Impact of repeat ablation of ventricular tachycardia in patients with structural heart disease

Abstract

Aims: Recurrences of ventricular tachycardia (VT) after initial catheter ablation is a significant clinical problem. In this study, we report the efficacy and risks of repeat VT ablation in patients with structural heart disease (SHD) in a tertiary single centre over a 7-year period.

Methods and results: Two hundred ten consecutive patients referred for repeat VT ablation after previous ablation in our institution were included in the analysis (53% ischaemic cardiomyopathy, 91% males, median age 65 years, mean left ventricular ejection fraction 35%). After performing repeat ablation, the clinical VTs were acutely eliminated in 82% of the patients, but 46% of the cohort presented with VT recurrence during the 25-month follow-up. Repeat ablation led to a 73% reduction of shock burden in the first year and 61% reduction until the end of follow-up. Similarly, VT burden was reduced 55% in the first year and 36% until the end of the study. Fifty-two patients (25%) reached the combined endpoint of ventricular assist device implantation, heart transplantation, or death. Advanced New York Heart Association functional class, anteroseptal substrate, and periprocedural complication after repeat ablation were associated with worse prognosis independently of the type of cardiomyopathy.

Conclusion: While complete freedom from VT after repeat ablation in SHD was difficult to achieve, ablation led to a significant reduction in VT and shock burden. Besides advanced heart failure characteristics, anteroseptal substrate and periprocedural complications predicted a worse outcome.

Keywords: Acute and long-term freedom from VT; Prognosis after repeat VT ablation; Repeat ablation in ventricular arrhythmias; Risks and complication management.

Graphical Abstract

Figure 1

(A) Illustration of shock burden of the cohort at baseline (left, only episodes up to 1 year before repeat ablation considered) and during the first year post repeat ablation (right). FU, follow-up. (B) Graphic of VT burden at baseline (left, only episodes up to 1 year before repeat ablation considered) and during the first year post repeat ablation (right, *patients admitted in incessant VT excluded). FU, follow-up. (C) Impact of cardiomyopathy on VT recurrence (blue line, ICM patients; green, NICM, n = number of patients).

Figure 2

Flowchart of VT recurrence management in SHD patients post repeat ablation. HF, heart failure; ICD, internal cardioverter defibrillator; LVAD, left ventricular assist device.

Figure 3

Pie graphic on cardiomyopathy classification of the cohort (A), in patients with anteroseptal substrate (B), and inferolateral substrate (C) with corresponding Kaplan–Meier curve depicting the impact of anteroseptal substrate on LVAD/HTX-free survival (D). Blue, anteroseptal group; green, inferolateral, n = number of patients.

Figure 4

Example of NICM patient of the cohort with septal substrate on the voltage map (A), with intramural LGE evidence in CMR (B) and corresponding anterosuperior and anteroseptal VT exits at the margin of late activation area in sinus rhythm endocardial (illustrated with CARTO-3 system). Both VT morphologies were clinical VTs. The activation map in sinus rhythm (C) demonstrates the areas of late activation at the basal anteroseptal area, where the VT exits were identified. After extensive substrate modification of the late activation area, no VTs were inducible at the end of the procedure.