title: Enhanced coagulation activation by in vitro lipopolysaccharide challenge in patients with ventricular fibrillation complicating acute myocardial infarction.
abstract: BACKGROUND
  Indicators of coagulation and inflammation are elevated in patients with coronary heart disease. A role of coagulation activation in ventricular fibrillation during acute myocardial infarction has not been described.
  
  
  RESULTS
  Whole blood samples of 21 patients with a history of acute myocardial infarction complicated by ventricular fibrillation and whole blood samples of 18 patients without ventricular fibrillation were incubated with lipopolysaccharide (LPS). In both groups, the in vitro blood coagulation time was measured with the ReoRox, a viscometric whole blood coagulometer. CD62P expression on platelets, tissue-factor binding on monocytes, and platelet-monocyte aggregates were measured with flow cytometry. Without LPS, no difference in the coagulation times were observed in both patient groups. After incubation with LPS, patients with a history of ventricular fibrillation showed a significantly decreased coagulation time compared to patients without ventricular fibrillation. The decrease of coagulation time after incubation with LPS also differed significantly in both groups. Expression of CD62P on platelets was significantly higher in patients with a history of ventricular fibrillation after incubation with LPS. Although in each patient group incubation with LPS induced a significantly increased amount of tissue factor on monocytes and a significantly increased the number of platelet-monocyte aggregates, the two groups did not differ significantly concerning tissue factor binding on monocytes and the amount of platelet-monocyte aggregates.
  
  
  CONCLUSIONS
  After in vitro LPS challenge, patients with a history of ventricular fibrillation during myocardial infarction show an enhanced coagulation activation, which may partly be due to an enhanced platelet activation.
authors.affiliation: 1st Department of Medicine, University Hospital Mannheim, Germany. thorsten.kaelsch@med.ma.uni-heidelberg.de
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: Nadine
authors.initials: N
authors.lastname: Grebert
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: D000328:Adult; D000368:Aged; D001777:Blood Coagulation / Q000187:drug effects*; D002449:Cell Aggregation / Q000187:drug effects; D003430:Cross-Sectional Studies; D005260:Female; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000502:physiology; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology; D015539:Platelet Activation / Q000187:drug effects; D012189:Retrospective Studies; D014693:Ventricular Fibrillation / Q000150:complications*
chemical_list: D008070:Lipopolysaccharides