Elevation of troponin I in sepsis and septic shock

Objective: To detect myocardial damage in severe systemic inflammation by c TnI measurements in patients without acute coronary syndromes. Design: Prospective case control study. Setting: Tertiary referral center. Participants: Twenty patients with sepsis, septic shock, and systemic infla mmatory response syndrome (SIRS) were examined and compared to controls wit hout coronary artery disease or myocarditis. Measurements and results: cTnI levels were assessed in patients with SIRS, sepsis, and septic shock. Eight patients (two female/six male) suffered fro m septic shock, nine (three female/six male) from sepsis without shock, and three (three male) from SIRS. Seventeen patients (85 %) showed elevated cT nI (median 0.57 mug/l; 0.17-15.4), whereas no patient in the control group showed elevated cTnI (P < 0.0001). Six patients (30 %), - three with septic shock and three with sepsis - died during hospitalization, five of them wi th elevated cTnI. Four out of five autopsies showed normal coronary arterie s. Coronary angiography, autopsy, and stress echocardiography ruled out sig nificant coronary artery disease in ten cTnI-positive patients (59 %). In 4 1 % of cTnI-positive patients, Streptococcus pneumoniae could be cultured, whereas no cTnI-negative or control patient showed signs of infection due t o S. pneumoniae. Conclusion: Cardiac troponin I was elevated in 85 % of patients with sepsis , septic shock or SIPS in our study. A high percentage showed infection cau sed by S. pneumoniae. In what way microorganisms cause cTnI elevations is n ot yet understood.