Diabetes Mellitus and Atrial Fibrillation: Mechanistic Insights and Therapeutic Impacts of Glucose-Lowering Drugs.
Level 5 - mechanism / opinion, no new human data
Narrative review without systematic search or meta-analysis
PubMed 41598171 · doi:10.3390/life16010016
What was done
Narrative review synthesizing epidemiological studies, mechanistic research, and cardiovascular outcome trials regarding the links between diabetes mellitus (DM) and atrial fibrillation (AF). The authors evaluated structural, electrical, autonomic, metabolic, and inflammatory arrhythmogenic pathways, along with clinical evidence on the impact of metformin, insulin, DPP-4 inhibitors, SGLT-2 inhibitors, and GLP-1 receptor agonists on AF incidence and recurrence.
What was found
The abstract reports no quantitative values or effect estimates. DM promotes AF through atrial fibrosis, electrical remodeling, autonomic dysfunction, oxidative stress, inflammation, glycemic fluctuations, and epicardial adipose tissue expansion. Clinically, antidiabetic drugs showed variable associations: metformin and SGLT-2 inhibitors showed favorable or neutral effects on AF risk; GLP-1 receptor agonists demonstrated cardiovascular benefits with uncertain AF-specific effects; insulin was associated with higher AF risk; and DPP-4 inhibitors showed neutral effects with inconsistent findings across studies.
Why it matters
Synthesizes the pathophysiological mechanisms linking diabetic metabolic disturbances to arrhythmogenic atrial remodeling and summarizes how distinct glucose-lowering drug classes influence AF risk.
Limits
Narrative review design without systematic search protocols, formal study selection criteria, risk-of-bias grading, or quantitative pooling. The abstract reports no numerical data, sample sizes, or specific trial endpoints. Associations for agents like insulin remain highly susceptible to confounding by diabetes duration and disease severity.
Cited by
- supports Metabolic disease and inflammation driven by blood sugar or insulin cause atrial muscle components to alter their conduction, causing atrial fibrillation.