title: Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction.
abstract: OBJECTIVE
  This study characterized clinical factors predictive of cardiogenic shock developing after thrombolytic therapy for acute myocardial infarction (AMI).
  
  
  BACKGROUND
  Cardiogenic shock remains a common and ominous complication of AMI. By identifying patients at risk of developing shock, preventive measures may be implemented to avert its development.
  
  
  METHODS
  We analyzed baseline variables associated with the development of shock after thrombolytic therapy in the Global Utilization of Streptikonase and Tissue-Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial. Using a Cox proportional hazards model, we devised a scoring system predicting the risk of shock. This model was then validated in the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO-III) cohort.
  
  
  RESULTS
  Shock developed in 1,889 patients a median of 11.6 h after enrollment. The major factors associated with increased adjusted risk of shock were age (chi2 = 285, hazard ratio [95% confidence interval] 1.47 [1.40, 1.53]), systolic blood pressure (chi2 = 280), heart rate (chi2 = 225) and Killip class (chi2 = 161, hazard ratio 1.70 [1.52, 1.90] and 2.95 [2.39, 3.63] for Killip II versus I and Killip III versus I, respectively) upon presentation. Together, these four variables accounted for >85% of the predictive information. These findings were transformed into an algorithm with a validated concordance index of 0.758. Applied to the GUSTO-III cohort, the four variables accounted for > 95% of the predictive information, and the validated concordance index was 0.796.
  
  
  CONCLUSIONS
  A scoring system accurately predicts the risk of shock after thrombolytic therapy for AMI based primarily on the patient's age and physical examination on presentation.
authors.affiliation: Rabin Medical Center, Petah Tikva, Israel.
authors.forename: D
authors.initials: D
authors.lastname: Hasdai
authors.forename: R M
authors.initials: RM
authors.lastname: Califf
authors.forename: T D
authors.initials: TD
authors.lastname: Thompson
authors.forename: J S
authors.initials: JS
authors.lastname: Hochman
authors.forename: E M
authors.initials: EM
authors.lastname: Ohman
authors.forename: M
authors.initials: M
authors.lastname: Pfisterer
authors.forename: E R
authors.initials: ER
authors.lastname: Bates
authors.forename: A
authors.initials: A
authors.lastname: Vahanian
authors.forename: P W
authors.initials: PW
authors.lastname: Armstrong
authors.forename: D A
authors.initials: DA
authors.lastname: Criger
authors.forename: E J
authors.initials: EJ
authors.lastname: Topol
authors.forename: D R
authors.initials: DR
authors.lastname: Holmes
mesh_terms: D000368:Aged; D000465:Algorithms; D004359:Drug Therapy, Combination; D005260:Female; D006493:Heparin / Q000008:administration & dosage / Q000009:adverse effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy*; D011379:Prognosis; D016016:Proportional Hazards Models; D012307:Risk Factors; D012770:Shock, Cardiogenic / Q000209:etiology* / Q000517:prevention & control; D013300:Streptokinase / Q000008:administration & dosage* / Q000009:adverse effects; D015912:Thrombolytic Therapy; D010959:Tissue Plasminogen Activator / Q000008:administration & dosage* / Q000009:adverse effects
chemical_list: D006493:Heparin; D013300:Streptokinase; D010959:Tissue Plasminogen Activator