Increases in serum levels of troponin I are associated with cardiac dysfunction and disease severity in pediatric patients with septic shock.

OBJECTIVES Myocardial cell injury may contribute to cardiac dysfunction in septic shock. Troponin I is a biochemical marker of myocardial cell injury and death. We hypothesized that troponin I is increased in pediatric patients with septic shock and correlates with cardiac dysfunction and disease severity. DESIGN Prospective, observational study. SETTING Children's medical center. PATIENTS Twenty-three patients with septic shock and cardiovascular failure were enrolled. MEASUREMENTS AND MAIN RESULTS Serum troponin I was measured at admission and serially over 72 hrs. Within 24 hrs of study enrollment, echocardiograms were performed to determine left ventricular ejection fraction, systolic fractional shortening, heart rate corrected mean velocity of circumferential fiber shortening, and end-systolic wall stress. Requirement for inotropic support (stratified as low, moderate, or high), number of organ system failures, and other demographic data (including Pediatric Risk of Mortality III) were collected. Troponin I was increased on admission in 13 of 23 patients (57%) and at 12 hrs in ten of 22 patients (46%). In all cases, troponin I was maximal within 12 hrs of admission. Admission troponin I was inversely correlated to ejection fraction and fractional shortening and directly correlated to wall stress. Patients who had increased admission troponin I had lower heart rate corrected mean velocity of circumferential fiber shortening (preload and heart rate independent measure of left ventricular systolic function) and higher wall stress (measure of afterload) compared with patients with normal troponin I. Admission troponin I correlated with Pediatric Risk of Mortality III and organ system failure but did not correlate with requirement for inotropic support. CONCLUSIONS Troponin I was increased in >50% of septic children early in their illness. Increased admission troponin I was associated with decreased measures of systolic cardiac function, as measured by echocardiography, and correlated with severity of illness. Early myocardial cell injury may contribute to the development of subsequent organ failure in septic shock, and measuring troponin I on admission may be helpful in assessing severity of sepsis.