January 10, 2026Reviews in Cardiovascular MedicineOpen Access

SGLT2i and GLP-1RA may help prevent AF onset by targeting metabolic alterations.

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Why the study?

Current therapeutic strategies often fail to prevent or durably control AF, prompting interest in targeting atrial metabolic remodeling and mitochondrial stress.

Design

Review

Key result

Targeting metabolic alterations, particularly with SGLT2 inhibitors and GLP-1 receptor agonists, may help prevent the onset of atrial fibrillation.

Authors

KGKonstantinos null Grigoriou PKPaschalis null Karakasis PTPanagiotis null Theofilis

Discussion

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Overview

May support metabolic-targeted AF prevention in diabetes/obesity; leaves open confirmation in prospective RCTs.

Key Points

The central aim is to understand how metabolic remodeling and mitochondrial stress contribute to atrial fibrillation.
Comprehensive analysis of mechanisms linking metabolic changes and atrial fibrillation.
Evaluation of therapeutic strategies including SGLT2 inhibitors and GLP-1 receptor agonists.
Integration of multi-omics data for understanding metabolic diversity in atrial fibrillation.
Assessment of next-generation imaging for detecting pathologic substrates.
Atrial metabolic remodeling and mitochondrial stress facilitate the onset of atrial fibrillation.
Targeted therapies may restore metabolic homeostasis and mitigate arrhythmia effects.
Emerging approaches enhance the customization of treatments based on individual metabolic profiles.

Cite This Study

Grigoriou et al. (2025) studied this question. Targeting metabolic alterations, particularly with SGLT2 inhibitors and GLP-1 receptor agonists, may help prevent the onset of atrial fibrillation.

synapsesocial.com/papers/6963224191e05aa366cb8d9e https://doi.org/10.31083/rcm44688

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January 10, 2026Reviews in Cardiovascular MedicineOpen Access

SGLT2i and GLP-1RA may help prevent AF onset by targeting metabolic alterations.

View Full Paper

Ask AI

Bookmark

Why the study?

Current therapeutic strategies often fail to prevent or durably control AF, prompting interest in targeting atrial metabolic remodeling and mitochondrial stress.

Design

Review

Key result

Targeting metabolic alterations, particularly with SGLT2 inhibitors and GLP-1 receptor agonists, may help prevent the onset of atrial fibrillation.

Authors

KGKonstantinos null Grigoriou PKPaschalis null Karakasis PTPanagiotis null Theofilis

Discussion

Member takes

Overview

May support metabolic-targeted AF prevention in diabetes/obesity; leaves open confirmation in prospective RCTs.

Key Points

The central aim is to understand how metabolic remodeling and mitochondrial stress contribute to atrial fibrillation.
Comprehensive analysis of mechanisms linking metabolic changes and atrial fibrillation.
Evaluation of therapeutic strategies including SGLT2 inhibitors and GLP-1 receptor agonists.
Integration of multi-omics data for understanding metabolic diversity in atrial fibrillation.
Assessment of next-generation imaging for detecting pathologic substrates.
Atrial metabolic remodeling and mitochondrial stress facilitate the onset of atrial fibrillation.
Targeted therapies may restore metabolic homeostasis and mitigate arrhythmia effects.
Emerging approaches enhance the customization of treatments based on individual metabolic profiles.

Cite This Study

Grigoriou et al. (2025) studied this question. Targeting metabolic alterations, particularly with SGLT2 inhibitors and GLP-1 receptor agonists, may help prevent the onset of atrial fibrillation.

synapsesocial.com/papers/6963224191e05aa366cb8d9e https://doi.org/10.31083/rcm44688

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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