The width of the QRS is often used to

The width of the QRS is often used to ascertain the distance of the site of origin from the conduction system. In the absence of antiarrhythmics, which result in conduction slowing, VTs with narrow QRS are located closer to the purkinje system or septum. VTs originating from the epicardium have been shown to have the widest QRS morphologies with delayed initial forces due to transmural activation from outside to inside prior to engaging the conduction system. Slurring or initial activation delay in the upstroke of the QRS, and Q waves in the limb leads are suggestive of epicardial sites, although these criteria may not be specific in the setting of structural heart disease [7–9]. The majority of patients that present with scar-mediated VT have ICDs. Therefore, the clinical presenting VT is seldom captured with 12-lead electrocardiography. While a far-field electrogram stored in the ICD log can be helpful, significant limitations in identifying and determining the “clinical” arrhythmia exist [10]. Out of practicality, VTs that are reproducibly induced or comparable in rate to ICD logs are often considered to be “clinical”. While the vast majority of VTs originate from regions with scar pathology, up to 9% patients with postinfarct scar have VTs from focal regions typically seen in idiopathic VT cases [11]. Therefore, the value of NIPS and EP study cannot be understated, taken with the limitations mentioned previously. In the setting of ischemic VT, the substrate that typically harbors reentrant circuits is revealed by Q waves on EKG, wall motion abnormalities seen on echocardiography, or perfusion defects on nuclear imaging. Delayed enhancement magnetic resonance can be helpful in characterizing the transmural location of scar [12]. Scar patterns in NICM are more typically midmyocardial and epicardial [13], in sphingosine to ICM, where necrosis from coronary artery occlusion originates subendocardially [14]. The scar has a perivalvular and basal lateral wall predilection in NICM [15]. (Fig. 2) The identification of scar detected on computed tomography, magnetic resonance imaging, or positron emission tomography can be registered and integrated with electroanatomic mapping to facilitate the targeting of arrhythmogenic scar while depicting adjacent structures and regional anatomy [16–19]. With magnetic resonance imaging, regions of heterogeneity can be visualized as “gray zones” [20,21]. Current MR technology is still subject to motion artifacts and partial volume effect and does not have the resolution of ex-vivo MRI to depict the spatial complexity of microfibrosis [22]. Despite this limitation, studies have demonstrated specificity of critical sites to regions of heterogeneous fibrosis, where regions of scar that exhibit >25% transmurality have been correlated with critical sites during ablation in ICM and NICM [23,24]. A novel wideband magnetic resonance sequence to minimize device-related artifacts can increase the diagnostic yield of imaging, as the majority of patients with scar-mediated VT have ICDs [25] (Fig. 3).
Scar reentry While polymorphic VT and VF represent spatially dynamic activation patterns of the ventricle with continuously changing QRS morphologies, the circuit for monomorphic VT is fixed and structurally defined by interspersed viable myocardium within scar. The initial understanding of reentry as the mechanism for VT was developed in postinfarction substrates. In the 1970s, Josephson et al. described continuous local electrical activity as “localized fibrillation” during diastole [26]. Reentry as the fundamental mechanism of arrhythmia was supported by reproducible initiation and termination of monomorphic VT by programmed stimulation [27]. Subendocardial resection and encircling ventriculotomy were shown to result in a significant reduction in recurrent VT and gave further support to the notion that the modification or elimination of critical regions of scar could be an effective therapy for recurrent VT [28–30]. In 1983, Hartzler et al. described the first catheter ablation using high energy unipolar direct current shock therapy for right ventricular outflow tract VT and septal infarct-related VT [31]. In the late 1980s, radiofrequency emerged as the preferred energy source as lesions were more controlled and homogeneous without any detrimental effects to global systolic function [32].