[The altered endothelial function in patients with arterial hypertension and different forms of atrial fibrillation]

Klinicheskaia Meditsina
|October 2, 2014
PubMed

Insights

Endothelial dysfunction, characterized by impaired vasodilation and increased Willebrand factor, is linked to arterial hypertension and persistent atrial fibrillation, indicating its role in cardiovascular disease progression.

Area of Science:

  • Cardiovascular Medicine
  • Vascular Biology
  • Clinical Research

Background:

  • Endothelial dysfunction (ED) is increasingly recognized as a precursor to cardiovascular diseases.
  • A strong association exists between ED and cardiac arrhythmias, particularly atrial fibrillation (AF).
  • ED precedes target organ damage in arterial hypertension (AH), highlighting its potential as an early marker.

Purpose of the Study:

  • To investigate endothelial function changes in patients diagnosed with arterial hypertension (AH) and atrial fibrillation (AF).
  • To assess the relationship between persistent AF, AH, and markers of endothelial health.

Main Methods:

  • Comparative study involving three groups: AH with paroxysmal AF (n=84), AH with permanent AF (n=20), and AH without AF (control, n=30).
  • Endothelial vasomotor function was assessed using reactive hyperemia via ultrasound.
  • Blood samples were analyzed for Willebrand factor (WF) collagen-binding activity.

Main Results:

  • Patients with AH and permanent AF exhibited significantly reduced endothelium-dependent vasodilation of the brachial artery.
  • Collagen-binding activity of WF was significantly elevated in patients with AH and permanent AF compared to other groups.
  • These findings suggest a marked alteration in endothelial function in this patient cohort.

Conclusions:

  • Patients experiencing both arterial hypertension and persistent atrial fibrillation demonstrate impaired endothelial function.
  • This impairment is evidenced by decreased brachial artery vasodilation and elevated WF activity.
  • Endothelial dysfunction is a significant factor in the pathophysiology of AH and persistent AF.
Abstract

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