。VF期间长时间标测需要机械循环支持,因为VF会导致完全的血流动力学崩溃。认识到通常存在引发临床VF发作的可靠触发心律失常,并且标测和消融这种触发因素的方法可能会成功,这些局限性已得到解决。此类触发因素可以是定位在浦肯野纤维/束支系统的PVC,在其他情况下,可以是来自流出道或心腔内结构(如乳头肌、假腱索或节制索)的异位搏动,或者可以是退化为VF的单形性VT或预激性心房颤动。最近,已经设计出直接针对VF基质而非消除触发因素的方法。这包括消除Brugada综合征患者心外膜右心室流出道的致心律失常基质,类似于消除缺血性和非缺血性心肌病疤痕区域内的致心律失常基质。此外,最近有人尝试在VF期间识别和消融可能对维持VF发作很重要的转子。这些在“治愈”VF方面的激动人心的进展正被证明对心律失常性死亡复苏幸存者具有救命作用。