Numerous reports have established that both cTnl and cTnT are biomarkers of myocardial injury in sepsis and septic shock or other systemic immune response syndromes (SIRSs), such as pancreatitis (27-32). Septic patients presenting to tertiary, urgent, and intensive care settings without documented heart disease have abnormal troponin results in a substantial proportion (31-85%) of cases. In a representative study among adult patients (n = 46) with septic shock, levels of cTnI (©0.4 Mg/L; Stratus II) and cTnT (>0.1 Mg/L; Elecsys 2010) were found to be elevated in 50 and 36%, respectively, with peak concentrations (median, interquartile range) of1.4 Mg/L (0.8-6.8 Mg/L) for cTnI and 0.66 Mg/L (0.19-1.51 ng/L) for cTnT (31).
The mechanism responsible for minor myocardial damage in this setting is not completely understood and a number of potential contributors should be considered. Certainly, elderly patients with sepsis are at risk of concomitant coronary atherosclerosis and may
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