Chest
Volume 129, Issue 5, May 2006, Pages 1349-1366
Journal home page for Chest

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

https://doi.org/10.1378/chest.129.5.1349Get rights and content

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.

Learning Objectives

  • 1. Assess myocardial dysfunction in sepsis and early recognition for administration of optimal therapy

  • 2. Analyze the elevation of cardiac troponins in patients with sepsis, severe sepsis or septic shock

  • 3. Evaluate the relationship between BNP (B-type natriuretic peptide) and both left ventricular ejection fraction and left-sided filling pressures

Section snippets

Definitions

Sepsis has been defined as the presence of the systemic inflammatory response syndrome (SIRS) in response to a culture-proven infection.19 However, SIRS can result not only from infection, but also from a variety of conditions such as autoimmune disorders, vasculitis, thromboembolism, and burns, or after surgery. The severity of sepsis is graded according to the associated organ dysfunction and hemodynamic compromise. The original definitions have been revisited by a group of experts,20 but,

Prevalence

Abnormalities of cardiac function are quite common in patients with sepsis. The prevalence of this transient phenomenon critically depends on the population studied, the definition applied, and the time point during the course of the disease. Approximately 50% of patients with severe sepsis and septic shock seem to have any form of impairment of left ventricular systolic function.4, 9

Pathomechanisms

The phenomenon of myocardial depression is mediated by circulating depressant substances,21, 22, 23, 24 which

Background

Cardiac troponins are regulatory proteins of the thin actin filaments of the cardiac muscle.30 Myocardial cell injury results in the release of cardiac troponin I (cTnI) and cardiac troponin T (cTnT), which differ from troponin isoforms of the skeletal muscle, and thus are highly sensitive and specific biomarkers of myocardial damage.30, 31 The measurement of cTnI and cTnT levels in blood is standard for diagnosis and risk stratification in patients with ACS.32 The currently employed tests use

Background

The 32-amino-acid B-type natriuretic peptide (BNP) and the 76-amino-acid N-terminal-pro-BNP (NT-proBNP) are the most extensively studied members of the family of natriuretic peptides. The prohormone pro-BNP is synthesized in bursts and cleaved into the active BNP and the biologically inactive NT-proBNP, which are constitutively released from ventricular myocytes. In contrast to A-type natriuretic peptide (ANP), BNP and NT-proBNP are not stored in granules, but BNP gene expression can increase

Relationship Between Cardiac Troponins and Natriuretic Peptides

Cardiac troponins and natriuretic peptides provide different information about myocardial dysfunction. Troponin release indicates minimal myocyte damage or loss of cell membrane integrity, and thus gives structural information, whereas BNP reflects wall stress, and thus provides functional information. Raised levels of both cardiac troponins and natriuretic peptides have been found in patients with a variety of conditions associated with overload or the damage of either or both cardiac

Conclusions and Recommendations

There is evidence from several small studies that elevated cardiac troponin levels in patients with sepsis indicate myocardial dysfunction and a poor prognosis. As far as the diagnosis of sepsis is obvious, and other conditions such as ACS, pulmonary embolism, or end-stage renal failure are excluded, elevated cardiac troponin levels may help to identify high-risk patients, who should undergo echocardiography, invasive hemodynamic monitoring, and optimized therapy. Unfortunately, the usefulness

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    The following authors have indicated to The ACCP that no significant relationships exist with any company/organization whose products or services may be discussed in this article: Micha Maeder, MD; Thomas Fehr, MD; Hans Rickli, MD; Peter Ammann, MD.

    Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).

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