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.

Heart Rhythm O2
|June 11, 2021
PubMed

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.

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