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Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
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Published on: July 20, 2022

Endothelial dysfunction and pathophysiological correlates in atrial fibrillation.

M Guazzi1, R Arena

  • 1Cardiopulmonary Unit, University of Milan, Milan, Italy. marco.guazzi@unimi.it

Heart (British Cardiac Society)
|December 26, 2008
PubMed
Summary

Atrial fibrillation (AF) is linked to endothelial dysfunction (ED), impairing blood vessel function. Mechanisms include altered blood flow, atrial activity, inflammation, and the renin-angiotensin system (RAS).

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Published on: February 26, 2013

Area of Science:

  • Cardiovascular Science
  • Vascular Biology
  • Integrative Physiology

Background:

  • Endothelial dysfunction (ED) is characterized by impaired nitric oxide (NO)-dependent vasorelaxation, increased oxidative stress, and inflammation.
  • Atrial fibrillation (AF) is recognized as a significant risk factor for developing ED.

Purpose of the Study:

  • To review the evidence linking AF to ED.
  • To explore the underlying mechanisms contributing to the AF-ED association.
  • To discuss the pathophysiological correlates of ED in AF patients.

Main Methods:

  • Review of existing literature on AF and ED.
  • Analysis of proposed mechanisms including rheology, atrial function, inflammation, and systemic factors like the renin-angiotensin system (RAS).
  • Examination of clinical manifestations of ED in AF.

Main Results:

  • AF is associated with impaired acetylcholine-mediated blood flow, reduced plasma nitrite/nitrate, and exacerbated ED by comorbidities.
  • Mechanisms include turbulent blood flow impairing NO release, reduced eNOS expression due to disorganized atrial contraction, inflammation, and RAS activation.
  • Clinical correlates include muscle underperfusion and lactic acidosis during exercise.

Conclusions:

  • AF significantly contributes to endothelial dysfunction through multiple interconnected pathways.
  • Understanding these mechanisms is crucial for managing AF patients and mitigating cardiovascular risk.
  • Targeting these pathways, such as RAS inhibition, may offer therapeutic benefits.