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.
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 cTnIpatients. 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.
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Authors: Claudio Ronco; Peter McCullough; Stefan D Anker; Inder Anand; Nadia Aspromonte; Sean M Bagshaw; Rinaldo Bellomo; Tomas Berl; Ilona Bobek; Dinna N Cruz; Luciano Daliento; Andrew Davenport; Mikko Haapio; Hans Hillege; Andrew A House; Nevin Katz; Alan Maisel; Sunil Mankad; Pierluigi Zanco; Alexandre Mebazaa; Alberto Palazzuoli; Federico Ronco; Andrew Shaw; Geoff Sheinfeld; Sachin Soni; Giorgio Vescovo; Nereo Zamperetti; Piotr Ponikowski Journal: Eur Heart J Date: 2009-12-25 Impact factor: 29.983