Aldosterone-Mediated Atrial Remodeling and Atrial Fibrillation: Molecular Mechanisms, Translational Insights and Implications for Cardiac Surgery
- 1Department of Cardiac Anesthesia and Intensive Care Unit, Cardiac Surgery, Ospedale dell’Angelo, Mestre, 30174 Venice, Italy
- 2Department of Neurosciences, Institute of Human Anatomy, University of Padova, 35121 Padova, Italy
Abstract
Atrial fibrillation (AF) has heterogeneous mechanisms, including structural atrial cardiomyopathy, electrical remodeling and primary ion-channel abnormalities. Aldosterone–mineralcorticoid receptor (MR) signaling may contribute to an arrhythmogenic atrial substrate through redox-sensitive, inflammatory, profibrotic and electrophysiological pathways; however, their direct demonstration in human atria varies. Primary aldosteronism is associated with excess AF risk, but circulating aldosterone, renin-independent secretion, tissue MR activation and MR-antagonist exposure are not interchangeable biological measures. This narrative review critically distinguishes evidence from human atrial tissue, atrial experimental systems and extrapolation from other cardiovascular models, with particular emphasis on the cardiac surgical setting. Preoperative aldosterone has been associated with postoperative atrial fibrillation (POAF), whereas perioperative MR-antagonist studies have reported discordant findings and observational analyses remain susceptible to confounding. We propose a testable, rather than established, two-hit framework in which a pre-existing endocrine-associated atrial substrate may interact with perioperative inflammation and hemodynamic stress. The review identifies gaps in endocrine phenotyping and the need for adequately powered prospective and interventional studies before aldosterone-directed POAF prevention can be recommended.
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BibTeX
@article{torre2026aldosteronemediated,
title = {{Aldosterone-Mediated Atrial Remodeling and Atrial Fibrillation: Molecular Mechanisms, Translational Insights and Implications for Cardiac Surgery}},
author = {Debora Emanuela Torre and Carmelo Pirri},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27219466},
url = {https://www.mdpi.com/1422-0067/27/21/9466},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Aldosterone-Mediated Atrial Remodeling and Atrial Fibrillation: Molecular Mechanisms, Translational Insights and Implications for Cardiac Surgery
AU - Debora Emanuela Torre
AU - Carmelo Pirri
PY - 2026
DA - 2026/10/23
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219466
UR - https://www.mdpi.com/1422-0067/27/21/9466
AB - Atrial fibrillation (AF) has heterogeneous mechanisms, including structural atrial cardiomyopathy, electrical remodeling and primary ion-channel abnormalities. Aldosterone–mineralcorticoid receptor (MR) signaling may contribute to an arrhythmogenic atrial substrate through redox-sensitive, inflammatory, profibrotic and electrophysiological pathways; however, their direct demonstration in human atria varies. Primary aldosteronism is associated with excess AF risk, but circulating aldosterone, renin-independent secretion, tissue MR activation and MR-antagonist exposure are not interchangeable biological measures. This narrative review critically distinguishes evidence from human atrial tissue, atrial experimental systems and extrapolation from other cardiovascular models, with particular emphasis on the cardiac surgical setting. Preoperative aldosterone has been associated with postoperative atrial fibrillation (POAF), whereas perioperative MR-antagonist studies have reported discordant findings and observational analyses remain susceptible to confounding. We propose a testable, rather than established, two-hit framework in which a pre-existing endocrine-associated atrial substrate may interact with perioperative inflammation and hemodynamic stress. The review identifies gaps in endocrine phenotyping and the need for adequately powered prospective and interventional studies before aldosterone-directed POAF prevention can be recommended.
SN - 1422-0067
ER -