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Source of inflammatory markers in patients with atrial fibrillation
Linköping University, Department of Medicine and Health Sciences, Cardiology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart Centre, Department of Cardiology.
Department of Cardiology, University Hospital Örebro, Örebro, Sweden.
Östergötlands Läns Landsting, Heart Centre, Department of Cardiology. Linköping University, Department of Medicine and Health Sciences, Cardiology . Linköping University, Faculty of Health Sciences.
Department of Cardiology, University Hospital Örebro, Örebro, Sweden.
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2008 (English)In: 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, ISSN 1532-2092, Vol. 10, no 7, 848-853 p.Article in journal (Refereed) Published
Abstract [en]

AIMS: Elevated levels of C-reactive protein and other inflammatory markers have been reported in some patients with atrial fibrillation (AF). Whether this finding is related to AF per se or to other conditions remains unclear. In addition, the source of inflammatory markers is unknown. Therefore, in the present study, we sought to assess the extent and the source of inflammation in patients with AF and no other concomitant heart or inflammatory conditions.

METHODS AND RESULTS: The study group consisted of 29 patients referred for radiofrequency catheter ablation: 10 patients with paroxysmal AF, 8 patients with permanent AF, and 10 control patients with Wolf-Parkinson-White (WPW) syndrome and no evidence of AF (mean age 54 +/- 11 vs. 57 +/- 13 vs. 43 +/- 16). No patient had structural heart diseases or inflammatory conditions. High-sensitive C-reactive protein, interleukin-6 (IL-6), and interleukin-8 (IL-8) were assessed in blood samples from the femoral vein, right atrium, coronary sinus, and the left and right upper pulmonary veins. All samples were collected before ablation. Compared with controls and patients with paroxysmal AF, patients with permanent AF had higher plasma levels of IL-8 in the samples from the femoral vein, right atrium, and coronary sinus, but not in the samples from the pulmonary veins (median values in the femoral vein: 2.58 vs. 2.97 vs. 4.66 pg/mL, P = 0.003; right atrium: 2.30 vs. 3.06 vs. 3.93 pg/mL, P = 0.013; coronary sinus: 2.85 vs. 3.15 vs. 4.07, P = 0.016). A high-degree correlation existed between the IL-8 levels in these samples (correlation coefficient between 0.929 and 0.976, P < 0.05). No differences in the C-reactive protein and IL-6 levels were noted between the three groups of patients.

CONCLUSION: The normal levels of C-reactive protein and IL-6, along with the elevated levels of IL-8 in patients with permanent AF but not in those with paroxysmal AF, suggest a link between a low-grade inflammatory reaction and long-lasting AF. The elevated IL-8 levels in the peripheral blood, right atrium, and coronary sinus but not in the pulmonary veins suggest a possible source of inflammation in the systemic circulation.

Place, publisher, year, edition, pages
2008. Vol. 10, no 7, 848-853 p.
Keyword [en]
Atrial fibrillation, Inflammation, Catheter ablation
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-20458DOI: 10.1093/europace/eun111PubMedID: 18523031OAI: oai:DiVA.org:liu-20458DiVA: diva2:234573
Available from: 2009-09-09 Created: 2009-09-09 Last updated: 2013-12-17Bibliographically approved
In thesis
1. Focal atrial tachycardia: Insights concerning the arrhythmogenic substrate based on analysis of intracardiac electrograms and inflammatory markers
Open this publication in new window or tab >>Focal atrial tachycardia: Insights concerning the arrhythmogenic substrate based on analysis of intracardiac electrograms and inflammatory markers
2009 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Background: Focal atrial tachycardias are tachycardias characterized by a radial spread of activation from a discrete area of the atrial myocardium. They account for 10-15% of supraventricular tachycardias and are generally poorly responsive to pharmacological treatment. The pathophysiologic substrate of these arrhythmias remains poorly understood. Computational studies suggest that a certain degree of intercellular uncoupling and anisotropy are important prerequisites for the development of focal arrhythmias. The anisotropy and intercellular uncoupling could promote focal arrhythmias by minimizing the suppressive effect of the surrounding atrial muscle on the pacemaking process in the focus. This hypothesis would be in agreement with the fact that fractionated electrograms, a marker of anisotropy and reduced intercellular coupling, are often recorded at the site of earliest activated site. Reduced intercellular coupling could be induced by factors enhancing the amount of intracardiac connective tissue, such as advancing age or cardiac disease states. Indeed, focal inflammatory processes have been reported in atrial specimens resected from patients with focal tachycardia undergoing arrhythmia surgery.

Methods: In a group of patients with paroxysmal and permanent atrial fibrillation we sought to assess whether there is a link between inflammation and the occurrence of atrial arrhythmia. We therefore analyzed different inflammatory markers (C-reactive protein and interleukin-6 and 8) in the systemic and pulmonary circulation as well as in the heart in these patients. In addition, we assessed the extent of intercellular uncoupling in the vicinity of tachycardia origin in patients with focal atrial tachycardia. We also assessed the impact of electrogram fractionation on the method of activation time determination, by comparing different methods for estimating activation time with regard to the appearance of the resultant activation maps and the location of the foci. We also assessed the observer variability in the estimation of activation time during mapping of these tachycardias.

Results: There was no evidence of elevated circulatory levels of inflammatory markers in patients with paroxysmal atrial fibrillation. However, patients with permanent atrial fibrillation had increased levels of inflammatory markers (interleukin-8) in the systemic circulation but not in the pulmonary circulation or in the heart. In patients with focal atrial tachycardia, a higher degree of electrogram fractionation existed in the region surrounding the earliest activation site and activated within the first 15 ms as compared with the remaining atrium. Moreover, within this region, from the periphery towards the earliest activated site, there was a gradual increase in electrogram fractionation as well as a gradual decrease in the peak-to-peak voltage. When comparing different methods for estimating local activation time we found that different methods can generate activation maps with different appearances and foci with different locations. However, regardless of the method of activation time determination, the foci tend to cluster within relatively large areas of low-amplitude fractionated electrograms. In addition we found significant observer variability in the estimation of the local activation time.

Conclusion: Patients with paroxysmal atrial fibrillation (and probably focal atrial tachycardia) do not have elevated levels of inflammatory markers. The increased levels of interleukin-8 in the systemic circulation suggest a link between long-lasting arrhythmia and inflammation. A relatively wide area of increased electrogram fractionation exists around the site of origin of focal atrial tachycardia. These findings suggest a sizeable atrial region with particular electrophysiological proprieties and raise the possibility of an anatomical substrate of the tachycardia. Increased electrogram fractionation can impact the process of activation determination, as suggested by the fact that different methods compute foci with different locations. In addition, there is significant observer variability in the estimation of local activation time in these patient.

Place, publisher, year, edition, pages
Linköp: Linköping University Electronic Press, 2009. 96 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 1148
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-20461 (URN)978-91-7393-556-2 (ISBN)
Public defence
2009-09-04, Berzeliussalen, Hälsouniversitetet, Campus US, Linköpings Universitet, Linköping, 13:00 (English)
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Note
Article II and III are the same article while article III is linked to the corrected article and article II to the original article.Available from: 2009-09-09 Created: 2009-09-09 Last updated: 2010-02-25Bibliographically approved

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Liuba, IoanJonasson, LenaSäfström, KågeWalfridsson, Håkan

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