title: Myocardial cell injury in septic shock.
abstract: OBJECTIVE
  To determine the presence of otherwise undetected myocardial cell injury in patients with septic shock using daily measurements of cardiac troponin I (cTN I).
  
  
  METHODS
  Prospective observational study.
  
  
  METHODS
  Intensive care unit of a tertiary institution.
  
  
  METHODS
  Fifteen consecutive patients with septic shock and six mechanically ventilated patients without septic shock.
  
  
  METHODS
  Daily collection of blood for the measurement of cTN I serum levels. Regular biochemical and hemodynamic assessment. Illness severity assessment and collection of demographic data.
  
  
  RESULTS
  Fifteen patients were studied for a median period of 3 days (range, 1 to 9 days). Serum cTN I concentrations were elevated to values otherwise considered diagnostic of acute myocardial infarction in 12 patients and were significantly higher than in critically ill controls (p = .01). All three patients who died in the intensive care unit and all four patients who did not survive beyond 28 days had elevated levels of cTN I. Survivors tended to lower levels of cTN I while in septic shock than nonsurvivors, and all three patients without increased cTN I survived. There was a significant positive correlation between vasoactive drug requirements and cTN I level (p = .04) and a significant negative correlation between cTN I concentration and left ventricular stroke work index (p = .01).
  
  
  CONCLUSIONS
  Myocardial cell injury appears to be common in patients with septic shock and correlates with cardiac dysfunction.
authors.affiliation: Department of Anesthesia and Intensive Care, Austin and Repatriation Medical Center, Heidelberg, Victoria, Australia.
authors.forename: A
authors.initials: A
authors.lastname: Turner
authors.forename: M
authors.initials: M
authors.lastname: Tsamitros
authors.forename: R
authors.initials: R
authors.lastname: Bellomo
mesh_terms: D018806:APACHE; D000328:Adult; D000368:Aged; D009202:Cardiomyopathies / Q000097:blood* / Q000188:drug therapy / Q000209:etiology* / Q000401:mortality; D016022:Case-Control Studies; D002395:Catecholamines / Q000627:therapeutic use; D003402:Creatine Kinase / Q000097:blood; D004305:Dose-Response Relationship, Drug; D006801:Humans; D019344:Lactic Acid / Q000097:blood; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D009336:Necrosis; D011446:Prospective Studies; D012772:Shock, Septic / Q000150:complications*; D018709:Statistics, Nonparametric; D016019:Survival Analysis; D019210:Troponin I / Q000097:blood*; D014662:Vasoconstrictor Agents / Q000627:therapeutic use; D016277:Ventricular Function, Left; D014739:Victoria / Q000453:epidemiology
chemical_list: D002395:Catecholamines; D019210:Troponin I; D014662:Vasoconstrictor Agents; D019344:Lactic Acid; D003402:Creatine Kinase