title: Cardiac troponin I predicts myocardial dysfunction and adverse outcome in septic shock.
abstract: OBJECTIVE
  The objectives of this study were to determine myocardial injury in patients with septic shock by measuring serum cardiac troponin I (cTnI), to evaluate relationship between elevated cTnI and myocardial dysfunction and to determine if cTnI is a predictor of outcome in these patients.
  
  
  METHODS
  Thirty-seven consecutive patients with septic shock were included in the study. Serum cTnI was measured at study entry and after 24 and 48 h. Transthoracic echocardiogram, electrocardiogram and regular biochemical and hemodynamic assessments were performed.
  
  
  RESULTS
  Sixteen (43%) patients had elevated serum cTnI. These patients had higher need for inotropic/vasopressor support (94% vs. 53%, p=0.018), higher APACHE II score (28 vs. 20, p=0.004), higher incidence of regional wall motion abnormalities on echocardiography (56% vs. 6%, p=0.002), lower ejection fraction (46% vs. 62%, p=0.04) and higher mortality (56% vs. 24%, p=0.04) compared to normal cTnI patients. By multiple logistic regression analysis, serum cTnI and APACHE II score were independent predictor of death and length of stay in intensive care unit. Serum cTnI, APACHE II score, anion gap and serum lactate were independent predictor of need for inotropic/vasopressor support. Receiver-operating characteristics of serum cTnI as a predictor of death in septic shock were significant. The elevated serum level of cTnI correlated with the lower left ventricular ejection fraction (p<0.001).
  
  
  CONCLUSIONS
  Myocardial injury can be determined in patients with septic shock by serum cTnI. Serum cTnI concentration correlates with myocardial dysfunction in septic shock. High serum cTnI predicts increased severity of sepsis and higher mortality. A close monitoring of patients with septic shock and elevated levels cTnI is warranted.
authors.affiliation: Division of Cardiology, Creighton University School of Medicine, 3006 Webster Street, Omaha, NE 68131, USA.
authors.forename: Nirav J
authors.initials: NJ
authors.lastname: Mehta
authors.forename: Ijaz A
authors.initials: IA
authors.lastname: Khan
authors.forename: Vipin
authors.initials: V
authors.lastname: Gupta
authors.forename: Ketan
authors.initials: K
authors.lastname: Jani
authors.forename: Ramesh M
authors.initials: RM
authors.lastname: Gowda
authors.forename: Peter R
authors.initials: PR
authors.lastname: Smith
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D009202:Cardiomyopathies / Q000097:blood* / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology*; D002316:Cardiotonic Agents / Q000627:therapeutic use; D005260:Female; D006801:Humans; D007362:Intensive Care Units; D007902:Length of Stay; D008297:Male; D008875:Middle Aged; D015588:Observer Variation; D011237:Predictive Value of Tests; D012720:Severity of Illness Index; D012772:Shock, Septic / Q000097:blood* / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology*; D013223:Statistics as Topic; D013318:Stroke Volume / Q000502:physiology; D016019:Survival Analysis; D019210:Troponin I / Q000097:blood*; D014662:Vasoconstrictor Agents / Q000627:therapeutic use; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000188:drug therapy / Q000453:epidemiology / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D002316:Cardiotonic Agents; D019210:Troponin I; D014662:Vasoconstrictor Agents