title: Enhanced expression of platelet CD40-ligand by in vitro lipopolysaccharide-challenge in patients with ventricular fibrillation complicating acute myocardial infarction.
abstract: BACKGROUND
  Acute myocardial infarction can be complicated by ventricular arrhythmias due to electrophysiological changes in the ischemic myocardium, but the exact predisposing factors causing ventricular fibrillation during myocardial infarction still remain unclear. A role of inflammatory stimulation on platelets as a potential risk factor for ventricular fibrillation during acute myocardial infarction has not been described yet.
  
  
  RESULTS
  Whole blood samples of 21 patients with a history of acute myocardial infarction (AMI) and ventricular fibrillation (VF) were incubated with lipopolysaccharide (LPS). As a control group, we studied 19 patients without VF during AMI. CD40-ligand and CD62P expression on platelets and tissue factor binding on monocytes were measured by flow cytometry. Platelet-monocyte aggregates were measured by CD41 expression on platelets adherent to monocytes. Soluble CD40-ligand plasma levels were measured with an ELISA. Without LPS, no significant difference between the patient groups concerning CD40L expression on platelets was observed, but plasma levels of soluble CD40L were significantly higher in patients with a history of AMI with VF. After LPS stimulation, patients with a history of VF showed a significantly increased expression of CD40L in comparison to the patients without ventricular fibrillation, based on a significantly higher increase of CD40L expression. CD62P expression on platelets was significantly increased in patients with a history of VF.
  
  
  CONCLUSIONS
  Patients with a history of VF complicating AMI show an enhanced expression of CD40L on platelets after in vitro lipopolysaccharide-challenge with an enhanced platelet activation.
authors.affiliation: Department of Cardiology, 1st Department of Medicine, University Hospital Mannheim, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany.
authors.forename: Thorsten
authors.initials: T
authors.lastname: Kälsch
authors.forename: Elif
authors.initials: E
authors.lastname: Elmas
authors.forename: Xuan Duc
authors.initials: XD
authors.lastname: Nguyen
authors.forename: Christian
authors.initials: C
authors.lastname: Wolpert
authors.forename: Harald
authors.initials: H
authors.lastname: Klüter
authors.forename: Martin
authors.initials: M
authors.lastname: Borggrefe
authors.forename: Karl Konstantin
authors.initials: KK
authors.lastname: Haase
authors.forename: Carl Erik
authors.initials: CE
authors.lastname: Dempfle
mesh_terms: D015415:Biomarkers / Q000097:blood; D023201:CD40 Ligand / Q000097:blood*; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008070:Lipopolysaccharides; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications*; D012189:Retrospective Studies; D014693:Ventricular Fibrillation / Q000097:blood* / Q000209:etiology
chemical_list: D015415:Biomarkers; D008070:Lipopolysaccharides; D023201:CD40 Ligand