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Ventricular tachycardia (VT) substrate in left ventricular (LV) nonischemic cardiomyopathy (NICM) consists of fibrosis with surviving myocardium.The purpose of this study was to determine whether, in patients with LV NICM and sustained VT, reduced QRS amplitude and QRSf during sinus rhythm can identify the presence and location of abnormal septal (S-NICM) and/or free-wall (FW-NICM) VT substrate.We compared patients with NICM and VT (group 1) with electroanatomic mapping septal (S-NICM; n = 21) or free-wall (FW-NICM; n = 20) VT substrate to a 38-patient reference cohort (group 2) with cardiac magnetic resonance imaging (cMRI) and NICM but no VT referred for primary prevention implantable cardioverter-defibrillator (26 [68.4%] with late gadolinium enhancement).Group 1 had lower QRS amplitude in leads II (0.60 ± 0.22 vs 0.86 ± 0.35, P.001), aVR (0.60 ± 0.24 vs 0.75 ± 0.31, P = .002), aVF (0.48 ± 0.20 vs 0.70 ± 0.28, P.001), and VIn LV NICM, low frontal plane QRS (0.55 mV in aVF) is associated with VT substrate. Although multilead QRS fractionation is associated with the presence and location of VT substrate, it is frequently identified in patients without VT with cMRI abnormalities.

Aim To describe clinical characteristics, procedural details, specific challenges, and outcomes in patients with HeartMate3™ (HM3), a left ventricular assist device system with a magnetically levitated pump, undergoing ventricular tachycardia ablation (VTA). Methods and results Data were collected from patients with an HM3 system who underwent VTA in seven tertiary centres. Data included baseline patient characteristics, procedural data, mortality, and arrhythmia-free survival. The study cohort included 19 patients with cardiomyopathy presenting with ventricular tachycardia (VT) (53% with VT storm). Ventricular tachycardias were induced in 89% of patients and a total of 41 VTs were observed. Severe electromagnetic interference was present on the surface electrocardiogram. Hence, VT localization required analysis of intra-cardiac signals or the use of filter in the 40–20 Hz range. The large house pump HM3 design obscured the cannula inflow and therefore multi imaging modalities were necessary to avoid catheter entrapment in the cannula. A total of 32 VTs were mapped and were successfully ablated (31% to the anterior wall, 38% to the septum and only 9% to the inflow cannula region). Non-inducibility of any VT was reached in 11 patients (58%). Over a follow-up of 429 (interquartile range 101–692) days, 5 (26%) patients underwent a redo VT ablation due to recurrent VTA and 2 (11%) patients died. Conclusions Ventricular tachycardia ablation in patients with HM3 is feasible and safe when done in the appropriate setup. Long-term arrhythmia-free survival is acceptable but not well predicted by non-inducibility at the end of the procedure.

Background: The substrate for ventricular tachycardia (VT) in left ventricular (LV) nonischemic cardiomyopathy may be epicardial. We assessed the prevalence, location, endocardial electrograms, and VT ablation outcomes in LV nonischemic cardiomyopathy with isolated epicardial substrate. Methods: Forty-seven of 531 (9%) patients with LV nonischemic cardiomyopathy and VT demonstrated normal endocardial (>1.5 mV)/abnormal epicardial bipolar low-voltage area (LVA, Results: Epicardial bipolar LVA (27.3 cm 2 [interquartile range, 15.8–50.0]) localized to basal (40), mid (8), and apical (3) LV with basal inferolateral LV most common (28/47, 60%). Of 44 endocardial maps available, 40 (91%) had endocardial unipolar LVA (24.5 cm 2 [interquartile range, 9.4–68.5]) and 29 (67%) had characteristic normal amplitude endocardial split electrograms opposite the epicardial LVA. At mean of 34 months, the VT-free survival was 55% after one and 72% after multiple procedures. Greater endocardial unipolar LVA than epicardial bipolar LVA (hazard ratio, 10.66 [CI, 2.63–43.12], P =0.001) and number of inducible VTs (hazard ratio, 1.96 [CI, 1.27–3.00], P =0.002) were associated with VT recurrence. Conclusions: In patients with LV nonischemic cardiomyopathy and VT, the substrate may be confined to epicardial and commonly basal inferolateral. LV endocardial unipolar LVA and normal amplitude bipolar split electrograms identify epicardial LVA. Ablation targeting epicardial VT and substrate achieves good long-term VT-free survival. Greater endocardial unipolar than epicardial bipolar LVA and more inducible VTs predict VT recurrence.

Background Low QRS amplitude (QRSa), QRS fractionation (QRSf) and longer QRS duration (QRSd) are markers of myocardial fibrosis and inflammation in non-ischemic cardiomyopathy (NICM). Objective To determine if reduction of inflammation with treatment of cardiac sarcoidosis (CS) may reverse these 12 lead ECG parameter changes. Methods 21 patients (pts) with CS and VT ablation with a positive baseline positron emission tomographic (PET 1) scan were studied. All pts received prednisone ≥40 mg for 4 to 8 weeks followed by a taper and maintenance with methotrexate ± low-dose prednisone, Results Pts in PET2(+) vs PET2(−) groups has similar gender (men 89% vs 100%, p=0.42), age (57±8 vs 56±10 years, p=0.8) and LV ejection fraction (41±11 vs 46±11, p=0.31). Baseline 12-lead ECGs showed similar QRSd, ≥2QRSf contiguous leads and QRSa for PET2(+) vs PET2(−); P all >0.15 (Table 1). At 1 yr there was a lower prevalence of ≥2QRSf contiguous leads and strong trend for shorter QRS duration and larger QRSa in lead DI if PET2(−) vs PET2(+). 4 pts demonstrated loss of QRSf 2 contiguous leads and/or increase in QRSa in DI by at least 0.15 mV from baseline if PET2(−) and none if PET2(+). Conclusions In pts with CS and VT, reversal of inflammation may result in a greater QRSa and reduction in QRSf. An increase in QRSa in lead 1 by >0.15mV and/or loss of QRSf identifies a clear positive response to treatment and negative PET at 1 year. Funding Acknowledgement Type of funding sources: Foundation. Main funding source(s): Richard T and Angela Clark Innovation Fund in Cardiovascular Medicine, the Mark S Marchlinski EP Research and Education Fund and the Winkelman Family Fund in Cardiovascular Innovation. Table 1