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There are limited data on the outcomes of cardiogenic shock (CS) and cardiac arrest (CA) complicating ST-segment-elevation myocardial infarction (STEMI).

Adult (>18 years) STEMI admissions were identified using the National Inpatient Sample (2000-2017) and classified as CS + CA, CS only, CA only and no CS/CA. Outcomes of interest included temporal trends, in-hospital mortality, hospitalization costs, use of do-not-resuscitate (DNR) status and palliative care referrals across the four cohorts.

Of the 4,320,117 STEMI admissions, CS, CA and both were noted in 5.8%, 6.2% and 2.7%, respectively. In 2017, compared to 2000, there was an increase in CA (adjusted odds ratio [aOR] 1.83 [95% confidence interval CI 1.79-1.86]), CS (aOR 3.92 [95% CI 3.84-4.01]) and both (aOR 4.09 [95% CI 3.94-4.24]) (all p < 0.001). The CS+CA (77.2%) cohort had higher rates of multiorgan failure than CS only (59.7%) and CA only (26.3%), p < 0.001. The CA only cohort had lower rates (64%) of coronary angiography compared to the other groups (>70%), p < 0.001. SHP099 supplier In-hospital mortality was higher in CS+CA compared to CS alone (adjusted OR 1.87 [95% CI 1.83-1.91]), CA alone (adjusted OR 1.99 [95% CI 1.95-2.03]) or neither (aOR 18.37 [95% CI 18.02-18.71]). The CS+CA cohort had higher use of palliative care and DNR status. The presence of CS, either alone or in combination with CA, was associated with higher hospitalization costs.

The combination of CS and CA was associated with higher rates of non-cardiac organ failure and in-hospital mortality in STEMI compared to those with either CS or CA alone.

The combination of CS and CA was associated with higher rates of non-cardiac organ failure and in-hospital mortality in STEMI compared to those with either CS or CA alone.

Cardiac arrest can activate blood coagulation, which clinically manifests as obstruction of the microcirculation and multiple organ dysfunction. Thromboelastography (TEG) provides a rapid and comprehensive assessment of hemostatic processes, but there are limited data on the use of sequential TEG values during targeted temperature management (TTM) in out-of-hospital cardiac arrest (OHCA) survivors. The aim of this study was to investigate the prognostic value of coagulopathy assessed by repeated TEG to predict neurologically intact survival.

A prospective cohort of consecutive non-trauma OHCA patients who were successfully resuscitated and treated with TTM. Patients with a target temperature of 36 ℃, no TEG data, and who declined appropriate treatment were excluded. TEG was measured at three time points of TTM (initial phase, target phase, and rewarming phase). The primary outcome was 28 day favorable neurologic function, defined as a Cerebral Performance Category of 1 or 2.

A total of 125 patients (mea associated with favorable neurologic outcome (OR, 4.508, 95% CI, 1.254-16.210).

TEG results are available within minutes, and shorted R values or the absence of prolonged LY30 values in the initial phase are an early predictor of neurologically intact survival in successfully resuscitated OHCA patients.

TEG results are available within minutes, and shorted R values or the absence of prolonged LY30 values in the initial phase are an early predictor of neurologically intact survival in successfully resuscitated OHCA patients.

To determine the effect of CPR delivery surface (e.g. firm mattress, floor, backboard) on patient outcomes and CPR delivery.

We searched Medline, Cochrane Library and Web of Science for studies published since 2009 that evaluated the effect of CPR delivery surface in adults and children on patient outcomes and quality of CPR. We included randomised controlled trials only. We identified pre-2010 studies from the 2010 ILCOR evaluation of this topic. Two reviewers independently screened titles/ abstracts and full-text papers, extracted data and assessed risk of bias. Evidence certainty for each outcome was evaluated using GRADE methodology. Where appropriate, we pooled data in a meta-analysis, using a random-effects model.

Database searches identified 2701 citations. We included seven studies published since 2009. We analysed these studies together with the four studies included in the previous ILCOR review. All included studies were randomised controlled trials in manikins. Certainty of evidence was very low. Increasing mattress stiffness or moving the manikin from the bed to the floor did not improve compression depth. Use of a backboard marginally improved compression depth (mean difference 3 mm (95% CI 1-4).

The use of a backboard led to a small increase in chest compression depth in manikin trials. Different mattress types or delivery of CPR on the floor did not affect chest compression depth. PROSPERO CRD42019154791.

The use of a backboard led to a small increase in chest compression depth in manikin trials. Different mattress types or delivery of CPR on the floor did not affect chest compression depth. PROSPERO CRD42019154791.Noroviruses are the main causative agents for acute viral gastroenteritis worldwide. RIG-I-like receptors (RLRs) triggered interferon (IFN) activation is essential for host defense against viral infections. In turn, viruses have developed sophisticated strategies to counteract host antiviral response. This study aims to investigate how murine norovirus (MNV) replicase interacts with RLRs-mediated antiviral IFN response. Counterintuitively, we found that the MNV replicase NS7 enhances the activation of poly (IC)-induced IFN response and the transcription of downstream interferon-stimulated genes (ISGs). Interestingly, NS7 protein augments RIG-I and MDA5-triggered antiviral IFN response, which conceivably involves direct interactions with the caspase activation and recruitment domains (CARDs) of RIG-I and MDA5. Consistently, RIG-I and MDA5 exert anti-MNV activity in human HEK293T cells with ectopic expression of viral receptor CD300lf. This effect requires the activation of JAK/STAT pathway, and is further enhanced by NS7 overexpression. These findings revealed an unconventional role of MNV NS7 as augmenting RLRs-mediated IFN response to inhibit viral replication.