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Published on: July 20, 2022
The Complex Interplay Between Aging, Cardiac Remodeling, and Atrial Fibrillation
Tammy Ryan1, Carlos A Morillo2, José Jalife3
1Libin Cardiovascular Institute, University of Calgary Health Research Innovation Centre, Calgary, Alberta, Canada.
Insights
Aging significantly increases atrial fibrillation risk. Research explores underlying mechanisms like fibrosis and inflammation to understand this public health challenge.
Area of Science:
- Cardiovascular Science
- Aging Research
- Pathophysiology
Background:
- Aging is a primary risk factor for atrial fibrillation.
- The aging global population exacerbates this public health concern.
- Specific mechanisms linking aging to atrial fibrillation are not fully understood.
Purpose of the Study:
- To review recent research on the link between aging and atrial fibrillation.
- To focus on the basic pathophysiological mechanisms involved.
- To identify areas for future research.
Main Methods:
- Literature review of studies from the last several years.
- Focus on basic science and pathophysiological mechanisms.
- Synthesis of current understanding and identification of knowledge gaps.
Main Results:
- Several biological processes implicated: fibrosis, DNA damage, chromatin remodeling, amyloid deposition, mitochondrial dysfunction, and inflammation.
- These processes contribute to structural and functional atrial changes.
- Current research highlights multiple contributing factors to age-related atrial remodeling.
Conclusions:
- Aging-associated pathophysiological changes are central to atrial fibrillation development.
- Further research is needed to fully elucidate the complex relationship between aging and atrial fibrillation.
- Understanding these mechanisms may lead to targeted interventions for age-related cardiovascular diseases.
Abstract:
Aging is one of the most significant risk factors for the development of atrial fibrillation, and given our aging population, this is likely to present a major public health challenge in the coming years. Although the specific mechanisms underlying this association remain poorly understood, several biological processes including fibrosis, DNA damage, chromatin remodeling, amyloid deposition, mitochondrial dysfunction, and inflammation have been implicated in the structural and functional deterioration that leads to the development of atrial fibrillation. Herein, we review work from the last several years that has contributed to our understanding of the link between aging and atrial fibrillation with a focus on the basic pathophysiological mechanisms. We also outline areas for future research aimed at better characterizing this complex relationship.
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