title: Atrial fibrillation is associated with high levels of monocyte-platelet-aggregates and increased CD11b expression in patients with aortic stenosis.
abstract: A growing body of evidence suggests a pivotal role of inflammatory processes in AF in a bidirectional manner. Infiltrating leukocytes seem to promote both structural and electrical remodelling processes in patients with AF. Monocyte-platelets-aggregates (MPAs) are sensitive markers of both platelets and monocyte activation. So far it is not clear whether the content of MPAs is affected by AF. The present study examined the content of MPAs and the activation of monocytes in elderly patients with an aortic stenosis in dependence of AF. These patients are known to have a high prevalence of AF. Flow-cytometric quantification analysis demonstrated that patients with AF have an increased content of MPAs (207 ± 13 cells/µl vs 307 ± 21 cells/µl, p< 0.001), and enhanced expression of CD11b on monocytes (p< 0.001), compared to patients in stable sinus rhythm (SR). The number of CD14+/CD16+ monocytes were only slightly elevated in patients with AF. These findings were seen in patients with permanent AF. But also patients with paroxysmal AF, even when presenting in SR, the MPAs were increased by 50 % (p< 0.05) as well as the CD11b expression, which was twice as high (p< 0.05) compared to stable SR. These results demonstrate for the first time a dependency of MPAs and CD11b expression on monocytes in the presence of AF and support the notion of a close relationship between AF, thrombogenesis and inflammation. The content of MPAs and the extent of activation on monocytes appear promising as biomarkers for paroxysmal AF and as possible future targets for developing novel pharmacological therapeutic strategies.
authors.affiliation: Dr. med. Christian Pfluecke, Fetscherstrasse 76, 01307 Dresden, Germany, Tel.: +49 351 4500, Fax: +49 351 450 1702, E-mail: christian.pfluecke@mailbox.tu-dresden.de.
authors.forename: Christian
authors.initials: C
authors.lastname: Pfluecke
authors.forename: Katharina
authors.initials: K
authors.lastname: Berndt
authors.forename: Sandy
authors.initials: S
authors.lastname: Wydra
authors.forename: Daniel
authors.initials: D
authors.lastname: Tarnowski
authors.forename: Peggy
authors.initials: P
authors.lastname: Barthel
authors.forename: Silvio
authors.initials: S
authors.lastname: Quick
authors.forename: Stefan
authors.initials: S
authors.lastname: Ulbrich
authors.forename: Marian
authors.initials: M
authors.lastname: Christoph
authors.forename: Nadine
authors.initials: N
authors.lastname: Waessnig
authors.forename: Uwe
authors.initials: U
authors.lastname: Speiser
authors.forename: Carsten
authors.initials: C
authors.lastname: Wunderlich
authors.forename: David M
authors.initials: DM
authors.lastname: Poitz
authors.forename: Ruth H
authors.initials: RH
authors.lastname: Strasser
authors.forename: Karim
authors.initials: K
authors.lastname: Ibrahim
mesh_terms: D000369:Aged, 80 and over; D001024:Aortic Valve Stenosis / Q000097:blood* / Q000150:complications* / Q000276:immunology; D001281:Atrial Fibrillation / Q000097:blood* / Q000150:complications* / Q000276:immunology; D015415:Biomarkers / Q000097:blood; D001792:Blood Platelets / Q000473:pathology; D039481:CD11b Antigen / Q000097:blood*; D002449:Cell Aggregation; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D009000:Monocytes / Q000276:immunology / Q000473:pathology; D015539:Platelet Activation; D010974:Platelet Aggregation; D013927:Thrombosis / Q000097:blood / Q000209:etiology / Q000276:immunology
chemical_list: D015415:Biomarkers; D039481:CD11b Antigen; C509295:ITGAM protein, human; D018836:Inflammation Mediators
keywords: Atrial fibrillation; inflammation; monocyte-platelet aggregates; monocytes; stroke