title: Do patients with drug-eluting stent thrombosis have a similar prognosis to patients presenting with st-Elevation myocardial infarction of de novo lesions?
abstract: BACKGROUND
  Despite significant advances in stent technology and pharmacotherapy, drug-eluting stent thrombosis (DES-ST) remains a major complication of percutaneous coronary intervention (PCI) and commonly presents as ST-elevation myocardial infarction (STEMI). There are currently little data comparing the in-hospital outcomes of patients presenting with STEMI due to DES-ST with those due to de novo coronary artery disease (CAD).
  
  
  METHODS
  Our study comprised 985 consecutive patients who underwent primary PCI for STEMI, 102 of whom were diagnosed as having a definite DES-ST. The primary end-point was the in-hospital composite of death or recurrent myocardial infarction (MI). The secondary end-point was the in-hospital maximum rise in creatine kinase (myocardial band [MB] fraction) and troponin I.
  
  
  RESULTS
  The DES-ST group had a higher proportion of patients with diabetes mellitus, hypercholesterolemia, history of ischemic heart disease, coronary revascularization, and chronic renal impairment. The adjusted primary end-point was higher in the DES-ST cohort (12.7% vs. 7.4%; P = 0.05). The 2 cohorts did not differ in the secondary end-point. The independent predictors of the primary end-point were age (hazard ratio [HR]= 1.04; 95% confidence interval [CI]= 1.01 - 1.06; P = 0.005), cardiogenic shock (HR = 11.5; 95% CI = 6.38 - 20.07, P < 0.001), and lesions involving the left anterior descending coronary artery (HR = 1.8; 95% CI = 1.03 - 3.13, P = 0.04). DES-ST was not an independent predictor of the primary end-point (HR = 1.18; 95% CI = 0.53-2.63, P = 0.38).
  
  
  CONCLUSIONS
  Patients with STEMI secondary to DES-ST have a poorer in-hospital outcome than do patients in whom STEMI is due to de novo CAD. This difference may be predominantly driven by differences in the baseline characteristics between these cohorts. (J Interven Cardiol 2011;24:320-325).
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Washington Hospital Center, District of Columbia.
authors.forename: Loic
authors.initials: L
authors.lastname: Belle
authors.forename: Michael
authors.initials: M
authors.lastname: Mahmoudi
authors.forename: Cedric
authors.initials: C
authors.lastname: Delhaye
authors.forename: Itsik
authors.initials: I
authors.lastname: Ben-Dor
authors.forename: Gabriel
authors.initials: G
authors.lastname: Maluenda
authors.forename: Michael A
authors.initials: MA
authors.lastname: Gaglia
authors.forename: Rebecca
authors.initials: R
authors.lastname: Torguson
authors.forename: Lowell F
authors.initials: LF
authors.lastname: Satler
authors.forename: Augusto D
authors.initials: AD
authors.lastname: Pichard
authors.forename: Ron
authors.initials: R
authors.lastname: Waksman
mesh_terms: D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000150:complications / Q000628:therapy*; D003328:Coronary Thrombosis / Q000209:etiology* / Q000401:mortality; D003402:Creatine Kinase / Q000097:blood; D054855:Drug-Eluting Stents / Q000009:adverse effects*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000209:etiology* / Q000401:mortality; D011379:Prognosis; D012189:Retrospective Studies; D019210:Troponin I / Q000097:blood
chemical_list: D019210:Troponin I; D003402:Creatine Kinase