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

Standard

Gut microbiota, dysbiosis and atrial fibrillation. Arrhythmogenic mechanisms and potential clinical implications. / Gawałko, Monika; Agbaedeng, Thomas A; Saljic, Arnela; Müller, Dominik N; Wilck, Nicola; Schnabel, Renate; Penders, John; Rienstra, Michiel; van Gelder, Isabelle; Jespersen, Thomas; Schotten, Ulrich; Crijns, Harry J G M; Kalman, Jonathan M; Sanders, Prashanthan; Nattel, Stanley; Dobrev, Dobromir; Linz, Dominik.

In: CARDIOVASC RES, Vol. 118, No. 11, 24.08.2022, p. 2415-2427.

Research output: SCORING: Contribution to journalSCORING: Review articleResearch

Harvard

Gawałko, M, Agbaedeng, TA, Saljic, A, Müller, DN, Wilck, N, Schnabel, R, Penders, J, Rienstra, M, van Gelder, I, Jespersen, T, Schotten, U, Crijns, HJGM, Kalman, JM, Sanders, P, Nattel, S, Dobrev, D & Linz, D 2022, 'Gut microbiota, dysbiosis and atrial fibrillation. Arrhythmogenic mechanisms and potential clinical implications', CARDIOVASC RES, vol. 118, no. 11, pp. 2415-2427. https://doi.org/10.1093/cvr/cvab292

APA

Gawałko, M., Agbaedeng, T. A., Saljic, A., Müller, D. N., Wilck, N., Schnabel, R., Penders, J., Rienstra, M., van Gelder, I., Jespersen, T., Schotten, U., Crijns, H. J. G. M., Kalman, J. M., Sanders, P., Nattel, S., Dobrev, D., & Linz, D. (2022). Gut microbiota, dysbiosis and atrial fibrillation. Arrhythmogenic mechanisms and potential clinical implications. CARDIOVASC RES, 118(11), 2415-2427. https://doi.org/10.1093/cvr/cvab292

Vancouver

Bibtex

@article{4a91e5ef99244331bc6c3183e1cf7a55,
title = "Gut microbiota, dysbiosis and atrial fibrillation. Arrhythmogenic mechanisms and potential clinical implications",
abstract = "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 antiarrhythmic 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.",
keywords = "Atrial Fibrillation, Dysbiosis, Ecosystem, Gastrointestinal Microbiome, Humans, Obesity",
author = "Monika Gawa{\l}ko and Agbaedeng, {Thomas A} and Arnela Saljic and M{\"u}ller, {Dominik N} and Nicola Wilck and Renate Schnabel and John Penders and Michiel Rienstra and {van Gelder}, Isabelle and Thomas Jespersen and Ulrich Schotten and Crijns, {Harry J G M} and Kalman, {Jonathan M} and Prashanthan Sanders and Stanley Nattel and Dobromir Dobrev and Dominik Linz",
note = "Published on behalf of the European Society of Cardiology. All rights reserved. {\textcopyright} The Author(s) 2021. For permissions please email: journals.permissions@oup.com.",
year = "2022",
month = aug,
day = "24",
doi = "10.1093/cvr/cvab292",
language = "English",
volume = "118",
pages = "2415--2427",
journal = "CARDIOVASC RES",
issn = "0008-6363",
publisher = "Oxford University Press",
number = "11",

}

RIS

TY - JOUR

T1 - Gut microbiota, dysbiosis and atrial fibrillation. Arrhythmogenic mechanisms and potential clinical implications

AU - Gawałko, Monika

AU - Agbaedeng, Thomas A

AU - Saljic, Arnela

AU - Müller, Dominik N

AU - Wilck, Nicola

AU - Schnabel, Renate

AU - Penders, John

AU - Rienstra, Michiel

AU - van Gelder, Isabelle

AU - Jespersen, Thomas

AU - Schotten, Ulrich

AU - Crijns, Harry J G M

AU - Kalman, Jonathan M

AU - Sanders, Prashanthan

AU - Nattel, Stanley

AU - Dobrev, Dobromir

AU - Linz, Dominik

N1 - Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2021. For permissions please email: journals.permissions@oup.com.

PY - 2022/8/24

Y1 - 2022/8/24

N2 - 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 antiarrhythmic 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.

AB - 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 antiarrhythmic 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.

KW - Atrial Fibrillation

KW - Dysbiosis

KW - Ecosystem

KW - Gastrointestinal Microbiome

KW - Humans

KW - Obesity

U2 - 10.1093/cvr/cvab292

DO - 10.1093/cvr/cvab292

M3 - SCORING: Review article

C2 - 34550344

VL - 118

SP - 2415

EP - 2427

JO - CARDIOVASC RES

JF - CARDIOVASC RES

SN - 0008-6363

IS - 11

ER -