title: Thrombin generation in patients with a first acute myocardial infarction.
abstract: BACKGROUND
  Despite improved treatment options, myocardial infarction is still an important cause of morbidity and mortality. One of the contributing mechanisms in the acute myocardial infarction (AMI) is plasma hypercoagulability.
  
  
  METHODS
  We investigated hypercoagulability in 135 (first) patients with AMI using thrombin generation (TG) testing. TG testing was performed in plasmas, drawn upon admission and before medication administration, and subsequently after 4 days, 3 and 6 months. Further, we evaluated determinants of thrombin generation using multiple regression analysis of major coagulation proteins and inhibitors. Admission TG results were also related to 1-year outcome: cardiovascular death, recurrent myocardial infarction, a second coronary intervention [percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG)] and ischemic stroke.
  
  
  RESULTS
  At day 0, the TG parameters peak height, endogenous thrombin potential (ETP) and lag time were increased compared with a reference population. Peak height and lag time stayed persistently increased in patients. The lowest half of the ETP values was statistically not significantly associated with an occurrence of endpoints. The lowest half of the ETP values combined with the upper half of the D-dimer values were associated with endpoints; odds ratio 5.8 (1.1-30.7). Tissue factor pathway inhibitor (TFPI) seems to be an important determinant of TG in AMI and healthy persons.
  
  
  CONCLUSIONS
  TG reflects acute hypercoagulability during AMI and partly also in the 6-month period after the acute event. TG shows a trend of an inverse association with risk of recurrent ischemic cardiovascular complications. Unraveling mechanisms in TG might improve our understanding of the pathophysiology of AMI and direct future improvements in medical care.
authors.affiliation: Laboratory for Clinical Thrombosis and Hemostasis, Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, the Netherlands. M.Smid@mumc.nl
authors.forename: M
authors.initials: M
authors.lastname: Smid
authors.forename: A W J H
authors.initials: AW
authors.lastname: Dielis
authors.forename: M
authors.initials: M
authors.lastname: Winkens
authors.forename: H M H
authors.initials: HM
authors.lastname: Spronk
authors.forename: R
authors.initials: R
authors.lastname: van Oerle
authors.forename: K
authors.initials: K
authors.lastname: Hamulyák
authors.forename: M H
authors.initials: MH
authors.lastname: Prins
authors.forename: J
authors.initials: J
authors.lastname: Rosing
authors.forename: J L
authors.initials: JL
authors.lastname: Waltenberger
authors.forename: H
authors.initials: H
authors.lastname: ten Cate
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001777:Blood Coagulation; D001779:Blood Coagulation Factors / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000209:etiology / Q000628:therapy; D012008:Recurrence; D013917:Thrombin / Q000096:biosynthesis*
chemical_list: D001779:Blood Coagulation Factors; D005338:Fibrin Fibrinogen Degradation Products; C036309:fibrin fragment D; D013917:Thrombin