Impact of underlying structural heart disease on survival after electrical storm

Thomas Fink (Bad Oeynhausen)1, M. Mörsdorf (Bad Oeynhausen)1, V. Sciacca (Bad Oeynhausen)1, D. Guckel (Bad Oeynhausen)1, M. Khalaph (Bad Oeynhausen)1, M. Braun (Bad Oeynhausen)1, M. El Hamriti (Bad Oeynhausen)1, S. Winnik (Wetzikon)2, G. Imnadze (Bad Oeynhausen)1, M. Didenko (Bad Oeynhausen)1, C. Sohns (Bad Oeynhausen)1, P. Sommer (Bad Oeynhausen)1

1Herz- und Diabeteszentrum NRW Klinik für Elektrophysiologie/ Rhythmologie Bad Oeynhausen, Deutschland; 2GZO Spital Wetzikon Klinik für Kardiologie und Angiologie Wetzikon, Schweiz

 

Background: Electrical storm (ES) is caused by frequent or incessant ventricular arrhythmia (VA) and most commonly occurs in individuals with structural heart diseases. ES is associated with high intrahospital mortality and therapy deliveries in patients with implantable cardioverter defibrillators (ICD). Treatment of ES is challenging and therapeutic success may be limited by specific pathologies of the underlying heart disease.

Objective: The purpose of this single-center study was to analyze the impact of different underlying heart diseases on clinical endpoints after treatment of ES.

Methods: Data from patients with structural heart disease who were admitted for treatment of ES from 2016 to 2021 were retrospectively analyzed. A composite clinical endpoint consisting of left ventricular assist device (LVAD) implantation, heart transplantation (HTX), death and freedom from VA events was investigated. VA events were defined as any sustained VA or adequate ICD therapy. Analysis was stratified by the underlying heart disease (ischemic cardiomyopathy (ICM) or non-ischemic cardiomyopathy (NICM)).

Results: A total of 150 patients (mean age 64.7±13.5 years) with structural heart disease who were admitted with ES to our VT unit were analyzed. There were 81 patients (54%) with ICM and 69 (46.0%) with NICM, 6 patients (4.0%) with arrhythmogenic right ventricular cardiomyopathy and 4 patients (2.7%) with hypertrophic cardiomyopathy. Mean left ventricular ejection fraction was 28.9±10.8%. ES treatment consisted of catheter ablation in 97 cases (64.7%) and conservative treatment in 53 patients (35.3%). Catheter ablation procedures were successful without inducibility of any sustained VA at the end of the procedure in 84/97 patients (86.6%).
Fourteen patients died within 30 days after admission for ES (10 patients with ICM and 5 patients with NICM; 11 patients who underwent catheter ablation and 4 patients with conservative treatment). The composite clinical endpoint was reached in 79 patients (52.7%; 36 patients [45.6%] with ICM and 43 patients [54.4%] with NICM, respectively) after a mean follow-up of 753±610 days. There was a trend for longer estimated event-free survival from the composite clinical endpoint in patients with ICM irrespective of interventional or conservative therapy for ES (log rank P=0.069) (Figure 1A). The estimated event-free survival in patients who underwent catheter ablation for ES treatment was significantly longer in patients with ICM than in patients with NICM (log rank P=0.018) (Figure 1B). VA recurrence occurred in 87patients (58%) after interventional or conservative ES treatment (31 ICM patients [35.6%] and 48 NICM patients [55.2%] with VA recurrence). Estimated VA-free survival was significantly longer in ICM patients compared to NICM patients in the total patient cohort (log rank P=0.0033) (Figure 2 A) and in patients who underwent catheter ablation for ES compared to patients with conservative management (log rank P=0.0015) (Figure 2 B).

Conclusion: Mortality, morbidity and recurrence of VA are common after ES. Patients with NICM experience significantly more adverse events and VA recurrences than patients with ICM. The effect is more pronounced in patients who undergo catheter ablation of ES, reflecting feasibility of VA ablation in ICM on the one hand and limitations of this technique in patients with NICM on the other.



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