2<\/sup>). Those patients were matched via propensity scoring to the same number of controls who did not initiate a GLP-1 and did not have AF at baseline. Participants in the GLP-1 group were stratified by change in weight (weight loss of 10% or more, weight loss of less than 10% or weight gain). <\/p>\nSurvival was higher among GLP-1 users compared with nonusers (HR = 0.35; 95% CI, 0.3-0.4; P<\/i> < .001), and the benefit in the GLP-1 group was consistent across weight group and individual GLP-1 medications (P<\/i> < .001 for all), according to the researchers.<\/p>\n
After accounting for the competing risk for death, Bilchick and colleagues determined that GLP-1 use was linked to reduced risk for incident AF (HR = 0.75; 95% CI, 0.64-0.88; P<\/i> < .001), and that the relationship was true regardless of weight-change category (weight loss of 10% or more, HR = 0.42; 95% CI, 0.25-0.69; P<\/i> < .001; weight loss of less than 10%, HR = 0.78; 95% CI, 0.63-0.97; P<\/i> = .028; weight gain, HR = 0.71; 95% CI, 0.54-0.93; P<\/i> = .014).<\/p>\n
\u201cThe effect of these medications on reducing atrial fibrillation did not seem to be dependent on weight loss,\u201d Bilchick told Healio. \u201cEven if you gained weight, you still had a reduction in the risk of atrial fibrillation. This is really one of the remarkable findings.\u201d<\/p>\n
Among specific GLP-1s, the strongest reduction in risk for AF occurred with semaglutide (Ozempic\/Wegovy, Novo Nordisk; HR = 0.67; 95% CI, 0.53-0.84, P<\/i> < .001), but reduced risk for AF also occurred in patients taking liraglutide (Victoza\/Saxenda, Novo Nordisk), dulaglutide (Trulicity, Eli Lilly) and tirzepatide (Mounjaro\/Zepbound, Eli Lilly), the researchers found. <\/p>\n
\u201cI think [the effect of GLP-1s on AF] is related to inflammation and reduction in inflammation and improvement in metabolic factors like glucose metabolism,\u201d Bilchick told Healio. \u201cWith respect to the inflammation, there\u2019s been a really interesting observation that there is fat around the heart that causes inflammation in the heart muscle and causes arrhythmias like atrial fibrillation. There are also data that support that these medications actually reduce inflammation systemically and also in this fat that is around the heart, changing the fatty acid composition, changing the way immune cells such as T cells and B cells work.\u201d<\/p>\n
The results could have implications for the prevention and treatment of AF, he said.<\/p>\n
\u201cWhat catheter ablation does not do is it doesn\u2019t modify someone\u2019s risk for atrial fibrillation in terms of inflammation and metabolism,\u201d Bilchick told Healio. \u201cAnd so there is a potential to change practice by having more patients, particularly with risk factors, be on these medications to treat … the systemic inflammation and metabolic abnormalities. And then in that way, the effects of these medications can be synergistic with the procedural interventions we have to treat atrial fibrillation, and that could lead to even more successful results and greater freedom from atrial fibrillation.\u201d<\/p>\n
For more information:<\/h2>\n Kenneth C. Bilchick, MD, MS,<\/b> can be reached at cardiology@healio.com.<\/p>\n\n
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Published by:<\/span>\n
Sources\/Disclosures<\/h3>\n Source: <\/h2>\n Bilchick KC, et al. Do GLP1 agonists have a role in the treatment of atrial fibrillation? Presented at: Heart Rhythm 2026; April 23-26, 2026; Chicago. <\/p>\n
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