Chest
Special FeaturesSepsis-Associated Myocardial Dysfunction: Diagnostic and Prognostic Impact of Cardiac Troponins and Natriuretic Peptides
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
References (105)
- et al.
Septic shock
Lancet
(2005) - et al.
Serum cardiac troponin T as a prognostic marker in early sepsis
Chest
(1998) - et al.
Troponin as a risk factor for mortality in critically ill patients without acute coronary syndromes
J Am Coll Cardiol
(2003) - et al.
Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis
Chest
(1992) - et al.
Role of interleukin 6 in myocardial dysfunction of meningococcal septic shock
Lancet
(2004) - et al.
Depressed left ventricular performance. Response to volume infusion in patients with sepsis and septic shock
Chest
(1988) - et al.
Right ventricular dysfunction and dilatation, similar to left ventricular changes, characterize the cardiac depression of septic shock in humans
Chest
(1990) - et al.
Release kinetics of serum cardiac troponin I in ischemic myocardial injury
Clin Biochem
(1996) - et al.
Common causes of troponin elevations in the absence of acute myocardial infarction: incidence and clinical significance
Chest
(2004) - et al.
Clinically recognized cardiac dysfunction: an independent determinant of mortality among critically ill patients
Chest
(1997)
Elevations of cardiac troponin I are associated with increased short-term mortality in noncardiac critically ill emergency department patients
Am J Cardiol
Early enzyme release from myocardial cells is not due to irreversible cell damage
J Mol Cell Cardiol
Diagnostic value of troponin T for alterations in left ventricular mass and function in dialysis patients
Kidney Int
B-type natriuretic peptide in cardiovascular disease
Lancet
Relationship between B-type natriuretic peptides and pulmonary capillary wedge pressure in the intensive care unit
J Am Coll Cardiol
Utility of B-type natriuretic peptide an N-terminal Pro B-type nariuretic peptide in evaluation of respiratory failure in critically ill patients
Chest
A rapid test for B-type natriuretic peptide correlates with falling wedge pressures in patients treated for decompensated heart failure: a pilot study
J Card Fail
Neurohormonal activation rapidly decreases after intravenous therapy with diuretics and vasodilators for class IV heart failure
J Am Coll Cardiol
Plasma brain natriuretic peptide as a biochemical marker of high left ventricular end-diastolic pressure in patients with symptomatic left ventricular dysfunction
Am Heart J
Bedside B-type natriuretic peptide in the emergency room diagnosis of heart failure with reduced or preserved ejection fraction
J Am Coll Cardiol
B-type natriuretic peptide levels are not a surrogate marker for invasive hemodynamics during management of patients with severe heart failure
Am Heart J
Predischarge B-type natriuretic peptide assay for identifying patients at high risk of re-admission after decompensated heart failure
J Am Coll Cardiol
Plasma brain natriuretic peptide levels increase in proportion to the extent of right ventricular dysfunction in pulmonary hypertension
J Am Coll Cardiol
Brain natriuretic peptide predicts right heart failure in patients with acute pulmonary embolism
Am Heart J
Increased plasma concentrations of brain natriuretic peptide in patients with acute lung injury
J Crit Care
B-type natriuretic peptide and renal function in the diagnosis of heart failure: an analysis from the Breathing Not Properly Multinational Study
Am J Kidney Dis
B-type natriuretic peptide for acute dyspnea in patients with kidney disease
Kidney Int
Secretion of brain natriuretic peptide in patients with aneurysmal subarachnoid haemorrhage
Lancet
Endothelin-1 and atrial natriuretic peptide in septic shock
Am Heart J
Left ventricular dysfunction predicted by early troponin I release after high-dose chemotherapy
J Am Coll Cardiol
High levels of plasma brain natriuretic peptide and interleukin-6 after optimized treatment for heart failure are independent risk factors for morbidity and mortality in patients with congestive heart failure
J Am Coll Cardiol
Effects of prolonged strenuous exercise on plasma levels of atrial natriuretic peptide and brain natriuretic peptide in healthy men
Am Heart J
Clinical significance of increased troponins T and I in participants of ultraendurance events
Am J Cardiol
Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care
Crit Care Med
Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial
JAMA
Brain natriuretic peptide: a marker of myocardial dysfunction and prognosis during severe sepsis
Crit Care Med
Cardiac troponin: a new serum marker of myocardial injury in sepsis
Intensive Care Med
Myocardial cell injury in septic shock
Crit Care Med
Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study
Intensive Care Med
Cardiac troponin I and T are biological markers of left ventricular dysfunction in septic shock
Clin Chem
Elevation of troponin I in sepsis and septic shock
Intensive Care Med
Cardiac troponin predicts myocardial dysfunction and adverse outcome in septic shock
Int J Cardiol
Plasma atrial natriuretic peptide and brain natriuretic peptide are increased in septic shock: impact of interleukin-6 and sepsis-associated left ventricular dysfunction
Intensive Care Med
B-type natriuretic peptide and the prediction of outcome in patients admitted to intensive care
Anaesthesia
Utility of B-type natriuretic peptide for the evaluation of intensive care unit shock
Crit Care Med
The prognostic value of serum troponin T in unstable angina
N Engl J Med
Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure
N Engl J Med
Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea
N Engl J Med
2001 SCCM/ESICM/ACCP/ATS/SIS International Sepsis Definitions Conference
Crit Care Med
A circulating myocardial depressant substance in humans with septic shock: septic shock patients with a reduced ejection fraction have a circulating factor that depressesin vitromyocardial cell performance
J Clin Invest
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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).