title: Prognostic implications of left ventricular end-diastolic pressure during primary percutaneous coronary intervention for ST-segment elevation myocardial infarction: Findings from the Assessment of Pexelizumab in Acute Myocardial Infarction study.
abstract: BACKGROUND
  Left ventricular end-diastolic pressure (LVEDP) is frequently measured during primary percutaneous coronary intervention (PCI). However, little is known of this measurement's utility in predicting outcomes or informing treatment decisions. We sought to determine the prognostic value of LVEDP measured during primary PCI for ST-segment elevation myocardial infarction (STEMI).
  
  
  METHODS
  We studied 1,909 (33.2%) of 5,745 STEMI patients in whom LVEDP was measured during primary PCI in the APEX-AMI trial. Cox regression analysis was used to evaluate whether LVEDP was an independent predictor of mortality and the composite of death, cardiogenic shock, or congestive heart failure (CHF) at 90 days.
  
  
  RESULTS
  The median (25th, 75th percentiles) LVEDP level was 22 mm Hg (16, 29); compared with patients with LVEDP ≤ 22 mm Hg, those with LVEDP > 22 mm Hg had higher rates of CHF (7.3% vs 3.1%, P < .001), cardiogenic shock (4.6% vs 1.7%, P < .001), and death (4.1% vs 2.2%, P = .014) at 90 days. After multivariable adjustment, LVEDP was associated with increased risk of mortality through 90 days (adjusted hazard ratio 1.22, 95% CI 1.02-1.46, per 5-mmHg increase, P = .044) and the composite of death, cardiogenic shock, or CHF within the first 2 days (adjusted hazard ratio 1.40, 95% CI 1.23-1.59, per 5-mm Hg increase, P < .001), but not from day 3 to 90 (P = .25).
  
  
  CONCLUSIONS
  Left ventricular end-diastolic pressure measured during primary PCI for STEMI is an independent predictor of inhospital and longer term cardiovascular outcomes. Measuring LVEDP may be useful to stratify patient risk and guide postinfarct treatment.
authors.affiliation: Duke Clinical Research Institute, Durham, NC. Electronic address: akshay.bagai@duke.edu.
authors.forename: Akshay
authors.initials: A
authors.lastname: Bagai
authors.forename: Paul W
authors.initials: PW
authors.lastname: Armstrong
authors.forename: Amanda
authors.initials: A
authors.lastname: Stebbins
authors.forename: Kenneth W
authors.initials: KW
authors.lastname: Mahaffey
authors.forename: Judith S
authors.initials: JS
authors.lastname: Hochman
authors.forename: W Douglas
authors.initials: WD
authors.lastname: Weaver
authors.forename: Manesh R
authors.initials: MR
authors.lastname: Patel
authors.forename: Christopher B
authors.initials: CB
authors.lastname: Granger
authors.forename: Renato D
authors.initials: RD
authors.lastname: Lopes
mesh_terms: D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D001794:Blood Pressure / Q000502:physiology*; D004311:Double-Blind Method; D005260:Female; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000401:mortality / Q000503:physiopathology* / Q000628:therapy; D062645:Percutaneous Coronary Intervention / Q000379:methods* / Q000401:mortality; D011379:Prognosis; D016016:Proportional Hazards Models; D012307:Risk Factors; D057127:Single-Chain Antibodies / Q000627:therapeutic use*; D015996:Survival Rate; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D057127:Single-Chain Antibodies; C402724:pexelizumab