0 3 6 9 12 15 18 21 24 27 30 33 36 Follow-up (months)
Fig. 3. Kaplan-Meier survival curves for patients with pulmonary edema. (Reproduced from ref. 25.)
develop myocardial ischemia during the stress ofmajor illness. However, elevated levels of troponin have been observed in children with meningococcal sepsis (62%) in the obvious absence of coronary artery disease (CAD). In addition, a substantial proportion of adults with abnormal levels ofcardiac troponin during sepsis have no evidence of obstructive CAD or histopathological evidence of irreversible myocardial injury. For example, in one study 58% of patients with elevated cTnl had no appreciable CAD when evaluated by coronary angiography, stress echocardiography, or pathological findings (32). Although disseminated microthrombi and small-vessel coronary obstruction should be considered, it is probable that myocardial injury during sepsis also can result from non-ischemic mechanisms. Transient myocardial dysfunction is present in up to 40% of patients with sepsis. The prevailing contemporary opinion relates this dysfunction to direct myocardial depressant effects of inflammatory mediators elaborated in SIRSs rather than global myocardial ischemia owing to disrupted coronary autoregulation, as once thought (29). Candidate mediators that may act as "myocardial depressant factors" in SIRSs include lipopolysac-charide, prostanoids, nitric oxide, and inflammatory cytokines such as tumor necrosis factor (TNF)-a and interleukin-1 p. Notably, patients with sepsis and impaired left ventricular function show greater increases in cardiac troponin, potentially tying myocardial toxic/ depressant effects of inflammatory cytokines to the release of cardiac troponin.
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