Serum troponin concentrations predict mortality in almost every clinical setting they have been examined, including sepsis. However, the causes for troponin elevations in sepsis are poorly understood. We hypothesized that detailed investigation of myocardial dysfunction by echocardiography can provide insight into the possible causes of troponin elevation and its association with mortality in sepsis.
Prospective, analytic cohort study.
Tertiary academic institute.
A cohort of ICU patients with severe sepsis or septic shock.
Advanced echocardiography using global strain, strain-rate imaging and 3D left and right ventricular volume analyses in addition to the standard echocardiography, and concomitant high-sensitivity troponin-T measurement in patients with severe sepsis or septic shock.
Two hundred twenty-five echocardiograms and concomitant high-sensitivity troponin-T measurements were performed in a cohort of 106 patients within the first days of severe sepsis or septic shock (2.1 ± 1.4 measurements/patient). Combining echocardiographic and clinical variables, left ventricular diastolic dysfunction defined as increased mitral E-to-strain-rate e′-wave ratio, right ventricular dilatation (increased right ventricular end-systolic volume index), high Acute Physiology and Chronic Health Evaluation-II score, and low glomerular filtration rate best correlated with elevated log-transformed concomitant high-sensitivity troponin-T concentrations (mixed linear model: t = 3.8, 3.3, 2.8, and –2.1 and p = 0.001, 0.0002, 0.006, and 0.007, respectively). Left ventricular systolic dysfunction determined by reduced strain-rate s′-wave or low ejection fraction did not significantly correlate with log(concomitant high-sensitivity troponin-T). Forty-one patients (39%) died in-hospital. Right ventricular end-systolic volume index and left ventricular strain-rate e′-wave predicted in-hospital mortality, independent of Acute Physiology and Chronic Health Evaluation-II score (logistic regression: Wald = 8.4, 6.6, and 9.8 and p = 0.004, 0.010, and 0.001, respectively). Concomitant high-sensitivity troponin-T predicted mortality in univariate analysis (Wald = 8.4; p = 0.004), but not when combined with right ventricular end-systolic volume index and strain-rate e′-wave in the multivariate analysis (Wald = 2.3, 4.6, and 6.2 and p = 0.13, 0.032, and 0.012, respectively).
Left ventricular diastolic dysfunction and right ventricular dilatation are the echocardiographic variables correlating best with concomitant high-sensitivity troponin-T concentrations. Left ventricular diastolic and right ventricular systolic dysfunction seem to explain the association of troponin with mortality in severe sepsis and septic shock.
1Division of Anesthesiology and Critical Care Medicine, Hadassah University Medical Center, Jerusalem, Israel.
2The Cardiovascular Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN.
3Division of Cardiology, Hadassah Hebrew University Medical Center, Jerusalem, Israel.
4The Bio-Medical Engineering, The Technion, Haifa, Israel.
* See also p. 975.
An abstract of this work was presented in the latest Society of Critical Care Medicine (SCCM) meeting (January 2013) and received the SCCM Annual Scientific Award.
Dr. Giora Landesberg’s institution received grant support from the International Anesthesia Research Society. Dr. Jaffe lectured for Roche and consulted for Beckman, Roche, Ortho, Alere, Abbott, Critical Diagnostics, Diadexus, Radiometer, and Amgen. Dr. Gilon’s institution received grant support from the International Anesthesia Research Society. Dr. Goodman’s institution received grant support from the International Anesthesia Research Society. Dr. Abu-Biah’s institution received grant support from the International Anesthesia Research Society. Dr. Beeri consulted for PiCardia. Dr. Weissman’s institution received grant support from the Israel Institute for Healthcare Policy. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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