Article

Role of inflammation in early atrial fibrillation recurrence.

Department of Cardiology, Thoraxcenter, University Medical Center Groningen, University of Groningen, PO Box 30.001, 9700 RB Groningen, The Netherlands.
Europace (Impact Factor: 2.77). 01/2012; 14(6):810-7. DOI: 10.1093/europace/eur402
Source: PubMed

ABSTRACT Outcome of rhythm control in atrial fibrillation (AF) is still poor due to various mechanisms involved in the initiation and perpetuation of AF. Differences in timing of AF recurrence may depend on different types of mechanisms. The aim of this study was to assess the mechanisms involved in early AF recurrence in patients with short-lasting AF.
Patients with short-lasting persistent AF undergoing rhythm control (n= 100) were included. Markers of mechanisms involved in the initiation and perpetuation of AF were assessed, including clinical factors, echocardiographic parameters, and biomarkers. Primary endpoint was early AF recurrence (recurrence <1 month). Secondary endpoint was progression to permanent AF. Median total AF history was short: 4.2 months. Early AF recurrences occurred in 30 patients (30%) after a median of 6 (inter-quartile range 2-14) days. Baseline log(2) interleukin (IL)-6 [adjusted hazard ratio (HR) 1.3, 95% confidence interval (CI) 1.0-1.7, P= 0.02] and present or previous smoking (adjusted HR 3.6, 95% CI 1.2-10.9, P= 0.03) were independently associated with early AF recurrence, suggesting that inflammation played an important role in early recurrences. Atrial fibrillation became permanent in 29 patients (29%). Baseline transforming growth factor-β1, left ventricular ejection fraction, and early AF recurrence were independently associated with progression to permanent AF.
In patients with short-lasting AF, early AF recurrence seemed to be associated with inflammation as represented by IL-6. Treatment aimed against inflammation may therefore prevent early AF recurrences, which can improve rhythm control outcome.

0 Bookmarks
 · 
87 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: ABSTRACT Purpose: Knowledge about the role of inflammation in the pathogenesis of arrhythmias in children is limited. Several studies have suggested a relationship between plasma IL-6 levels and/or the -174G>C IL-6 gene polymorphism and atrial fibrillation in adults. Our present study was performed to investigate whether serum IL-6, -174G>C IL-6 polymorphism and C-reactive protein (CRP) are associated with arrhythmias of unknown origin in children. Methods: The study included 126 children diagnosed with supraventricular or ventricular arrhythmia. Patients with congenital heart defects as well as arrhythmias of known origin were excluded from the study. The control group comprised 37 healthy children. The 24 hour Holter electrocardiography monitoring was performed. Serum IL-6, -174 GC IL-6 polymorphism and CRP concentrations were measured on admission. Results: There were no differences in IL-6, CRP and -174 G>C IL-6 genotype distribution between the control and patient groups. No significant differences in IL-6, CRP and -174 G>C IL-6 genotypes were observed between children with supraventricular or ventricular arrhythmias. The severity of arrhythmias showed also no associations with IL-6, CRP or -174 G>C IL-6 genotypes. Conclusion: The results suggest that idiopathic cardiac arrhythmias of unknown origin in children are not associated with selected pro-inflammatory markers of infections i.e. elevated IL-6, CRP or -174 G>C IL-6 polymorphism. This new information can effectively reduce the total financial cost of unnecessary diagnosis and treatment of children affected by cardiac arrhythmias.
    Advances in Medical Sciences 11/2013; · 0.80 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Substantial literature exists linking inflammation with arrhythmia, in particular with regards to serological markers of systemic inflammation. Regional inflammation can be identified using positron emission tomography (PET) with the radiotracer F18-fluorodeoxyglucose (F18-FDG). In the current series, we demonstrate novel applications of cardiac PET using F18-FDG and N13-ammonia radiotracers in the evaluation and treatment of arrhythmia associated with cardiac sarcoidosis. These applications include defining the cause of arrhythmia, identifying arrhythmias that will be amenable to medical management, and guiding therapy using serial scanning. Though these applications are promising, prospective multicenter studies are needed to provide better understanding of the utility of PET imaging in the diagnosis and treatment of arrhythmias.
    The international journal of cardiovascular imaging 11/2013; · 2.15 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The historical origin of the term ‘lone atrial fibrillation (AF)’ predates by 80 years our current understanding of the pathophysiology of AF, the multitude of known etiologies for AF, and our ability to image and diagnose heart disease. The term was meant to indicate AF in whom subsequent investigations could not demonstrate heart disease, but for many practitioners has become synonymous with ‘idiopathic AF’. As the list of heart diseases has expanded and diagnostic techniques have improved, the prevalence of ‘lone AF’ has fallen. The legacy of the intervening years is that definitions of ‘lone AF’ in the literature are inconsistent such that studies of ‘lone AF’ are not comparable Guidelines provide a vague definition of ‘lone AF’ but do not provide direction about how much or what kind of imaging and other testing are necessary to exclude heart disease. There has been an explosion in the understanding of the pathophysiology of AF in the last 20 years in particular. Nevertheless, there are no apparently unique mechanisms for AF in patients categorized as ‘lone AF’. In addition, the term ‘lone AF’ is not invariably useful in making treatment decisions, and other tools for doing so have been more thoroughly and carefully validated. It is therefore recommended that use of the term ‘lone AF’ be avoided.
    Journal of the American College of Cardiology 01/2014; · 14.09 Impact Factor