Consecutive patients with SHD who were referred for electrophysiological study and first ablation of VT between January 2016 and February 2022 were included in this study.

VT was mostly documented by ICD and if available by 12-lead electrocardiogram (ECG), ECG tele-monitoring, or in case of unstable course or during resuscitation by external defibrillator monitoring [8]. The definition of respective underlying cardiomyopathy was performed according to European guidelines [9, 10]. Patients with toxic cardiomyopathy, arrhythmia-induced cardiomyopathy, and primary valvular abnormalities were excluded. Patients with reduced LVEF and proven substrate but without comprehensible heart disease were rendered as “idiopathic.”

Standardized transthoracic echocardiographic examinations were usually performed before hospital discharge and admission, and values of left ventricular ejection fraction (LVEF) were retrieved before discharge to assess LVEF beyond the acute phase of VT. The documentation period lasted from index VT ablation until November 2022.

All patients gave written informed consent to all pre- and post-ablation diagnostics and the ablation procedure. The study was carried out according to the principles of the Declaration of Helsinki and was approved by the local medical ethics committee of the Heart Centre Bad Neustadt, Germany. All patients gave informed consent for participation in this retrospective analysis.

In most patients, VT ablation was performed under analgosedation (analgesia-first-based sedation) and in the fasting state using a continuous propofol infusion in conjunction with morphine derivatives. General anesthesia was only used when necessary, at the discretion of the operator, and only in minor part (< 5%). For all procedures, a high-density three-dimensional electroanatomic mapping system (CARTO 3, Biosense Webster, Diamond Bar, CA, USA; Ensite Precision, Abbott, St. Paul, MN, USA; Rhythmia, Boston Scientific, Natick, MA, USA) was used.

Our standard approach includes a high-density voltage map acquired with a high-density multipolar mapping catheter (Pentaray, Biosense Webster, Diamond Bar, CA, USA; Advisor HD Grid, Abbott, St. Paul, MN, USA; Intellamap Orion, Boston Scientific, Natick, MA, USA). Bipolar areas with voltage values ≤ 0.5 mV were defined as scar and low-voltage areas with values of ≤ 1.5 mV but > 0.5 mV as initially defined by Marchlinski et al. [11]. As additional criteria to identify abnormal ventricular tissue late potentials, local abnormal ventricular potentials and fractionated low amplitude potentials were annotated [12].

An epicardial approach was obtained in some cases using the percutaneous subxiphoid approach at the discretion of the operator. Prior to epicardial access, anticoagulation with non-vitamin-K oral antagonists (NOACs) was stopped the day before the procedure, and vitamin-K antagonists (VKAs) were stopped as appropriate in order to reach an INR level below 1.5, if the procedure could be planned.

All ablation procedures were performed according to our institutional standardized protocol by experienced operators. High-density mapping to characterize the underlying electrophysiological substrate in low-voltage areas and short episodes of inducible VT for activation and entrainment mapping was performed. Ablation targets were as follows: (1) identified critical VT isthmuses and (2) late potentials in low-voltage areas. All ablations were performed with irrigated RF ablation of 45W and standard lesion parameters. The endpoint of ablation procedures was evaluated at least once at the end of the procedure: (1) partial short-term success if non-inducibility of the clinical VT but other VTs were still inducible; (2) complete short-term success as elimination of any inducible VT; (3) ablation of all tagged abnormal electrograms. At the end of the procedure, usually, PVS was performed with stimuli 2 ms in duration at twice diastolic threshold up to 4 extrastimuli at 2 basic drive cycle lengths (500 and 400 ms), at the right ventricular apex, and at at least one left ventricular site. Coupling intervals of extrastimuli were decreased in 20-ms intervals until refractoriness or induced VT.

The reason for deferring NIPS was repeated non-inducibility at the beginning and during the procedure, spontaneous VT recurrence between VT ablation and before planned NIPS, and upon patients’/operators’ preference. NIPS was performed in all clinically stable patients without VT recurrences during the initial post-ablation phase via implanted ICD several days after ablation before hospital discharge. In most patients, antiarrhythmic drug therapy was discontinued except beta-blockers. In the fasting state under beta-blocker therapy in the awake state from the right ventricular ICD lead, drive trains of 500 and 400 ms with up to 4 extrastimuli were applied as feasible based on ICD specifications. Coupling intervals of extrastimuli were decreased in 20 ms intervals until refractoriness or induced VT. The output was set at 5 V/2 ms. In patients with biventricular pacing devices, also, trains of 500 and 400 ms with up to 4 extrastimuli were applied via LV-only pacing as feasible based on ICD specifications. Only patients with ICD feasible of NIPS were included. Sedation with midazolam was used only in case of induction of any VT for the purpose of ICD shock.

The endpoint “clinical VT inducible” was categorized, if any sustained monomorphic VT was induced matching the spontaneous VTs. “Non-clinical VT inducible” was categorized if only sustained monomorphic or polymorphic VTs were induced not matching the clinical VTs in QRS morphology and cycle length. “No VT inducible” was categorized if no sustained monomorphic VT was inducible. In the case of VT induction during NIPS, ICD programming was adopted accordingly to record all induced VT-cycle lengths.

Patient data including all adverse events and deaths were collected until discharge and documented. ICD programming after VT ablation typically included the slowest clinical and/or induced VT zone. VT with a CL equal to or longer than the clinical VT documented via ICD or having the same QRS morphology on event 12-lead ECG was considered recurrent clinical VT recurrence.

The endpoint was the recurrence of any sustained ventricular arrhythmia (VA) documented either by ICD interrogations during follow-up in most cases or ECG.

Quantitative data are presented as mean ± standard error of mean (SEM), median and interquartile range (IQR), and ranges depending on the distribution of the data and were compared using Student’s t test for normally distributed data or the Mann–Whitney U test for nonparametric data. Deviations from a Gaussian distribution were tested by the Kolmogorov–Smirnov test. Spearman’s rank correlation for nonparametric data was used to test univariate correlations. Qualitative data are presented as absolute and relative frequencies and compared using the Chi2 test or Fisher’s exact test, as appropriate.

Continuous variables were evaluated by logistic regression; categorical variables were analyzed by contingency tables. Univariate regression analysis was performed for significant and clinically relevant variables. The result of a statistical test was considered significant for p < 0.05, and p values ≤ 0.1 were defined as a statistical trend. SAS, release 9.4 (SAS Institute Inc., Cary, NC, USA) and SPSS (Version 25, IBM Armonk, New York, USA) were used for statistics. The Sankey diagram was designed using R Studio with the packages “Rcmdr,” “dplyr,” and “NetworkD3” as well as the BioRender software.