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Cardiac troponin I predicts myocardial dysfunction and adverse outcome in septic shock
Nirav J Mehta1, Ijaz A Khan, Vipin Gupta
1Division of Cardiology, Creighton University School of Medicine, 3006 Webster Street, Omaha, NE 68131, USA.
Insights
Elevated serum cardiac troponin I (cTnI) indicates myocardial injury in septic shock patients. High cTnI levels correlate with myocardial dysfunction and predict increased sepsis severity and mortality.
Area of Science:
- Cardiology
- Critical Care Medicine
- Biochemistry
Background:
- Septic shock frequently leads to myocardial dysfunction.
- Assessing myocardial injury in septic shock is crucial for patient outcomes.
Purpose of the Study:
- To determine myocardial injury in septic shock using serum cardiac troponin I (cTnI).
- To evaluate the relationship between elevated cTnI and myocardial dysfunction.
- To assess cTnI as a predictor of outcomes in septic shock patients.
Main Methods:
- Thirty-seven septic shock patients were enrolled.
- Serum cTnI levels were measured at baseline, 24, and 48 hours.
- Echocardiography, ECG, and hemodynamic assessments were performed.
Main Results:
- 43% of patients exhibited elevated cTnI.
- Elevated cTnI correlated with increased need for vasopressors, higher APACHE II scores, and wall motion abnormalities.
- Higher cTnI levels were associated with lower ejection fraction and increased mortality.
Conclusions:
- Serum cTnI effectively identifies myocardial injury in septic shock.
- Elevated cTnI correlates with myocardial dysfunction and predicts worse outcomes.
- Close monitoring of septic shock patients with elevated cTnI is recommended.
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.
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