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Reduction of atrial fibrillation burden by pulmonary vein isolation leads to a decrease of CD11b expression on inflammatory cells
- Source :
- EP Europace. 20:459-465
- Publication Year :
- 2017
- Publisher :
- Oxford University Press (OUP), 2017.
-
Abstract
- Aims It is hypothesized that inflammation could promote structural and electrical remodelling processes in atrial fibrillation (AF). Atrial infiltration of monocytes and granulocytes has been shown to be dependent on CD11b expression. The aim of this study was to investigate whether treatment of AF by pulmonary vein isolation (PVI) may lead to reduced inflammation, as indicated by a decrease of CD11b expression on monocytes and granulocytes. Methods and results Flow-cytometric quantification analysis and determination of systemic inflammatory markers of peripheral blood were performed in 75 patients undergoing PVI 1 day before and 6 months after PVI. The extent of activation of monocytes and granulocytes was measured by quantifying the cell adhesion molecule CD11b. The mean expression of CD11b on monocytes (20.9 ± 2.5 vs. 10.2 ± 1.4; P
- Subjects :
- Male
0301 basic medicine
medicine.medical_specialty
Time Factors
Action Potentials
Down-Regulation
Inflammation
030204 cardiovascular system & hematology
Gastroenterology
Monocytes
Pulmonary vein
03 medical and health sciences
0302 clinical medicine
Downregulation and upregulation
Heart Rate
Risk Factors
Physiology (medical)
Internal medicine
Atrial Fibrillation
Heart rate
Humans
Medicine
Atrium (heart)
Aged
CD11b Antigen
biology
business.industry
Cell adhesion molecule
Atrial fibrillation
Atrial Remodeling
Middle Aged
medicine.disease
Treatment Outcome
030104 developmental biology
medicine.anatomical_structure
Integrin alpha M
Pulmonary Veins
Immunology
Catheter Ablation
biology.protein
Female
Inflammation Mediators
medicine.symptom
Cardiology and Cardiovascular Medicine
business
Granulocytes
Subjects
Details
- ISSN :
- 15322092 and 10995129
- Volume :
- 20
- Database :
- OpenAIRE
- Journal :
- EP Europace
- Accession number :
- edsair.doi.dedup.....e17fa5739bf1da0e694dda406c822123