• 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • Since the first description of epicardial VT ablation with


    Since the first description of epicardial VT ablation with percutaneous subxiphoid access in 1996, epicardial mapping and ablation have been widely performed for the treatment of scar-related VT [55]. Svenson et al. reported that bafilomycin a1 autophagy epicardial VT circuits are particularly common in patients after inferior wall infarction [56]. In 14 patients with post-infarction of the inferior wall, 7 of 30 VTs had a reentry circuit identified and ablated from the epicardium [57]. In patients with stable post-infarction VT, the critical isthmus was considered to be located epicardially in approximately 10–15% of patients [57,58]. Soejima et al. reported that a prior surgical procedure in post-infarction patients poses a technical challenge to percutaneous epicardial access in the electrophysiology laboratory due to pericardial adhesions that can be overcome by limited direct subxiphoid surgical approaches [59]. In patients with non-ischemic dilated cardiomyopathy, the epicardial VT substrate is more frequently identified, and combined endocardial and epicardial ablation has been used to achieve better outcomes [60–62]. However, Nakahara et al. reported that success rate of VT ablation in non-ischemic cardiomyopathy appears to be worse than that in ischemic cardiomyopathy [48]. Tung et al. demonstrated no significant difference in VT-free survival in patients with non-ischemic cardiomyopathy who underwent a combined endo- and epicardial approach compared with those who underwent endo-only ablation (36% versus 33%) [63]. Patients with non-ischemic cardiomyopathy remain at high risk for recurrent VT despite epicardial ablation. In patients with ARVC, the VT substrate is predominantly distributed on the epicardium, as the pathological hallmark of ARVC, fibrofatty replacement of the right ventricle, starts from the epicardium and proceeds to the endocardium [64–67]. Therefore, combined endocardial and epicardial ablation yields higher long-term control of ventricular tachycardia off antiarrhythmic therapy than endocardial ablation alone [67–69]. There are potential risks associated with epicardial ablation, such as pericardial bleeding and injury of coronary vessels or the phrenic nerve [70–72]. Della Bella et al. reported a 4.1% rate of major complications in 218 patients in 6 European centers [71]. Sacher et al. reported a complication rate of 7% for 156 epicardial procedures at 3 institutions [72]. In a recent experimental study by Sacher et al., contact force not directed toward the heart resulted in pulmonary lesions [73]. A recent report from the Bordeaux group provided important information and insight on the issues of epicardial ablation [34]. Successful elimination of epicardial LAVA using endocardial ablation is feasible and most likely to be successful in patients with ARVC and ischemic cardiomyopathy in whom the epicardial substrate is located in a thin myocardial wall (Fig. 7). The data provide important clinical implications, raising the possibility that endocardial ablation can be useful in some circumstances in which epicardial ablation may be limited by the proximity to coronary vessels or the phrenic nerve. Furthermore, a subset of epicardial LAVA disappeared after complete elimination of endocardial LAVA. These data suggest that endocardial ablation could be performed first during substrate ablation procedures to reduce or obviate the need for epicardial ablation.
    Endpoint of substrate ablation Although some studies demonstrated that acute VT ablation success as defined by non-inducibility of VT following ablation was associated with reduced cardiac mortality [74–78], this has not been a consistent finding. Whereas the inducibility of any VT is a poor prognostic sign, the absence of inducibility does not mean VT will not recur [13,79,80]. A VT stimulation protocol may lack reproducibility and may be unable to induce the target VTs at the beginning of procedure despite clinical documentation [1,81]. The degree of sedation, the intensity of the induction protocol, and the pacing site (from the right ventricular apex, left ventricle, or within the scar) may all affect the result of an inducibility test. In the instance in which the patient is non-inducible at the start of the procedure, the value of this particular endpoint is uncertain. Furthermore, whether the goal should be non-inducibility of any VT or whether the absence of clinical VT but persistent inducibility of non-clinical VT is reasonable is the subject of ongoing controversy.