Patients with type 2 diabetes mellitus (T2DM) and heart failure (HF) have an elevated risk of arrhythmic events and worse prognosis [1]. For these patients, the implantable cardioverter-defibrillator (ICD) is the mainstay of treatment [2]. Indeed, the ICD could treat ventricular arrhythmias and prevent cardiac deaths [2]. Despite this, T2DM patients with ICD have still poor prognosis [3]. Indeed, T2DM could favor ventricular arrhythmias and cardiac deaths, via over- inflammation and sympathetic tone dysfunction [4]. These effects increase the intra-myocardial fluid accumulation and cause abnormalities in cardiac ionic currents and action potentials [5]. Notably, the ICD interrogation could provide information regarding arrhythmic events, and shocks, and monitor the sensing, pacing, and impedance leads parameters [5]. These parameters could reflect the cardiac electrophysiological properties and report information about the electrical and functional properties of cardiac cells [5]. These parameters are correlated to serum inflammation and to worse clinical outcomes [5]. In this context, the sodium-glucose cotransporter-2 inhibitors (SGLT2i) are anti-T2DM and anti-HF medications with pleiotropic effects and anti-arrhythmic properties [6]. Indeed, SGLT2i could reduce arrhythmic events in T2DM patients treated with ICDs and/or cardiac resynchronization therapy with a defibrillator (CRTd), [6]. Intriguingly, the SGLT2i could exert cardio-protective effects by modulating inflammatory stress and sympathetic tone activity [7], [8]. Notably, the SGLT2i could stabilize the cardiac action potentials and significantly reduce ventricular arrhythmias and cardiac deaths in T2DM patients [9]. Furthermore, we might speculate that SGLT2i might lead to anti-arrhythmic effects in T2DM patients with ICD/CRTd, by improving the cardiac electrophysiological properties. The amelioration of cardiac electrophysiological properties might be due to the reduction of inflammatory burden and the modulation of sympathetic tone. These effects might consequently reduce ventricular arrhythmic events and ICD interventions, and lead to the best clinical outcomes. On the other hand, this study hypothesis has not been fully investigated before. Thus, to address this study hypothesis, here we investigated the effects of SGLT2i on the cardiac electrophysiological properties, at baseline and at 1 year of follow-up, in T2DM patients with ICD/CRTd treated with SGLT2i (SGLT2i-users) versus those not receiving SGLT2i therapy (non-SGLT2i users), by interrogation of implanted cardiac devices. Then, we investigated in the SGLT2i-users vs. non-SGLT2i users the serum inflammatory cellular and biomarkers expression, and the sympathetic tone activity, via heart rate (HR) and serum catecholamines values, at baseline and at 1 year of follow-up. Finally, we evaluated the events of sustained ventricular arrhythmias, ICD shocks, HF hospitalizations, and cardiac deaths in these cohorts of patients at 1 year of follow-up.