Abstract 17263: Curative Treatment of Atrial Fibrillation by Pulmonary Vein Isolation Causes Reduced Cd11b Expression on Inflammatory Cells
Introduction: Inflammation plays a significant role in the genesis and perpetuation of atrial fibrillation (AF). These remodeling processes further sustain the existence of AF, known as the “AF begets AF”-phenomenon. The expression of CD11b on monocytes and granulocytes could be associated with the prevalence of AF and its thrombogenicity. The infiltration of inflammatory cells in atrial myocardium is known to be mediated by CD11b which furthermore could be associated with the development of atrial fibrosis as well as the receptiveness for AF.
Hypothesis: Curative treatment of AF by pulmonary vein isolation (PVI) could lead to reduced markers of inflammation, especially to a decrease of CD11b expression on monocytes and granulocytes.
Methods: Flow-cytometric quantification analyses and determination of systemic inflammatory markers of peripheral blood, like CRP, IL-6, TNFα and PCT, were detected at baseline as well as on the day of follow-up, six months after PVI. All 75 patients completed the study. The extent of activation of monocytes and granulocytes was measured by quantifying the cell adhesion molecule CD11b.
Results: The mean expression of CD11b on monocytes (20.9 ± 2.5 vs. 10.2 ± 1.4; p<0.001) and on granulocytes (13.9 ± 1.6 vs. 6.8 ± 0.5; p<0.001) as well as the relative count of CD11b positive monocytes (p<0.05) and CD11b positive granulocytes (p<0.01) was significantly reduced, comparing the same patients before PVI to six months after performed intervention. Patients with unsuccessful PVI and ongoing AF on day of follow-up showed no decrease in CD11b expression. Moreover, patients with running AF on the day of follow-up showed an increased expression of CD11b than those patients with sinus rhythm. Systemic inflammatory parameters, such as CRP and PCT, showed only a declining tendency after six months.
Conclusions: Curative treatment of AF with catheter ablation significantly reduced expression of activated CD11b on monocytes and granulocytes. AF itself seems to promote proinflammatory processes at cellular level, giving further proof for the bidirectional interaction between AF and inflammation. It highlights another mechanism of the interdependency of AF and inflammation which may contribute to remodeling processes in patients with AF.
- Arrhythmias, treatment of
- Atrial fibrillation
- Inflammation and inflammatory markers
- Catheter ablation
Author Disclosures: C. Pfluecke: None. D. Tarnowski: None. L. Plichta: None. F.M. Heidrich: None. P. Barthel: None. M. Forkmann: None. S. Ulbrich: None. M. Christoph: None. D.M. Poitz: None. C. Wunderlich: None. R.H. Strasser: None. K. Ibrahim: None.
- © 2016 by American Heart Association, Inc.