title: Is fibrin formation and thrombin generation increased during and after an acute coronary syndrome?
abstract: METHODS
  In order to study coagulation and fibrinolysis in acute coronary syndrome (ACS) we used a recently developed assay, called OH-index, which provides simultaneous measurements of fibrin formation and fibrinolysis (fibrin degradation) in the patients' plasma. We also investigated thrombin generation using the calibrated automated thrombogram (CAT), and assessed thrombin generation in vivo by measuring F1+2 plasma concentrations. In addition, to better characterize the patients we also assessed markers of inflammation and endothelial function. Eighty-seven ACS patients were sampled at admission, within 24 hours during treatment with low molecular weight heparin (LMH), and 6 months later; 65 healthy controls were also sampled.
  
  
  RESULTS
  As assessed by OH-index fibrin formation was slightly depressed at admission, profoundly depressed during LMH treatment and comparable to controls at 6 months, whereas fibrin degradation was elevated, particularly during LMH treatment. F1+2 levels decreased during LMH treatment but did not deviate significantly from controls at admission or in convalescence. CAT data showed that peak thrombin was higher at admission and after 6 months compared to controls, whereas the endogenous thrombin potential only tended to be elevated. Both variables were strongly reduced during LMH treatment. Patients had elevated levels of markers of inflammation and endothelial function as expected.
  
  
  CONCLUSIONS
  ACS-patients have an increased capacity to generate thrombin and an enhanced capacity to degrade fibrin in the acute phase. Increased thrombin generation persists also 6 months after the event.
authors.affiliation: Karolinska Institutet, Department of Clinical Sciences, Danderyd Hospital, Division of Cardiovascular Medicine, Stockholm, Sweden. mika.skeppholm@ds.se
authors.forename: Mika
authors.initials: M
authors.lastname: Skeppholm
authors.forename: Anders
authors.initials: A
authors.lastname: Kallner
authors.forename: Karin
authors.initials: K
authors.lastname: Malmqvist
authors.forename: Margareta
authors.initials: M
authors.lastname: Blombäck
authors.forename: Håkan
authors.initials: H
authors.lastname: Wallén
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood* / Q000473:pathology / Q000503:physiopathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000502:physiology; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000502:physiology; D005260:Female; D005337:Fibrin / Q000378:metabolism*; D005342:Fibrinolysis / Q000502:physiology; D006801:Humans; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D013917:Thrombin / Q000096:biosynthesis*
chemical_list: D015415:Biomarkers; D005337:Fibrin; D013917:Thrombin