Why the study?
Although SGLT2 inhibitors are core heart failure therapy and ICD and CRT-D devices provide continuous physiological data, it remained unclear whether the physiological effects of ertugliflozin are detectable using device-based remote monitoring.
Does ertugliflozin alter ICD/CRT-D-derived physiological parameters (such as heart rate, heart rate variability, physical activity, and thoracic impedance) compared with placebo in patients with ICD or CRT-D devices?
RCT (n=46)
Placebo-controlled
Randomized
Does ertugliflozin alter ICD/CRT-D-derived physiological parameters (such as heart rate, heart rate variability, physical activity, and thoracic impedance) compared with placebo in patients with ICD or CRT-D devices?
In this small exploratory post-hoc analysis of the ERASe trial, ertugliflozin did not produce detectable changes in ICD/CRT-D-derived physiological parameters over 12 months, highlighting the need for larger studies to evaluate device-based digital biomarkers during SGLT2 inhibitor therapy.
Aims: Implantable cardioverter-defibrillators (ICD) and cardiac resynchronization therapy defibrillators (CRT-D) provide continuous physiological data reflecting heart failure (HF) status and autonomic tone. Sodium–glucose cotransporter-2 inhibitors (SGLT2i) are core HF therapy, but it remains unclear whether their physiological effects are detectable using device-based remote monitoring. Following the ERASe trial, which showed reduced ventricular arrhythmias with ertugliflozin, this post-hoc analysis evaluated its impact on ICD/CRT-D-derived parameters. Methods: In this prospective, randomized ERASe post-hoc analysis, ertugliflozin was compared with placebo over 12 months in patients with ICD or CRT-D devices. Device-derived parameters including 24 h heart rate, night heart rate, heart rate variability, physical activity, and thoracic impedance were assessed at baseline and follow-up. Analyses were predefined as exploratory. Results: Forty-six patients (22 ertugliflozin, 24 placebo) had ≥1 analysable parameter. Paired longitudinal data were available for 29 patients for 24 h heart rate (HR), 19 for night HR, 17 for HR variability, and 9 for thoracic impedance. No significant between-group differences were observed in 24 h HR, physical activity or thoracic impedance. No significant differential longitudinal treatment effects were observed for the evaluated device-derived parameters, although estimates were imprecise because of limited parameter-specific data availability. Assessment of associations with arrhythmic and heart-failure outcomes was precluded by small event numbers and incomplete parameter-specific data. Conclusions: Ertugliflozin did not significantly alter individual device-derived parameters. Larger studies are needed to determine whether device-based physiological signals can identify treatment-related changes.
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Rohrer et al. (2026) conducted an RCT in Heart failure in patients with ICD or CRT-D devices (n=46). Ertugliflozin vs. Placebo was evaluated on Device-derived parameters including 24 h heart rate, night heart rate, heart rate variability, physical activity, and thoracic impedance.
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