Background: Emerging evidence shows that coronavirus disease 2019 (COVID-19) is commonly complicated by coagulopathy, and venous thromboembolism (VTE) is considered to be a potential cause of unexplained death. Information on the incidence of VTE in COVID-19 patients, however, remains unclear. Conclusions: This meta-analysis revealed that the estimated VTE incidence was 25% in hospitalized COVID-19 patients. Higher incidence of VTE was observed in COVID-19 patients with a severe condition or with a low rate of pharmacologic thromboprophylaxis. Assessment of VTE risk is strongly recommended in COVID-19 patients, and effective measures of thromboprophylaxis should be taken in a timely manner for patients with high risk of VTE.

Left atrial strain derived by cardiac MRI was associated major adverse cardiac events after ST-segment elevation myocardial infarction, overriding outcome predictors such as left atrial volume and left ventricular function. Key Results STEMI patients with impaired left atrial reservoir strain (21.8% or less) and conduit strain (10.5% or less) had significantly higher long-term risk of major adverse cardiac events than patients with reservoir strain larger than 21.8% and conduit strain larger than 10.5% (Log rank P < .001). Left atrial reservoir (hazard ratio, 0.84; P < .001) and conduit (hazard ratio, 0.81; P < .001) strains were independent predictors of major adverse cardiac events after STEMI, after adjusting for all included clinical and cardiac MRI outcome markers. The models including left atrial reservoir and conduit strains on top of traditional outcome markers had higher prognostic accuracy in predicting major adverse cardiac events than the model with only traditional outcome markers (Uno's C statistic, 0.

Nonalcoholic fatty liver disease (NAFLD), characterized by hepatic steatosis, insulin resistance and inflammation, poses a high risk of cardiometabolic disorders. Ubiquitin specific protease 4 (USP4), a deubiquitinating enzyme, is pivotally involved in regulating multiple inflammatory pathways; however, the role of USP4 in NAFLD is unknown. Here we report that USP4 expression was dramatically downregulated in the livers from NAFLD patients and different NAFLD mouse models induced by a high fat diet (HFD) or a genetic deficiency (ob/ob) as well as in palmitate-treated hepatocytes. Hepatocyte-specific USP4 depletion exacerbated hepatic steatosis, insulin resistance and inflammatory response in HFD-induced NAFLD mice. Conversely, hepatic USP4 overexpression notably alleviated the pathological alterations in two different NAFLD models. Mechanistically, hepatocyte USP4 directly bound to and deubiquitinated transforming growth factor-β activated kinase 1 (TAK1), leading to a suppression of the activation of downstream NF-κB and JNK cascades, which in turn reversed the disruption of the IRS-AKT-GSK3β signaling. In addition, USP4-TAK1 interaction and subsequent TAK1 deubiquitination were required for the amelioration of metabolic dysfunctions. Collectively, the present study provides the first evidence that USP4 functions as a pivotal suppressor in NAFLD and related metabolic disorders. This article is protected by copyright. All rights reserved.