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Resume Pour une revue medicale, la diffusion a grande echelle de chacun de ses articles est aujourd’hui indispensable pour toucher un large public scientifique. Dans ce contexte, l’utilisation du reseau social Twitter permet a chaque nouvelle publication d’etre diffusee tres rapidement, a faible cout, pour des lecteurs precis et partout dans le monde. C’est de loin le reseau social le plus utilise pour partager les publications en 2021. Les reflexions autour de ce sujet ont ainsi abouti a la creation en novembre 2020 de la Social Media Team (SoMe Team) d’Anaesthesia Critical Care and Pain Medicine, le journal anglophone international de la Societe francaise d’anesthesie et de reanimation (SFAR). Cette equipe est coordonnee par un editeur en charge des reseaux sociaux, en lien direct avec le redacteur en chef du journal. Il elabore le planning des tweets en fonction du programme de publication du journal, il fleche le type de contenu qui y sera associe et sollicite les auteurs pour l’obtention d’images ou de courtes videos de presentation de leur publication. Le contenu graphique et la diffusion sur Twitter sont assures par les membres de l’equipe dediee aux reseaux sociaux.

International audience; War is back in Europe. With all its horrific pictures and live videos.In its report issued on the 24th of March 2022, the World Health Organization (WHO) [1] states that the Ukrainian conflict has involved 18 million persons so far, with 3.4 million refugees in bordering countries and 6.4 million persons internally displaced (Fig. 1). In this report, 1,035 deaths and 1,650 civilian injuries were reported in Ukraine without any reported data from Russia.

Resume Le syndrome post-reanimation (SPR) ou post-intensive care syndrome (PICS) correspond a un ensemble de troubles somatiques mais aussi psychologiques qui sont courants chez les patients qui survivent a une maladie grave et aux soins intensifs. Certaines etudes estiment que 50 % a 70 % des survivants des unites de soins intensifs developpent un PICS. Les troubles cognitifs rapportes dans le cadre du PICS sont particulierement frequents et persistent dans le temps, allant de plus de 64 % a la sortie de l’hopital, de 32 % a 57 % a 6 mois et plus de 30 % a 1 an suivant les etudes. Les troubles psychologiques semblent etre presents chez un patient survivant sur trois en sortie de soins intensifs et peuvent persister dans le temps ; leurs principaux facteurs de risques sont les troubles psychologiques preexistants et les souvenirs difficiles de l’hospitalisation en soins intensifs. Les proches des patients hospitalises en reanimation et eventuellement survivants sont aussi affectes. Des symptomes d’anxiete, de depression ou de stress chez ces aidants ont ainsi ete decrits. Un accompagnement de ces proches devrait etre envisage. Les consequences ou effets secondaires des soins de reanimation pourraient etre reduits par une reeducation physique et cognitive multidisciplinaire precoce en reanimation mais aussi poursuivie a la sortie du sejour en unite de soins intensifs. Les resultats d’evaluation des strategies de traitement des consequences psychologiques, en particulier de la depression, sont a ce jour plutot decevants.

Over the past decade, endoplasmic reticulum (ER) stress has emerged as an important mechanism involved in the pathogenesis of cardiovascular diseases including heart failure. Cardiac therapy based on ER stress modulation is viewed as a promising avenue toward effective therapies for the diseased heart. Here, we tested whether sirtuin-1 (SIRT1), a NAD+-dependent deacetylase, participates in modulating ER stress response in the heart. Using cardiomyocytes and adult-inducible SIRT1 knockout mice, we demonstrate that SIRT1 inhibition or deficiency increases ER stress-induced cardiac injury, whereas activation of SIRT1 by the SIRT1-activating compound STAC-3 is protective. Analysis of the expression of markers of the three main branches of the unfolded protein response (i.e., PERK/eIF2α, ATF6 and IRE1) showed that SIRT1 protects cardiomyocytes from ER stress-induced apoptosis by attenuating PERK/eIF2α pathway activation. We also present evidence that SIRT1 physically interacts with and deacetylates eIF2α. Mass spectrometry analysis identified lysines K141 and K143 as the acetylation sites on eIF2α targeted by SIRT1. Furthermore, mutation of K143 to arginine to mimic eIF2α deacetylation confers protection against ER stress-induced apoptosis. Collectively, our findings indicate that eIF2α deacetylation on lysine K143 by SIRT1 is a novel regulatory mechanism for protecting cardiac cells from ER stress and suggest that activation of SIRT1 has potential as a therapeutic approach to protect the heart against ER stress-induced injury.

Worsening of renal failure is a frequent complication of acute decompensated right heart failure. Right heart failure may lead to chronic kidney disease that may be aggravated during acute episodes. In addition to treat the cause of this acute heart failure, renal dysfunction related to acute right side failure requires a thorough evaluation of patient volume status, an optimization of blood pressure and cardiac output and an active decongestion. An echocardiographic follow-up of RV function and tricuspid valve regurgitation are of utmost importance. Biomarkers associated with congestion (BNP, CD146,…) may be of help to prevent and treat this complication.

Background Sepsis still represents a major health issue, with persistent high morbidity and mortality rates. Cardiovascular dysfunction occurs frequently during sepsis. Adrenomedullin has been identified as a key mediator in vascular tone regulation. A non-neutralizing anti-adrenomedullin antibody, Adrecizumab, may improve haemodynamic dysfunction during caecal ligation and puncture-induced septic shock in a murine model. Our objective was to determine the role of Adrecizumab on haemodynamics in a rat model of sepsis. Methods For the induction of sepsis, caecal ligation and puncture were performed in Wistar male rats. Single blinded administration of Adrecizumab (2 mg/kg) or placebo was injected i.v. 24 h after the surgery, and norepinephrine was infused as the standard of care. There were > 7 animals per group. Invasive blood pressure and cardiac function (by echocardiography) were assessed until 3 h after Adrecizumab injection. Results A single therapeutic injection of Adrecizumab in septic rats induced rapid haemodynamic benefits with an increase in systolic blood pressure in septic-Adrecizumab rats versus untreated-septic rats (p = 0.049). The shortening fraction did not differ between the untreated-septic and septic-Adrecizumab groups. However, cardiac output increased during the 3 h after a single dose of Adrecizumab compared to untreated septic rats (p = 0.006). A single dose of Adrecizumab resulted in similar haemodynamics to the continuous administration of norepinephrine. Three hours after a single injection of Adrecizumab, there was no change in the inflammatory phenotype (TNFα, IL-10) in the hearts of the septic rats. By contrast, 3 h after a single Adrecizumab injection, free-radical production decreased in the hearts of septic-Adrecizumab vs untreated septic rats (p

The present study involved both human cohorts and animal experiments to explore the performance of soluble CD146 (sCD146), a marker of endothelial function, as a diagnostic marker of acutely decompensated heart failure (ADHF), to determine the influence of patients' characteristics on that performance and to explore the potential application of CD146 in the pathophysiology of ADHF.NT-proBNP and sCD146 were measured in three hundred ninety-one patients admitted to the emergency department for acute dyspnea. ROC curve analysis demonstrated that AUCs for ADHF diagnosis in dyspneic patients were 0.86 (95% CI: 0.82-0.90) for sCD146 and 0.90 (95% CI: 0.86-0.92) for NT-proBNP. Subgroup analyses demonstrated that adding sCD146 to NT-proBNP improved the diagnostic performance for patients lying in the gray zone of NT-proBNP (p=0.02) and could be especially useful for ruling-out ADHF. An experimental model of ADHF in rats using thoracic aortic constriction suggests that CD146 is expressed in the intima of large arteries and associated with both left ventricular function and organ congestion.sCD146, a marker of endothelial function, seems to be as powerful as NT-proBNP is used to detect the cardiac origin of an acute dyspnea. The combination of sCD146 and NT-proBNP may have better performance than NT-proBNP used alone in particular for patients underlying in the "gray" zone and could therefore be an improved option for ruling-out ADHF. Both experimental and human data suggest that CD146 is related to systolic left ventricular function and to organ congestion.

Background Maintaining adequate organ perfusion during high-risk surgery requires continuous monitoring of cardiac output to optimise haemodynamics. Oesophageal Doppler Cardiac Output monitoring (DCO) is commonly used in this context, but has some limitations. Recently, the cardiac output estimated by pulse pressure analysis- (PPCO) was developed. This study evaluated the agreement of cardiac output variations estimated with 9 non-commercial algorithms of PPCO compared with those obtained with DCO. Methods High-risk patients undergoing neurosurgery were monitored with invasive blood pressure and DCO. For each patient, 9 PPCO algorithms and DCO were recorded before and at the peak effect for every haemodynamic challenge. Results Sixty-two subjects were enrolled; 284 events were recorded, including 134 volume expansions and 150 vasopressor boluses. Among the 9 algorithms tested, the Liljestrand-Zander model led to the smallest bias (0.03 litre min−1 [−1.31, +1.38] (0.21 litre min−1 [−1.13; 1.54] after volume expansion and −0.13 litre min−1 [−1.41, 1.15] after vasopressor use). The corresponding percentage of the concordance was 91% (86% after volume expansion and 94% after vasopressor use). The other algorithms, especially those using the Winkessel concept and the area under the pressure wave, were profoundly affected by the vasopressor. Conclusions Among the 9 PPCO algorithms examined, the Liljestrand-Zander model demonstrated the least bias and best limits of agreement, especially after vasopressor use. Using this particular algorithm in association with DCO calibration could represent a valuable option for continuous cardiac output monitoring of high risk patients. Clinical Trial Registration Comite d'ethique de la Societe de Reanimation de Langue Francaise No. 11–356.

Introduction L’hemorragie sous-arachnoidienne anevrysmale (aHSA) grave justifie une prise en charge en reanimation, et ses consequences precoces (HTIC, hematomes intracerebraux) ou tardives (vasospasme, infections secondaires) sont difficiles a predire. Par ailleurs, une immunodepression innee, traduite par la baisse de l’expression monocytaire d’HLA-DR (mHLA-DR), semble associee a l’atteinte cerebrale en general [1] , et a l’aHSA [2] en particulier. L’objectif de cette etude etait de tester l’association entre l’expression de mHLA-DR avec la severite initiale ainsi qu’avec l’incidence des complications. Materiel et methodes Les aHSA admis en reanimation dont 1 mesure au moins d’mHLA-DR (cytometrie en flux, AB/C), realisee en routine bi-hebdomadaire, etait obtenue dans les 3 jours apres l’admission, etaient inclus. Les procedures diagnostiques, therapeutiques, et les complications (infections secondaires, vasospasme ou deces) ont ete recueillies. La pente d’evolution avant evenement d’mHLA-DR a ete estimee. Les resultats sont exprimes en mediane et 25 e –75 e interquartiles ou nombre et pourcentage, et obtenus au moyen de tests statistiques non parametriques, avec un risque alpha de 0,05. Resultats Entre 2009 et 2011, 55 patients ont ete inclus dans cette etude observationnelle retrospective de soins courants (autorisation de la CNIL). Les patients necessitant une ventilation mecanique > 72 heures etaient discrimines par leur expression de mHLA-DR initiale ( Tableau 1 ). Ceux dont cette premiere valeur etait inferieure a la mediane (9309 [6100–13 007,5] AB/C) avaient une incidence accrue de pneumopathie (63 % vs 29 % ; p = 0,02) et de deces [7 (25,9 %) vs 1 (3,6 %) ; p = 0,051]. La pente de recuperation de mHLA-DR etait inferieure chez les patients avant une infection secondaire (157,2 [100,7–190,5] vs 241,3 [153,2–296,3] AB/C par jour ; p = 0,02), ou avant le deces en reanimation (269 [75–334] vs 437 [258–568] AB/C par jour ; p = 0,05). Discussion Les patients admis en reanimation avaient une expression de mHLA-DR initiale basse, associee a l’infection secondaire ou au deces, mais pas au vasospasme. La predominance du traitement endovasculaire (78 %) attenue l’impact de la chirurgie sur ces resultats. La lenteur de la recuperation de mHLA-DR pourrait predire la survenue de complications autres que le vasospasme.

Introduction QSOX1 a ete identifie comme un marqueur diagnostic de l’insuffisance cardiaque aigue (ICA), plus performant que le BNP dans sa zone de grise chez l’homme. Des modeles murins ont permis de montrer que l’expression de QSOX1 est specifiquement induite dans le cœur au cours de l’ICA. De plus un stress cardiaque aigu par injection d’isoproterenol (ISO) associe a un « knock-down » de QSOX1 aggrave la dysfonction cardiaque des animaux traites. Nous avons voulu investiguer le role de QSOX1 au cours du developpement et analyser la reponse de QSOX1 dans un modele cellulaire HL-1 apres differents stress. Materiel et methodes Des souris knock-out pour QSOX1 et porteur de gene LacZ en aval du promoteur de QSOX1 ont ete utilises. Les animaux ont ete preleves a E12, E15 et E18, J1, J10, J21 et adultes. Le marquage par β-galactosidase a ete etudie au niveau macroscopique et cellulaire. Les ARNm intra-cardiaques de ces animaux ont ete etudies. Le modele cellulaire utilise une lignee de cardiomyocytes auriculaires immortalises. Les cellules ont ete soumises a plusieurs stress, tels que l’isoproterenol, la deprivation, l’hypoxie et le stress oxydant. Les ARNm en reponse a ces stress ont ete analyses par PCR quantitative ( QSOX1 , ANP , BNP , QSOX2 , et CTGF ). Resultats Au cours du developpement, QSOX1 est exprime de maniere stable au niveau de la jonction atrio-ventriculaire, de l’aorte, de l’artere pulmonaire, de l’arbre respiratoire et de l’uretere. L’absence de QSOX1 n’entraine pas de modification de l’expression des transcrits testes. Les experiences in vitro montre que le traitement des cellules HL-1 par l’ISO recapitule le phenotype in vivo, mais que le stress oxydant et l’hypoxie decouple l’induction de QSOX1 de celle des peptides natriuretiques ; la deprivation ayant un effet intermediaire ( Fig. 1 ). Discussion QSOX1 est exprime de maniere constante au cours du developpement dans le cœur et son absence n’entraine pas de phenotype cardiaque macroscopique ni moleculaire. Dans un modele in vitro, QSOX1 est regule de maniere independante des peptides natriuretiques.

IntroductionQSOX1 was identified as a plasma biomarker of acute heart failure (AHF). QSOX1 being a sulfhydryl oxidase, our aim was to decipher the role of QSOX1 in the heart face to an AHF event.MethodsAHF was provoked by IP injections of Isoproterenol (ISO, 300mg/kg/12h) for 2 days in mice (C57Bl/6 J) whereas control (C) received NaCl 9‰. Mice were killed at day 3, after echocardiography. QSOX1 KO (C57Bl/6 J) mice were generated using a QSOX1tm1a embryonic stem cell clone (KOMP). The KO construct contains a promoter-less lacZ gene under the control of the QSOX1 regulatory sequences. The mRNA levels were analyzed by RT-qPCR. The cellular level of oxidative stress was detected by using DHE. Fibrosis was analysed by Sirius red and collagen mRNA.ResultsAt baseline QSOX1-/- adult mice did not display any cardiac or vascular phenotype. After ISO, lacZ expression dramatically increased in QSOX1+/- hearts with the strongest β-galactosidase staining in the atria. In mice receiving ISO, a pulmonary congestion, BNP (x2 p

QSOX1 was identified as a new biomarker of acute heart failure (AHF). Using a proteomics strategy on plasma, QSOX1, which exists in 2 isoforms (short S and long L form), emerged as a promising marker to differentiate dyspnea caused by AHF from other syndromes. Preliminary results from our group suggested a protective role of OSOX1 cardiac induction in AHF. We developed an AHF murine model by isoproterenol injections. To further study the role of QSOX1 during AHF, we used antisense oligonucleotides (AOs) and we generated a knock-out (KO) mouse for QSOX1. AHF was provoked by two daily injections of 150 mg/kg of Isoproterenol (ISO) for two days; control mice (C) received NaCl 0.09‰ injections. Mice were sacrificed the third day, after cardiac function has been assessed by echocardiography. To silence QSOX1 expression, mice were treated by intraperitoneal injection of antisense oligonucleotides (AOs) for QSOX1. QSOX1 cardiac expression was analyzed by RT-qPCR, immunoblotting and immonofluorescence. In parallel, embryonic stem cell clone QSOX1tm1a (KOMP), in which the QSOX1 gene is invalidated, were injected into mouse blastocysts (SEAT platform, France). The KO constructs contain a promoter-less lacZ gene that is under the control of the QSOX1 regulatory sequences. QSOX1+/- heterozygotes mice were obtained from chimeric mice. The ISO mice exhibited a decrease in shortening fraction (C = 35.0 ± 0.4 %; ISO = 27.2 ± 3.3 %; p