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      Monocyte subsets predict mortality after cardiac arrest

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          Abstract

          After successful cardiopulmonary resuscitation (CPR), many patients show signs of an overactive immune activation. Monocytes are a heterogeneous cell population that can be distinguished into 3 subsets by flow cytometry (classical monocytes [CM: CD14 ++CD16 ], intermediate monocytes [IM: CD14 ++CD16 +CCR2 +] and non‐classical monocytes [NCM: CD14 +CD16 ++CCR2 ]). Fifty‐three patients admitted to the medical intensive care unit (ICU) after cardiac arrest were included. Blood was taken on admission and after 72 h. The primary endpoint of this study was survival at 6 months and the secondary endpoint was neurological outcome as determined by cerebral performance category (CPC)‐score at 6 months. Median age was 64.5 (49.8‐74.3) years and 75.5% were male. Six‐month mortality was 50.9% and survival with good neurological outcome was 37.7%. Monocyte subset distribution upon admission to the ICU did not differ according to survival. Seventy‐two hours after admission, patients who died within 6 months showed a higher percentage of the pro‐inflammatory subset of IM (8.3% [3.8‐14.6]% vs. 4.1% [1.5–8.2]%; P = 0.025), and a lower percentage of CM (87.5% [79.9–89.0]% vs. 90.8% [85.9–92.7]%; P = 0.036) as compared to survivors. In addition, IM were predictive of outcome independent of time to ROSC and witnessed cardiac arrest, and correlated with CPC‐score at 6 months ( R = 0.32; P = 0.043). These findings suggest a possible role of the innate immune system in the pathophysiology of post cardiac arrest syndrome.

          Graphical Abstract

          In patients admitted to an ICU after surviving a cardiac arrest, an increase of intermediate monocytes after 72 hours was associated with poor outcome.

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          Most cited references39

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          Heart Disease and Stroke Statistics—2019 Update: A Report From the American Heart Association

          Circulation, 139(10)
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            Ischemia and reperfusion--from mechanism to translation.

            Ischemia and reperfusion-elicited tissue injury contributes to morbidity and mortality in a wide range of pathologies, including myocardial infarction, ischemic stroke, acute kidney injury, trauma, circulatory arrest, sickle cell disease and sleep apnea. Ischemia-reperfusion injury is also a major challenge during organ transplantation and cardiothoracic, vascular and general surgery. An imbalance in metabolic supply and demand within the ischemic organ results in profound tissue hypoxia and microvascular dysfunction. Subsequent reperfusion further enhances the activation of innate and adaptive immune responses and cell death programs. Recent advances in understanding the molecular and immunological consequences of ischemia and reperfusion may lead to innovative therapeutic strategies for treating patients with ischemia and reperfusion-associated tissue inflammation and organ dysfunction.
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              The fate and lifespan of human monocyte subsets in steady state and systemic inflammation

              Using stable isotope labeling, Patel et al. establish the lifespan of all three human monocyte subsets that circulate in dynamic equilibrium; in steady state, classical monocytes are short-lived precursors with the potential to become intermediate and nonclassical monocytes. They highlight that systemic inflammation induces an emergency release of classical monocytes into the circulation.
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                Author and article information

                Contributors
                walter.speidl@meduniwien.ac.at
                Journal
                J Leukoc Biol
                J Leukoc Biol
                10.1002/(ISSN)1938-3673
                JLB
                Journal of Leukocyte Biology
                John Wiley and Sons Inc. (Hoboken )
                0741-5400
                1938-3673
                05 October 2020
                June 2021
                : 109
                : 6 ( doiID: 10.1002/jlb.v109.6 )
                : 1139-1146
                Affiliations
                [ 1 ] Division of Cardiology Department of Internal Medicine II Medical University of Vienna Vienna Austria
                [ 2 ] Ludwig Boltzmann Cluster for Cardiovascular Research Vienna Austria
                [ 3 ] 3rd Medical Department Wilhelminen Hospital Vienna Austria
                [ 4 ] Core Facilities Medical University of Vienna Vienna Austria
                Author notes
                [*] [* ] Correspondence

                Walter S. Speidl, Department of Internal Medicine II, Medical University of Vienna, Austria.

                Email: walter.speidl@ 123456meduniwien.ac.at

                Author information
                https://orcid.org/0000-0002-7267-3138
                Article
                JLB10822
                10.1002/JLB.5A0420-231RR
                8247267
                33020969
                a888aa9f-1efe-4c59-b878-396e6a097d10
                © 2020 The Authors. Journal of Leukocyte Biology published by Wiley Periodicals LLC on behalf of Society for Leukocyte Biology

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 14 September 2020
                : 10 April 2020
                : 14 September 2020
                Page count
                Figures: 4, Tables: 2, Pages: 8, Words: 5766
                Categories
                Article
                Translational and Clinical Immunology
                Custom metadata
                2.0
                June 2021
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.0.2 mode:remove_FC converted:01.07.2021

                Hematology
                cardiac arrest,innate immunity,monocyte subsets,monocytes
                Hematology
                cardiac arrest, innate immunity, monocyte subsets, monocytes

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