4.7 Review

Gut microbiota, dysbiosis and atrial fibrillation. Arrhythmogenic mechanisms and potential clinical implications

Journal

CARDIOVASCULAR RESEARCH
Volume 118, Issue 11, Pages 2415-2427

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvab292

Keywords

Arrhythmia; Atrial fibrillation; Cardiometabolic; Gut microbiota; Metabolites

Funding

  1. Canadian Institutes of Health Research [148401]
  2. Heart and Stroke Foundation of Canada [18-0022032]
  3. National Institutes of Health [R01HL136389, R01HL131517, R01HL089598]
  4. German Research Foundation (DFG) [Do 769/4-1]
  5. European Union (large-scale integrative project MEASTRIA) [965286]

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Recent studies suggest that imbalances in gut microbiota composition may contribute to atrial fibrillation (AF), a condition where the heart beats irregularly. The gut microbiota is a complex ecosystem of trillions of microorganisms that can be influenced by factors such as diet and drugs, in addition to individual characteristics. Research explores the potential bidirectional relationship between AF and gut microbiota, examining how the microbiota's metabolites could affect AF development. Additionally, investigations into modifying gut microbiota through pharmacological and dietary interventions are discussed as potential methods to prevent AF progression.
Recent preclinical and observational cohort studies have implicated imbalances in gut microbiota composition as a contributor to atrial fibrillation (AF). The gut microbiota is a complex and dynamic ecosystem containing trillions of microorganisms, which produces bioactive metabolites influencing host health and disease development. In addition to host-specific determinants, lifestyle-related factors such as diet and drugs are important determinants of the gut microbiota composition. In this review, we discuss the evidence suggesting a potential bidirectional association between AF and gut microbiota, identifying gut microbiota-derived metabolites as possible regulators of the AF substrate. We summarize the effect of gut microbiota on the development and progression of AF risk factors, including heart failure, hypertension, obesity, and coronary artery disease. We also discuss the potential anti-arrhythmic effects of pharmacological and diet-induced modifications of gut microbiota composition, which may modulate and prevent the progression to AF. Finally, we highlight important gaps in knowledge and areas requiring future investigation. Although data supporting a direct relationship between gut microbiota and AF are very limited at the present time, emerging preclinical and clinical research dealing with mechanistic interactions between gut microbiota and AF is important as it may lead to new insights into AF pathophysiology and the discovery of novel therapeutic targets for AF.

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