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Updated: Nov 2, 2025

Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Atrial remodeling and atrial fibrillation in acquired forms of cardiovascular disease
Hailey J Jansen1,2, Loryn J Bohne1,2, Anne M Gillis1
1Department of Cardiac Sciences, Libin Cardiovascular Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Insights
Atrial fibrillation (AF) is linked to heart disease, diabetes, hypertension, and aging. This review explores cellular and molecular changes causing AF remodeling in these conditions.
Area of Science:
- Cardiology
- Electrophysiology
- Gerontology
Background:
- Atrial fibrillation (AF) is common in cardiovascular diseases like diabetes mellitus (DM), hypertension, cardiac hypertrophy, and heart failure.
- Aging is an independent risk factor for AF, with significant health status variations (frailty) even among individuals of the same chronological age.
- AF pathogenesis involves atrial electrical and structural remodeling, including ion channel changes, fibrosis, myocyte hypertrophy, and adiposity.
Purpose of the Study:
- To review the cellular and molecular factors driving atrial electrical and structural remodeling.
- To identify similarities and differences in remodeling mechanisms across various conditions: DM, hypertension, hypertrophy, heart failure, aging, and frailty.
Main Methods:
- Focused review of existing literature.
- Analysis of human patient data and animal models of cardiovascular disease and associated risk factors.
Main Results:
- Electrical remodeling involves ion channel alterations; structural remodeling includes fibrosis, hypertrophy, and adiposity.
- Remodeling mechanisms differ across conditions like DM, hypertension, heart failure, aging, and frailty.
- These remodeling processes contribute to AF initiation and maintenance through triggered activity and electrical re-entry.
Conclusions:
- Understanding the distinct cellular and molecular bases of atrial remodeling in various conditions is crucial for targeted AF therapies.
- Frailty assessment may reveal heterogeneity in aging-related AF risk.
- Further research into specific remodeling pathways can elucidate AF pathogenesis in diverse patient populations.
Abstract:
Atrial fibrillation (AF) is prevalent in common conditions and acquired forms of heart disease, including diabetes mellitus (DM), hypertension, cardiac hypertrophy, and heart failure. AF is also prevalent in aging. Although acquired heart disease is common in aging individuals, age is also an independent risk factor for AF. Importantly, not all individuals age at the same rate. Rather, individuals of the same chronological age can vary in health status from fit to frail. Frailty can be quantified using a frailty index, which can be used to assess heterogeneity in individuals of the same chronological age. AF is thought to occur in association with electrical remodeling due to changes in ion channel expression or function as well as structural remodeling due to fibrosis, myocyte hypertrophy, or adiposity. These forms of remodeling can lead to triggered activity and electrical re-entry, which are fundamental mechanisms of AF initiation and maintenance. Nevertheless, the underlying determinants of electrical and structural remodeling are distinct in different conditions and disease states. In this focused review, we consider the factors leading to atrial electrical and structural remodeling in human patients and animal models of acquired cardiovascular disease or associated risk factors. Our goal is to identify similarities and differences in the cellular and molecular bases for atrial electrical and structural remodeling in conditions including DM, hypertension, hypertrophy, heart failure, aging, and frailty.
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