title: Acute and subacute stent thrombosis after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction: incidence, predictors and clinical outcome.
abstract: BACKGROUND
  Early coronary stent thrombosis occurs most frequent after primary percutaneous coronary intervention (PCI) for ST-segment elevation myocardial infarction (STEMI).
  
  
  OBJECTIVE
  To identify the specific predictors of, respectively, acute and subacute stent thrombosis in patients after primary PCI for STEMI.
  
  
  METHODS
  Consecutive STEMI patients with angiographically confirmed early stent thrombosis were enrolled and compared in a 2 : 1 ratio with a matched control group. Clinical outcome was collected up to 1 year.
  
  
  RESULTS
  Of 5842 STEMI patients treated with primary PCI, 201 (3.5%) presented with a definite early stent thrombosis. Of these, 97 (1.7%) had acute stent thromboses and 104 (1.8%) had subacute stent thromboses. Postprocedurally discovered dissection, undersizing and smaller stent diameter were the strongest predictors for acute stent thrombosis. No glycoprotein IIb/IIIa therapy and the use of drug-eluting stents were also associated with acute stent thrombosis. Lack of clopidogrel therapy in the first 30 days after the index PCI was the strongest predictor for subacute stent thrombosis. Mortality rates at 1-year follow-up were lower for acute stent thrombosis than for subacute stent thrombosis (8.3% vs. 13.2%, P = 0.294). The incidence of definite recurrent stent thrombosis at 1-year follow up was significantly lower after a first definite acute stent thrombosis than after a first definite subacute stent thrombosis (6.4% vs. 19.3%, P = 0.007 at 1 year).
  
  
  CONCLUSIONS
  The specific risk factors for, respectively, acute and subacute stent thrombosis after primary PCI vary greatly. Mortality rates are high for both categories of stent thrombosis. However, recurrent stent thrombosis occurs more frequently after subacute stent thrombosis.
authors.affiliation: Department of Cardiology, Medisch Centrum Alkmaar, Alkmaar, The Netherlands.
authors.forename: A A C M
authors.initials: AA
authors.lastname: Heestermans
authors.forename: J W
authors.initials: JW
authors.lastname: van Werkum
authors.forename: B
authors.initials: B
authors.lastname: Zwart
authors.forename: J A
authors.initials: JA
authors.lastname: van der Heyden
authors.forename: J C
authors.initials: JC
authors.lastname: Kelder
authors.forename: N J
authors.initials: NJ
authors.lastname: Breet
authors.forename: A W J
authors.initials: AW
authors.lastname: van't Hof
authors.forename: J-H E
authors.initials: JH
authors.lastname: Dambrink
authors.forename: J J
authors.initials: JJ
authors.lastname: Koolen
authors.forename: B R G
authors.initials: BR
authors.lastname: Brueren
authors.forename: F
authors.initials: F
authors.lastname: Zijlstra
authors.forename: J M
authors.initials: JM
authors.lastname: ten Berg
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000379:methods*; D000077144:Clopidogrel; D005260:Female; D006801:Humans; D015994:Incidence; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology / Q000628:therapy*; D009426:Netherlands; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D012042:Registries; D012307:Risk Factors; D015607:Stents / Q000009:adverse effects; D013927:Thrombosis / Q000150:complications* / Q000209:etiology* / Q000628:therapy; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D010975:Platelet Aggregation Inhibitors; D000077144:Clopidogrel; D013988:Ticlopidine