title: Impact of time-to-treatment on myocardial perfusion after primary percutaneous coronary intervention with Gp IIb-IIIa inhibitors.
abstract: BACKGROUND
  Primary angioplasty has been shown to be superior to thrombolysis. However, previous reports have shown a negative impact of longer time-to-treatment on myocardial perfusion and survival even with mechanical reperfusion. However, these deleterious effects might potentially be overcome by an extensive use of glycoprotein (Gp) IIb-IIIa inhibitors. Thus, the aim of the current study was to evaluate the prognostic role of the interval from symptoms onset to reperfusion in a large cohort of patients undergoing primary angioplasty with Gp IIb-IIIa inhibitors.
  
  
  METHODS
  Our population is represented by 1560 patients undergoing primary angioplasty for ST-segment elevation myocardial infarction (STEMI) included in the EGYPT (Early Glycoprotein IIb-IIIa Inhibitors in Primary Angiography) database. Myocardial perfusion was evaluated by angiography or ST-segment resolution, whereas infarct size was estimated by using peak creatine kinase and creatine kinase-MB (CK-MB). Follow-up data were collected between 30 days and 1 year after primary angioplasty.
  
  
  RESULTS
  Time-to-treatment was significantly associated with age and female sex, diabetes and previous myocardial infarction (MI), but inversely related to smoking. Time-to-treatment affected the rate of postprocedural thrombolysis in myocardial infarction (TIMI) 3 flow (P < 0.0001), myocardial blush grade 2-3 (P = 0.052), complete ST-resolution (P < 0.0001) and distal embolization (P = 0.038). This relationship was confirmed after correction for baseline confounding factors for postprocedural TIMI 3 flow (P = 0.008) and complete ST-segment resolution (P = 0.003). Furthermore, time-to-treatment significantly affected enzymatic infarct size, even after correction for baseline confounding factors [odds ratio (OR) 95% confidence interval (95% CI) = 1.002 (1.001-1.003), P = 0.004]. At 208 ± 160 days follow-up, time-to-treatment was associated with a significantly higher mortality (P = 0.006). The impact was confirmed when time-to-treatment was evaluated as a continuous variable (P < 0.001), even after correction for baseline confounding factors [age, sex, diabetes, smoking, hypertension, previous myocardial infarction (MI), preprocedural TIMI 3 flow, multivessel disease, coronary stenting and early Gp IIb-IIIa inhibitors] (P = 0.001).
  
  
  CONCLUSIONS
  This study showed that time-to-treatment is a major determinant of mortality in ST-segment elevation myocardial infarction patients undergoing primary angioplasty. Impaired epicardial and myocardial perfusion and larger infarct size associated with longer ischemia time contribute to explain this finding.
authors.affiliation: aDivision of Cardiology, 'Maggiore della Carità' Hospital, Eastern Piedmont University, Novara, Italy bTIMI Study Group, Cardiovascular Division, Brigham & Women's Hospital, Boston, Massachusetts, USA cDivision of Cardiology, Division of Cardiology, Hospital 'De Weezenlanden', Zwolle, Netherlands dInterventional Cardiology Section, Beth Israel Deaconess Medical Center, Boston, Massachusets, USA eCenter for Intensive Internal Medicine, University Medical Center, Ljubljana, Slovenia fPrato Hospital, Prato, Italy gDivision of Cardiology, Herzzentrum Ludwigshafen, Ludwigshafen, Germany hDivision of Cardiology, Hospital de Santa Maria, Lisboa, Portugal iSiyami Ersek Thoracic and Cardiovascular Surgery Center, Istanbul, Turkey jII Department of Cardiology, Institute of Cardiology, Jagiellonian University, Krakow, Poland kDepartment of Cardiology, Medical University of Vienna l3rd Department of Medicine (Cardiology and Emergency Medicine) Wilhelminenspital, Vienna, Austria.
authors.forename: Giuseppe
authors.initials: G
authors.lastname: De Luca
authors.forename: Michael C
authors.initials: MC
authors.lastname: Gibson
authors.forename: Arnoud W J Van't
authors.initials: AW
authors.lastname: Hof
authors.forename: Donald
authors.initials: D
authors.lastname: Cutlip
authors.forename: Uwe
authors.initials: U
authors.lastname: Zeymer
authors.forename: Marko
authors.initials: M
authors.lastname: Noc
authors.forename: Mauro
authors.initials: M
authors.lastname: Maioli
authors.forename: Simona
authors.initials: S
authors.lastname: Zorman
authors.forename: Mesquita H
authors.initials: MH
authors.lastname: Gabriel
authors.forename: Gioel Gabrio
authors.initials: GG
authors.lastname: Secco
authors.forename: Ayse
authors.initials: A
authors.lastname: Emre
authors.forename: Dariusz
authors.initials: D
authors.lastname: Dudek
authors.forename: Tomasz
authors.initials: T
authors.lastname: Rakowski
authors.forename: Maryann
authors.initials: M
authors.lastname: Gyongyosi
authors.forename: Kurt
authors.initials: K
authors.lastname: Huber
authors.forename: Francesco
authors.initials: F
authors.lastname: Bellandi
mesh_terms: D000367:Age Factors; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D017023:Coronary Angiography; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form / Q000097:blood; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000401:mortality / Q000473:pathology / Q000628:therapy*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D012737:Sex Factors; D061665:Time-to-Treatment; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form