Ventricular arrhythmia events in patients with implantable cardioverter-defibrillator before and after the treatment with sodium-glucose co-transporter 2 inhibitors

The role of sodium-glucose co-transporter 2 inhibitors (SGLT2i) in the treatment of chronic heart failure is expanding. However, the timing of implantable cardioverter-defibrillator (ICD) implantation for primary prevention in relation to the use of SGLT2i remains unclear. A small case series has described appropriate shocks from ICD in two patients following the initiation of SGLT2i, but a comprehensive analysis is lacking in the literature.

This study aimed to investigate the rate of ventricular arrhythmic burden and appropriate anti-tachycardia therapy from ICD before and after the initiation of SGLT2i therapy. We conducted a retrospective single-center analysis, comparing ventricular events from home monitoring reports three months before and three months after SGLT2i therapy initiation.

Seventeen patients were enrolled in the study. At baseline, clinical characteristics were as follows: 13 (76%) were male, 9 (53%) had ischemic, 2 (12%) had valvular, and 6 (35%) had idiopathic cardiomyopathy. The mean end-diastolic volume (EDV) was 203 ± 90 ml, and the mean left ventricular ejection fraction was 0.36 ± 0.09. All patients were treated with beta-blockers, 14 (82%) with sacubitril-valsartan, 13 (76%) with aldosterone antagonists, 16 (94%) with furosemide, and 5 (29%) with amiodarone. SGLT2i started with dapagliflozin for 13 patients (76%), empagliflozin for 3 patients (18%), and canagliflozin for 1 patient (6%). Ten patients (59%) had single-chamber or dual-chamber ICDs, and 7 had implantable cardiac resynchronization therapy (CRT) defibrillators.

In the three months before SGLT2i treatment, 4/17 patients had non-sustained ventricular tachycardia (NSVT), compared to 8/17 (23% vs. 47%, p-value 0.23) patients with NSVT after treatment. Seven patients (41%) experienced an increase in the rate of NSVT events, with one patient having 28 NSVT events after treatment versus none before treatment. No patients had anti-tachycardia therapy in the three months before treatment, while in the three months after SGLT2i treatment, 1 patient had ventricular tachycardia treated with anti-tachycardia pacing (110 days after the beginning of the treatment), and 2 patients had ventricular tachycardia treated with appropriate shocks (2 and 25 days after the initiation of SGLT2i treatment).

This small retrospective analysis revealed an increase in ventricular arrhythmic events in the three months following the initiation of SGLT2i. These findings highlight the need for a more extensive analysis to establish a stronger statistical correlation.