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Updated: May 5, 2026

Catheter Ablation in Combination With Left Atrial Appendage Closure for Atrial Fibrillation
Published on: February 26, 2013
[Relations between FANS, PPI and atrial fibrillation].
Fabrizio Ricci1, Raffaele De Caterina
1Istituto di Cardiologia e Centro per gli Studi sull'Invecchiamento, Università Gabriele d'Annunzio, Chiete.
Non-steroidal anti-inflammatory drugs (NSAIDs) may increase atrial fibrillation risk. This is linked to inflammation, myocardial fibrosis, and potential gastroesophageal reflux associated with NSAID use.
Area of Science:
- Cardiology
- Pharmacology
Context:
- Growing evidence links non-steroidal anti-inflammatory drug (NSAID) use to increased atrial fibrillation (AF) risk.
- Chronic inflammation is a known risk factor for myocardial fibrosis, a condition contributing to AF.
Purpose:
- To explore the potential mechanisms underlying the association between NSAID use and atrial fibrillation.
- To investigate the role of atrial inflammatory remodeling and gastroesophageal reflux in NSAID-induced AF.
Summary:
- NSAIDs may elevate AF risk through mechanisms involving atrial inflammatory remodeling and subsequent myocardial fibrosis.
- Fibrosis leads to atrial conduction abnormalities, promoting AF development and persistence.
- Gastroesophageal reflux, common with NSAID use, is also considered a potential trigger for AF.
Impact:
- Highlights potential cardiovascular risks associated with widely used anti-inflammatory medications.
- Suggests further research into the specific pathways linking NSAIDs, inflammation, fibrosis, and arrhythmias.
- Informs clinical practice regarding patient monitoring and risk assessment for individuals on long-term NSAID therapy.
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