The inflammatory response is related to circulatory failure after out-of-hospital cardiac arrest: A prospective cohort study

Langeland, Halvor; Damås, Jan Kristian; Mollnes, Tom Eirik; Ludviksen, Judith Krey; Ueland, Thor; Michelsen, Annika E.; Løberg, Magnus; Bergum, Daniel; Nordseth, Trond; Skjærvold, Nils Kristian; Klepstad, Pål

doi:10.1016/j.resuscitation.2021.11.026

Cited by 33 publications

(30 citation statements)

References 41 publications

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“…Multiple novel biomarkers have been studied in the past in patients after cardiac arrest [ 6 , 7 , 20 ]. Moreover, classical indicators of inflammation such as leukocyte and neutrophil counts were associated with a worse medium- to long-term outcome after resuscitation [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, most pro-inflammatory cytokines and chemokines show temporal dynamics within the first 72 h after CA, whereas various standard interventions, such as targeted temperature management, have been observed to affect these biomarker levels [ 6 , 20 , 23 ]. The pro-inflammatory chemokines interleukin-8 and MCP-1 are certainly among the most studied novel biomarkers [ 6 , 7 ]. Regarding “classical inflammatory markers” in our study, a difference was only shown for C-reactive protein but not leukocyte counts.…”

Section: Discussionmentioning

confidence: 99%

“…Total DNase activity was measured using a single radial enzyme diffusion (SRED) assay as previously published [ 7 ]. An example is shown in Appendix A , Figure A1 .…”

Section: Methodsmentioning

confidence: 99%

“…A graphical overview of the pathophysiological role of NETs in the context of PCAS is shown in Figure 1 . The role of the pro-inflammatory chemokines interleukin-8 and monocyte chemotactic protein-1 (MCP-1) has also been studied previously in patients after CA [ 6 , 7 ]. The generalized inflammatory response in the context of regaining circulation after cardiac arrest represents a stress state in the body, which shares similarities with the pathophysiology of sepsis, but on the other hand is unique as an entity due to the short-term complete ischemia and reperfusion injury [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

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Cell-Free Double-Stranded DNA to DNase Ratio Predicts Outcome after Primary Survived Cardiac Arrest

Rezar

Lichtenauer

Paar

et al. 2022

Cells

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(1) Double-stranded DNA (dsDNA) and deoxyribonuclease (DNase) as surrogate parameters for accumulating inflammatory hazards are insufficiently studied in resuscitation research. (2) Blood samples of 76 individuals after CA were analyzed 24 and 96 h after ICU admission. Plasma levels of dsDNA, interleukin-8, and monocyte chemoattractant protein-1 and activity of DNase were assessed along with baseline characteristics, intensive care measures, and outcome data. DsDNA/DNase ratio was used as main prognostication parameter. After calculating an optimal empirical cut-off for outcome prediction (death or Cerebral Performance Category ≥3 at 6 months), multivariable logistic regression was applied. (3) Using receiver operating characteristic (ROC) analysis, an area under the curve (AUC) of 0.65 (95% CI 0.50–0.79) was found for dsDNA/DNase after 24 h versus 0.83 (95% CI 0.73–0.92) after 96 h (p = 0.03). The empirical cut-off for dsDNA/DNase ratio after 96 h was 149.97 (Youden). DsDNA/DNase ratio was associated with unfavorable outcome at six months (aOR 1.006, 95% CI 1.0017–1.0094, p = 0.005). In multivariable analysis, the association of dsDNA/DNase ratio independently predicted outcome as a continuous variable (aOR 1.004, 95% CI 1.0004–1.0079, p = 0.029) after adjusting for potential confounders. (4) DsDNA/DNase ratio at 96 h demonstrates good predictive performance for estimating outcome after CA.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Total DNase activity was measured using a single radial enzyme diffusion (SRED) assay as previously published [ 7 ]. An example is shown in Appendix A , Figure A1 .…”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cell-Free Double-Stranded DNA to DNase Ratio Predicts Outcome after Primary Survived Cardiac Arrest

Rezar

Lichtenauer

Paar

et al. 2022

Cells

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“…Postcardiac arrest syndrome (PCAS) is characterized by reperfusion injury from systemic ischemia, myocardial dysfunction, brain, and other vital organ injury, superimposed on underlying diseases, all of which explain the low survival rate of hospital discharge. After CA, a systemic inflammatory response occurs that has been shown to occur in the reperfusion stage, with the release of pro-inflammatory cytokines by leukocytes and endothelial cells through the activation of leukocytes and endothelial cells and the release of secondary cytokines [ 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 ]. EC expresses a wide spectrum of cytokines and chemokines, including pro-inflammatory interleukins; IL-1β, IL-3, IL-5, IL-6, IL-8, IL-11, IL-15, and tumor necrosis factor (TNF-α), as well as anti-inflammatory cytokines such as IL-1 receptor antagonist (IL-1ra), IL-10, IL-13, and transforming growth factor beta (TGF-β) [ 61 , 62 , 63 ].…”

Section: Models Of Endothelial Activationmentioning

confidence: 99%

Non-Invasive Pulsatile Shear Stress Modifies Endothelial Activation; A Narrative Review

2022

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The monolayer of cells that line both the heart and the entire vasculature is the endothelial cell (EC). These cells respond to external and internal signals, producing a wide array of primary or secondary messengers involved in coagulation, vascular tone, inflammation, and cell-to-cell signaling. Endothelial cell activation is the process by which EC changes from a quiescent cell phenotype, which maintains cellular integrity, antithrombotic, and anti-inflammatory properties, to a phenotype that is prothrombotic, pro-inflammatory, and permeable, in addition to repair and leukocyte trafficking at the site of injury or infection. Pathological activation of EC leads to increased vascular permeability, thrombosis, and an uncontrolled inflammatory response that leads to endothelial dysfunction. This pathological activation can be observed during ischemia reperfusion injury (IRI) and sepsis. Shear stress (SS) and pulsatile shear stress (PSS) are produced by mechanical frictional forces of blood flow and contraction of the heart, respectively, and are well-known mechanical signals that affect EC function, morphology, and gene expression. PSS promotes EC homeostasis and cardiovascular health. The archetype of inducing PSS is exercise (i.e., jogging, which introduces pulsations to the body as a function of the foot striking the pavement), or mechanical devices which induce external pulsations to the body (Enhanced External Pulsation (EECP), Whole-body vibration (WBV), and Whole-body periodic acceleration (WBPA aka pGz)). The purpose of this narrative review is to focus on the aforementioned noninvasive methods to increase PSS, review how each of these modify specific diseases that have been shown to induce endothelial activation and microcirculatory dysfunction (Ischemia reperfusion injury-myocardial infarction and cardiac arrest and resuscitation), sepsis, and lipopolysaccharide-induced sepsis syndrome (LPS)), and review current evidence and insight into how each may modify endothelial activation and how these may be beneficial in the acute and chronic setting of endothelial activation and microvascular dysfunction.

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Cardiac arrest related lung edema: examining the role of downtimes in transpulmonary thermodilution analysis

Voigt,

Mighali,

Wieneke

et al. 2023

Intern Emerg Med

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The inflammatory response is related to circulatory failure after out-of-hospital cardiac arrest: A prospective cohort study

Cited by 33 publications

References 41 publications

Cell-Free Double-Stranded DNA to DNase Ratio Predicts Outcome after Primary Survived Cardiac Arrest

Cell-Free Double-Stranded DNA to DNase Ratio Predicts Outcome after Primary Survived Cardiac Arrest

Non-Invasive Pulsatile Shear Stress Modifies Endothelial Activation; A Narrative Review

Cardiac arrest related lung edema: examining the role of downtimes in transpulmonary thermodilution analysis

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