title: Markers of thrombin generation are associated with myocardial necrosis and left ventricular impairment in patients with ST-elevation myocardial infarction.
abstract: BACKGROUND
  Platelet activation, thrombin generation and fibrin formation play important roles in intracoronary thrombus formation, which may lead to acute myocardial infarction. We investigated whether the prothrombotic markers D-dimer, pro-thrombin fragment 1 + 2 (F1 + 2) and endogenous thrombin potential (ETP) are associated with myocardial necrosis assessed by Troponin T (TnT), and left ventricular impairment assessed by left ventricular ejection fraction (LVEF) and N-terminal pro b-type natriuretic peptide (NT-proBNP).
  
  
  METHODS
  Patients (n = 987) with ST-elevation mycardial infarction (STEMI) were included. Blood samples were drawn at a median time of 24 h after onset of symptoms.
  
  
  RESULTS
  Statistically significant correlations were found between both peak TnT and D-dimer (p < 0.001) and F1 + 2 (p < 0.001), and between NT-proBNP and D-dimer (p = 0.001) and F1 + 2 (p < 0.001). When dividing TnT and NT-proBNP levels into quartiles there were significant trends for increased levels of both markers across quartiles (all p < 0.001) D-dimer remained significantly associated with NT-proBNP after adjustments for covariates (p = 0.001) whereas the association between NTproBNP and F1 + 2 was no longer statistically significant (p = 0.324). A significant inverse correlation was found between LVEF and D-dimer (p < 0.001) and F1 + 2 (p = 0.013). When dichotomizing LVEF levels at 40 %, we observed significantly higher levels of both D-dimer (p < 0.001) and F1 + 2 (p = 0.016) in the group with low EF (n = 147).
  
  
  CONCLUSIONS
  In our cohort of STEMI patients we demonstrated that levels of D-dimer and F1 + 2 were significantly associated with myocardial necrosis as assessed by peak TnT. High levels of these coagulation markers in patients with low LVEF and high NTproBNP may indicate a hypercoagulable state in patients with impaired myocardial function.
authors.affiliation: Center for Clinical Heart Research, Oslo University Hospital Ullevål, PB 4956 Nydalen, N-4956 Oslo, Norway ; Departement of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway.
authors.forename: C H
authors.initials: CH
authors.lastname: Hansen
authors.affiliation: Center for Clinical Heart Research, Oslo University Hospital Ullevål, PB 4956 Nydalen, N-4956 Oslo, Norway ; Departement of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway ; Faculty of Medicine, University of Oslo, Oslo, Norway.
authors.forename: V
authors.initials: V
authors.lastname: Ritschel
authors.affiliation: Departement of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway ; Faculty of Medicine, University of Oslo, Oslo, Norway.
authors.forename: S
authors.initials: S
authors.lastname: Halvorsen
authors.affiliation: Center for Clinical Heart Research, Oslo University Hospital Ullevål, PB 4956 Nydalen, N-4956 Oslo, Norway ; Departement of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway.
authors.forename: G Ø
authors.initials: GØ
authors.lastname: Andersen
authors.affiliation: Departement of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway.
authors.forename: R
authors.initials: R
authors.lastname: Bjørnerheim
authors.affiliation: Departement of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway.
authors.forename: J
authors.initials: J
authors.lastname: Eritsland
authors.affiliation: Center for Clinical Heart Research, Oslo University Hospital Ullevål, PB 4956 Nydalen, N-4956 Oslo, Norway ; Faculty of Medicine, University of Oslo, Oslo, Norway.
authors.forename: H
authors.initials: H
authors.lastname: Arnesen
authors.affiliation: Center for Clinical Heart Research, Oslo University Hospital Ullevål, PB 4956 Nydalen, N-4956 Oslo, Norway ; Departement of Cardiology, Oslo University Hospital Ullevål, Oslo, Norway ; Faculty of Medicine, University of Oslo, Oslo, Norway.
authors.forename: I
authors.initials: I
authors.lastname: Seljeflot
keywords: D-dimer; Myocardial function; Myocardial infarction; Prothrombin fragment 1 + 2