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Sepsis-Associated Myocardial Dysfunction*: Diagnostic and Prognostic Impact of Cardiac Troponins and Natriuretic Peptides

Micha Maeder, MD; Thomas Fehr, MD; Hans Rickli, MD; Peter Ammann, MD
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*From the Division of Cardiology (Drs. Maeder, Rickli, and Ammann), Department of Internal Medicine, Kantonsspital St. Gallen, Switzerland; and Transplantation Biology Research Center (Dr. Fehr), Massachusetts General Hospital/Harvard Medical School, Boston, MD.

Correspondence to: Micha Maeder, MD, Division of Cardiology, University Hospital, Petersgraben 4, CH-4031 Basel, Switzerland; e-mail: micha.maeder@bluewin.ch



Chest. 2006;129(5):1349-1366. doi:10.1378/chest.129.5.1349
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Myocardial dysfunction, which is characterized by transient biventricular impairment of intrinsic myocardial contractility, is a common complication in patients with sepsis. Left ventricular systolic dysfunction is reflected by a reduced left ventricular stroke work index or, less accurately, by an impaired left ventricular ejection fraction (LVEF). Early recognition of myocardial dysfunction is crucial for the administration of the most appropriate therapy. Cardiac troponins and natriuretic peptides are biomarkers that were previously introduced for diagnosis and risk stratification in patients with acute coronary syndrome and congestive heart failure, respectively. However, their prognostic and diagnostic impact in critically ill patients warrants definition. The elevation of cardiac troponin levels in patients with sepsis, severe sepsis, or septic shock has been shown to indicate left ventricular dysfunction and a poor prognosis. Troponin release in this population occurs in the absence of flow-limiting coronary artery disease, suggesting the presence of mechanisms other than thrombotic coronary artery occlusion, probably a transient loss in membrane integrity with subsequent troponin leakage or microvascular thrombotic injury. In contrast to the rather uniform results of studies dealing with cardiac troponins, the impact of raised B-type natriuretic peptide (BNP) levels in patients with sepsis is less clear. The relationship between BNP and both LVEF and left-sided filling pressures is weak, and data on the prognostic impact of high BNP levels in patients with sepsis are conflicting. Mechanisms other than left ventricular wall stress may contribute to BNP release, including right ventricular overload, catecholamine therapy, renal failure, diseases of the CNS, and cytokine up-regulation. Whereas cardiac troponins may be integrated into the monitoring of myocardial dysfunction in patients with severe sepsis or septic shock to identify those patients requiring early and aggressive supportive therapy, the routine use of BNP and other natriuretic peptides in this setting is discouraged at the moment.

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