Life-threatening heart failure in meningococcal septic shock in children: non-invasive measurement of cardiac parameters is of important prognostic value

Wiegman, Albert; Hoek, G.; Vreede, W. B.; Derkx, H. H. F.

doi:10.1007/s004310050070

Cited by 10 publications

(4 citation statements)

References 41 publications

(44 reference statements)

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“…There were no deaths in those children with normal cardiac function. These findings that children with more severe illness have impaired cardiac performance, or that deaths are found only among the group of children who have a disturbance of cardiac function have since been confirmed by other investigators [9,21,22].…”

Section: Assessment Of Cardiac Dysfunctionsupporting

confidence: 54%

Myocardial dysfunction in meningococcal septic shock

Makwana¹,

Baines²

2005

Current Opinion in Critical Care

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Accepting that myocardial dysfunction may be an important cause of the shock state in overwhelming meningococcal disease, the approach to management may need to be tailored appropriately. Although presently there is no targeted treatment, it may be that therapy focused on inhibiting or antagonising interleukin-6 will be helpful in the future. Regardless of the importance of myocardial depression, fluid resuscitation remains a cornerstone in the management of severe meningococcal disease.

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Section: Assessment Of Cardiac Dysfunctionsupporting

confidence: 54%

Myocardial dysfunction in meningococcal septic shock

Makwana¹,

Baines²

2005

Current Opinion in Critical Care

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“…The septic shock is characterized by a profound vasodilation, reduced ventricular contractility, vascular leakage reducing the circulation blood volume and a gradual development of inflammation-induced cardiac failure, manifested by increased left ventricle volume and decreasing ejection fraction (Boucek et al, 1984;Mercier et al, 1988;Hagmolen of ten Have et al, 2000;Thiru et al, 2000;Brandtzaeg, 2006;Martin et al, 2019). The septic cardiac failure and vasodilation have been associated with increased production of nitric oxide (NO) in endothelial cells, high levels of tumor necrosis factor (TNF), interleukin 1β (IL-1β), IL-6, vasoactive intestinal polypeptide and persistent high levels tumor necrosis factor; TNFAIP3, Tumor necrosis factor, alpha-induced protein 3; TNFAIP6, Tumor Necrosis Factor-Inducible Gene 6 Protein (alias TSG-6); TNIP1, TNFAIP3-interacting protein 1; TREM1, Triggering receptor expressed on myeloid cells 1; UPR, unfolded protein response; VCAM-1, vascular cell adhesion molecule 1; YWHAE, Tyrosine 3-Monooxygenase/Tryptophan 5-Monooxygenase Activation Protein Epsilon (alias 14-3-3 protein epsilon).…”

Section: Introductionmentioning

confidence: 99%

Extensive Changes in Transcriptomic “Fingerprints” and Immunological Cells in the Large Organs of Patients Dying of Acute Septic Shock and Multiple Organ Failure Caused by Neisseria meningitidis

Brusletto

Løberg

Hellerud

et al. 2020

Front. Cell. Infect. Microbiol.

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Background: Patients developing meningococcal septic shock reveal levels of Neisseria meningitidis (10 6-10 8 /mL) and endotoxin (10 1-10 3 EU/mL) in the circulation and organs, leading to acute cardiovascular, pulmonary and renal failure, coagulopathy and a high case fatality rate within 24 h. Objective: To investigate transcriptional profiles in heart, lungs, kidneys, liver, and spleen and immunostain key inflammatory cells and proteins in post mortem formalin-fixed, paraffin-embedded (FFPE) tissue samples from meningococcal septic shock patients. Patients and Methods: Total RNA was isolated from FFPE and fresh frozen (FF) tissue samples from five patients and two controls (acute non-infectious death). Differential expression of genes was detected using Affymetrix microarray analysis. Lung and heart tissue samples were immunostained for T-and B cells, macrophages, neutrophils and the inflammatory markers PAI-1 and MCP-1. Inflammatory mediators were quantified in lysates from FF tissues. Results: The transcriptional profiles showed a complex pattern of protein-coding and non-coding RNAs with significant regulation of pathways associated with organismal death, cell death and survival, leukocyte migration, cellular movement, proliferation of cells, cell-to-cell signaling, immune cell trafficking, and inflammatory responses in an organ-specific clustering manner. The canonical pathways including acute phase response-, EIF2-, TREM1-, IL-6-, HMBG1-, PPAR signaling, and LXR/RXR activation were associated with acute heart, pulmonary, and renal failure. Fewer genes were regulated in the liver and particularly in the spleen. The main upstream regulators were TNF, IL-1β, IL-6, RICTOR, miR-6739-3p, and CD3. Increased numbers of inflammatory cells (CD68+, MPO+, CD3+, and CD20+) were found in lungs and heart. PAI-1 inhibiting Brusletto et al. Transcriptional Profiles in MSS Organs fibrinolysis and MCP-1 attracting leukocyte were found significantly present in the septic tissue samples compared to the controls. Conclusions: FFPE tissue samples can be suitable for gene expression studies as well as immunostaining of specific cells or molecules. The most pronounced gene expression patterns were found in the organs with highest levels of Neisseria meningitidis DNA. Thousands of protein-coding and non-coding RNA transcripts were altered in lungs, heart and kidneys. We identified specific biomarker panels both protein-coding and non-coding RNA transcripts, which differed from organ to organ. Involvement of many genes and pathways add up and the combined effect induce organ failure.

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“…In pediatric literature, normal values for systolic function of the left ventricle differ from shortening fraction by more than 28% or more than 30%. [15][16][17][18] Systolic function of the right ventricle was determined by measuring tricuspid annular plane systolic excursion (TAPSE). There are no known reference data in the pediatric literature for TAPSE.…”

Section: Methodsmentioning

confidence: 99%