Empagliflozin linked to milder sleep apnea in heart failure
Among 70 adults with heart failure, empagliflozin was linked to an adjusted 11.04-point greater reduction in a sleep-apnea severity score than background therapy alone at three months.
Limit: Only 70 participants were analyzed, limiting precision of the sleep apnea effect
Edited by Boris Djordjevic · AgingResearch.News
Seventy adults with heart failure and predominantly obstructive sleep apnea took part in a randomized trial with blinded outcome assessment. Researchers assigned 37 to empagliflozin, 10 mg daily, plus background heart-failure therapy and 33 to background therapy alone. They assessed participants at three and six months. Both groups began continuous positive airway pressure, which keeps airways open during sleep, after month three.
Before airway-pressure therapy began, empagliflozin initiation was associated with a greater reduction in the apnea–hypopnea index, a measure of breathing interruptions during sleep. The adjusted difference in change between groups was 11.04 points. Exploratory measures also indicated improved oxidative balance—the balance between reactive molecules and defenses that counter them—in the drug group at both follow-ups.
Why it matters
For heart failure, an age-related disease, the authors called for further investigation of empagliflozin’s effects on breathing and oxidative balance when sleep apnea coexists.
Caveats
The oxidative-balance outcomes were exploratory, and shared airway-pressure therapy prevented separation of drug and airway-pressure effects after month three. The results do not establish effects in people without both conditions; the abstract did not report side effects or other harms.
From the paper
- Participants
A total of 135 patients with HF at high risk of sleep-disordered breathing (STOP-Bang score > 4) underwent a sleep study; 87 (64.4%) were diagnosed with OSA.
- Follow-up
Participants assigned to the study group (n = 37) additionally initiated empagliflozin 10 mg once daily at baseline and continued treatment throughout the 6-month follow-up, whereas those assigned to the control group (n = 33) did not initiate an SGLT2 inhibitor as part of the study intervention.
- Result
The baseline-adjusted between-group difference in AHI change from baseline to month 3 (study minus control) was −11.04 (95% CI −16.72 to −5.35; p < 0.001).
Results, 3.2. Longitudinal Analyses of AHI and Oxidative Stress Markers
- Events by group
AHI < 15 was achieved by 3/37 (8.1%) in the study group and 1/33 (3.0%) in the controls at month 3 (p = 0.616), and by 36/37 (97.3%) and 30/33 (90.9%) at month 6 (p = 0.337), respectively.
Results, 3.2. Longitudinal Analyses of AHI and Oxidative Stress Markers
- Limitation
First, this was a single-center trial with a modest sample size and 6-month follow-up, limiting statistical precision, generalizability, and the ability to assess the durability of the observed redox effects or their relationship with hard clinical outcomes.
Quoted word for word from the full text on mdpi.com.
- Empagliflozin
- Continuous positive airway pressure
- Oxidative stress and ROS signaling
- Heart failure
- Obstructive sleep apnea
- Humans
Empagliflozin is part of Bryan Johnson's Blueprint
The paper
Medical University of Białystok
Antioxidants, Oct 22, 2026, Open access, CC BY
