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Source of inflammatory markers in patients with atrial fibrillation

Ioan Liuba1, Henrik Ahlmroth, Lena Jonasson

  • 1Department of Cardiology, University Hospital Linköping, 581 85 Linköping, Sweden. ioan.liuba@imv.liu.se

Europace : European Pacing, Arrhythmias, and Cardiac Electrophysiology : Journal of the Working Groups on Cardiac Pacing, Arrhythmias, and Cardiac Cellular Electrophysiology of the European Society of Cardiology
|June 5, 2008
PubMed

Insights

Permanent atrial fibrillation (AF) is linked to a low-grade inflammatory reaction, specifically elevated interleukin-8 (IL-8) in systemic circulation. This suggests systemic inflammation, not AF itself, may drive elevated IL-8 in permanent AF patients.

Area of Science:

  • Cardiology
  • Immunology
  • Biochemistry

Background:

  • Elevated inflammatory markers are observed in some atrial fibrillation (AF) patients, but their origin and relation to AF are unclear.
  • The source of inflammation in AF remains unknown, necessitating research into localized versus systemic inflammatory processes.

Purpose of the Study:

  • To investigate the extent and source of inflammation in patients with AF, specifically differentiating between paroxysmal and permanent AF.
  • To assess inflammatory markers in blood samples from various locations to pinpoint the origin of inflammation in AF patients without other confounding conditions.

Main Methods:

  • Blood samples were collected from the femoral vein, right atrium, coronary sinus, and pulmonary veins of 29 patients (paroxysmal AF, permanent AF, and controls with WPW syndrome).
  • High-sensitive C-reactive protein, interleukin-6 (IL-6), and interleukin-8 (IL-8) were measured in all samples prior to radiofrequency catheter ablation.
  • No patients had structural heart disease or inflammatory conditions.

Main Results:

  • Patients with permanent AF showed significantly higher plasma IL-8 levels in the femoral vein, right atrium, and coronary sinus compared to controls and paroxysmal AF patients.
  • No significant differences in IL-8 levels were found in pulmonary vein samples between the groups.
  • C-reactive protein and IL-6 levels did not differ significantly across the three patient groups.

Conclusions:

  • Elevated IL-8 in permanent AF patients, particularly in systemic circulation, suggests a link between long-lasting AF and a low-grade systemic inflammatory reaction.
  • The absence of elevated IL-8 in pulmonary veins indicates that the inflammation source is likely systemic rather than originating within the pulmonary vasculature.
  • These findings differentiate permanent AF from paroxysmal AF regarding inflammatory profiles and suggest systemic circulation as the source of elevated IL-8.
Abstract

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