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Original Research: Critical Care Medicine |

Myocardial Dysfunction in Severe Sepsis and Septic ShockInflammatory Cytokines and Myocardial Dysfunction: No Correlation With Inflammatory Cytokines in Real-life Clinical Setting

Giora Landesberg, MD, DSc; Phillip D. Levin, MA, BChir; Dan Gilon, MD; Sergey Goodman, MD; Milena Georgieva, MD; Charles Weissman, MD; Allan S. Jaffe, MD; Charles L. Sprung, MD, FCCP; Vivian Barak, PhD
Author and Funding Information

From the Departments of Anesthesiology and Critical Care Medicine (Drs Landesberg, Levin, Goodman, Georgieva, Weissman, and Sprung), the Department of Cardiology (Dr Gilon), and the Immunology Laboratory (Dr Barak), Hadassah – Hebrew University Medical Center, Jerusalem, Israel; and the Cardiovascular Department of Laboratory Medicine and Pathology (Dr Jaffe), Mayo Clinic, Rochester, MN.

CORRESPONDENCE TO: Giora Landesberg, MD, DSc, Department of Anesthesiology and Critical Care Medicine, Hadassah – Hebrew University Medical Center, Jerusalem 91120, Israel; e-mail: giora.lan@mail.huji.ac.il


FUNDING/SUPPORT: This study was funded in major part by the International Anesthesia Research Association (IARS) 2006 Clinical Scholar Research Award (CSRA) and in part by a grant from Hadassah Hospital.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(1):93-102. doi:10.1378/chest.14-2259
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BACKGROUND:  In vitro studies suggested that circulating inflammatory cytokines cause septic myocardial dysfunction. However, no in vivo clinical study has investigated whether serum inflammatory cytokine concentrations correlate with septic myocardial dysfunction.

METHODS:  Repeated echocardiograms and concurrent serum inflammatory cytokines (IL-1β, IL-6, IL-8, IL-10, IL-18, tumor necrosis factor-α, and monocyte chemoattractant protein-1) and cardiac biomarkers (high-sensitivity [hs] troponin-T and N-terminal pro-B-type natriuretic peptide [NT-proBNP]) were examined in 105 patients with severe sepsis and septic shock. Cytokines and biomarkers were tested for correlations with systolic and diastolic dysfunction, sepsis severity, and mortality.

RESULTS:  Systolic dysfunction defined as reduced left ventricular ejection fraction (LVEF) < 50% or < 55% and diastolic dysfunction defined as e′-wave < 8 cm/s on tissue-Doppler imaging (TDI) or E/e′-ratio were found in 13 (12%), 24 (23%), 53 (50%), and 26 (25%) patients, respectively. Forty-four patients (42%) died in-hospital. All cytokines, except IL-1, correlated with Sequential Organ Failure Assessment and APACHE (Acute Physiology and Chronic Health Evaluation) II scores, and all cytokines predicted mortality. IL-10 and IL-18 independently predicted mortality among cytokines (OR = 3.1 and 28.3, P = .006 and < 0.0001). However, none of the cytokines correlated with LVEF, end-diastolic volume index (EDVI), stroke-volume index (SVI), or s′-wave and e′-wave velocities on TDI (Pearson linear and Spearman rank [ρ] nonlinear correlations). Similarly, no differences were found in cytokine concentrations between patients dichotomized to high vs low LVEF, EDVI, SVI, s′-wave, or e′-wave (Mann-Whitney U tests). In contrast, NT-proBNP strongly correlated with both reduced LVEF and reduced e′-wave velocity, and hs-troponin-T correlated mainly with reduced e′-wave.

CONCLUSIONS:  Unlike cardiac biomarkers, none of the measured inflammatory cytokines correlates with systolic or diastolic myocardial dysfunction in severe sepsis or septic shock.

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