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Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Atrial Fibrillation and Endothelial Dysfunction: A Potential Link?
Michel T Corban1, Takumi Toya1, Ali Ahmad1
1Department of Cardiovascular Diseases, Mayo Clinic College of Medicine and Science, Rochester, MN.
Insights
Atrial fibrillation (AF) and atherosclerosis share common risk factors and mechanisms, like endothelial dysfunction. Targeting these shared factors may improve outcomes for both conditions.
Area of Science:
- Cardiology
- Vascular Biology
- Internal Medicine
Background:
- Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia, while coronary atherosclerosis is a leading cause of mortality globally.
- Endothelial dysfunction represents the earliest detectable stage of atherosclerosis.
- Current AF treatments have limitations, potentially due to an incomplete understanding of its complex pathophysiology.
Purpose of the Study:
- To explore mechanistic links between endothelial dysfunction and AF.
- To investigate a novel vascular perspective on AF pathophysiology.
- To highlight evidence associating endothelial dysfunction, AF, and stroke, and discuss potential common therapies.
Main Methods:
- Review of existing research on AF pathophysiology and endothelial dysfunction.
- Analysis of mechanistic links including inflammation, oxidative stress, ischemia, genetics, shear stress, and FGF-23.
- Synthesis of evidence linking systemic vascular endothelial dysfunction with AF and stroke.
Main Results:
- Shared risk factors for AF and atherosclerosis, such as inflammation and oxidative stress, impact both conditions.
- Endothelial dysfunction may represent a key link in the pathophysiology of AF.
- Evidence supports a connection between systemic vascular endothelial dysfunction, AF, and stroke risk.
Conclusions:
- Understanding the vascular dimension of AF pathophysiology is crucial.
- Targeting shared risk factors and endothelial dysfunction may offer a unified therapeutic approach for AF, atherosclerosis, and stroke prevention.
- Further research into common mechanistic pathways is warranted.
Abstract:
Atrial fibrillation (AF) is the most common cardiac arrhythmia, and coronary atherosclerosis is the leading cause of death in the United States and worldwide. Endothelial dysfunction is the earliest clinically detectable form of atherosclerosis. Control of shared AF and coronary atherosclerosis risk factors improves both AF-free survival and vascular endothelial function. Decades of AF research have yielded fundamental insight into AF pathophysiology, but current pharmacological and catheter-based invasive AF therapies have limited long-term efficacy and substantial side effects, possibly because of incomplete understanding of underlying complex AF pathophysiology. We hereby discuss potential mechanistic links between endothelial dysfunction and AF (risk-factor-associated systemic inflammation and oxidative stress, myocardial ischemia, common gene variants, vascular shear stress, and fibroblast growth factor-23), explore a potential new vascular dimension to AF pathophysiology, highlight a growing body of evidence supporting an association between systemic vascular endothelial dysfunction, AF, and stroke, and discuss potential common effective therapies.
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