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Chronic heart failure is the end stage of cardiac diseases. With a high prevalence and a high mortality rate worldwide, chronic heart failure is one of the heaviest health-related burdens. In addition to the standard neurohormonal blockade therapy, several medications have been developed for chronic heart failure treatment, but the population-wide improvement in chronic heart failure prognosis over time has been modest, and novel therapies are still needed. Mechanistic discovery and technical innovation are powerful driving forces for therapeutic development. On the one hand, the past decades have witnessed great progress in understanding the mechanism of chronic heart failure. It is now known that chronic heart failure is not only a matter involving cardiomyocytes. Instead, chronic heart failure involves numerous signaling pathways in noncardiomyocytes, including fibroblasts, immune cells, vascular cells, and lymphatic endothelial cells, and crosstalk among these cells. The complex regulatory network includes protein–protein, protein–RNA, and RNA–RNA interactions. These achievements in mechanistic studies provide novel insights for future therapeutic targets. On the other hand, with the development of modern biological techniques, targeting a protein pharmacologically is no longer the sole option for treating chronic heart failure. Gene therapy can directly manipulate the expression level of genes; gene editing techniques provide hope for curing hereditary cardiomyopathy; cell therapy aims to replace dysfunctional cardiomyocytes; and xenotransplantation may solve the problem of donor heart shortages. In this paper, we reviewed these two aspects in the field of failing heart signaling cascades and emerging therapeutic strategies based on modern biological techniques.

Background Current guidelines recommend rhythm control for improving symptoms and quality of life in symptomatic patients with atrial fibrillation (AF). However, the long-term prognostic outcomes of rhythm control compared with rate control are still inconclusive. In this meta-analysis, we aimed to assess the effects of early rhythm control compared with rate control on clinical outcomes in newly diagnosed AF patients. Methods We systematically searched the PubMed and Embase databases up to August 2022 for randomized and observational studies reporting the associations of early rhythm control (defined as within 12 months of AF diagnosis) with effectiveness outcomes. The primary outcome was a composite of death, stroke, admission to hospital for heart failure (HF), or acute coronary syndrome (ACS). Hazard ratios (HRs) and 95% confidence intervals (CIs) from each study were pooled using a random-effects model, complemented with an inverse variance heterogeneity or quality effects model. Results A total of 8 studies involving 447,202 AF patients were included, and 23.5% of participants underwent an early rhythm-control therapy. In the pooled analysis using the random-effects model, compared with rate control, the early rhythm-control strategy was significantly associated with reductions in the primary composite outcome (HR = 0.88, 95% CI: 0.86–0.89) and secondary outcomes, including stroke or systemic embolism (HR = 0.78, 95% CI: 0.71–0.85), ischemic stroke (HR = 0.81, 95% CI: 0.69–0.94), cardiovascular death (HR = 0.83, 95% CI: 0.70–0.99), HF hospitalization (HR = 0.90, 95% CI: 0.88–0.92), and ACS (HR = 0.86, 95% CI: 0.76–0.98). Reanalyses using the inverse variance heterogeneity or quality effects model yielded similar results. Conclusions Our current meta-analysis suggested that early initiation of rhythm control treatment was associated with improved adverse effectiveness outcomes in patients who had been diagnosed with AF within 1 year. Registration The study protocol was registered to PROSPERO (CRD42021295405).

BackgroundAnticoagulant treatment in non-valvular atrial fibrillation (AF) patients with severe chronic kidney disease (CKD) or on dialysis remains a matter of debate. The object of this study was to quantify the benefit-risk profiles of rivaroxaban or apixaban versus warfarin in AF patients with stage 4–5 CKD or on dialysis.MethodA comprehensive search of the Cochrane Library, PubMed, Ovid, and Google Scholar databases was performed for eligible studies that comparing the effect and safety of rivaroxaban or apixaban versus warfarin in AF patients with stage 4–5 CKD or on dialysis. Hazard ratios (HRs) and 95% confidence intervals (CIs) were abstracted, and then pooled using a random-effects model.ResultsA total of seven studies, one post hoc analysis of RCT and six observational cohorts, were included in this meta-analysis. Compared with warfarin use, the use of rivaroxaban or apixaban was significantly associated with reduced risks of all-cause death (HR = 0.82, 95% CI 0.72–0.93) and gastrointestinal bleeding (HR = 0.87, 95% CI 0.80–0.95). There were no significant differences in the risks of stroke or systemic embolism (rivaroxaban, HR = 0.71, 95% CI 0.43–1.19; apixaban, HR = 0.86, 95%CI 0.68–1.09) and major bleeding (rivaroxaban, HR = 0.96, 95% CI 0.64–1.45; apixaban, HR = 0.56, 95%CI 0.28–1.12).ConclusionsCurrent evidence suggests that rivaroxaban or apixaban are safe and at least as effective as warfarin in patients with AF and stage 4–5 CKD or on dialysis.

Background Epicardial adipose tissue (EAT) has been suggested to exert deleterious effects on myocardium and cardiovascular disease (CVD) consequence. We evaluated the associations of EAT thickness with adverse outcomes and its potential mediators in the community. Methods Participants without heart failure (HF) who had undergone cardiac magnetic resonance (CMR) to measure EAT thickness over the right ventricular free wall from the Framingham Heart Study were included. The correlation of EAT thickness with 85 circulating biomarkers and cardiometric parameters was assessed in linear regression models. The occurrence of HF, atrial fibrillation, coronary heart disease (CHD), and other adverse events was tracked since CMR was implemented. Their associations with EAT thickness and the mediators were evaluated using Cox regression and causal mediation analysis. Results Of 1554 participants, 53.0% were females. Mean age, body mass index, and EAT thickness were 63.3 years, 28.1 kg/m 2 , and 9.8 mm, respectively. After fully adjusting, EAT thickness positively correlated with CRP, LEP, GDF15, MMP8, MMP9, ORM1, ANGPTL3, and SERPINE1 and negatively correlated with N-terminal pro-B-type natriuretic peptide (NT-proBNP), IGFBP1, IGFBP2, AGER, CNTN1, and MCAM. Increasing EAT thickness was associated with smaller left ventricular end-diastolic dimension, thicker left ventricular wall thickness, and worse global longitudinal strain (GLS). During a median follow-up of 12.7 years, 101 incident HF occurred. Per 1-standard deviation increment of EAT thickness was associated with a higher risk of HF (adjusted hazard ratio [HR] 1.43, 95% confidence interval [CI] 1.19–1.72, P  < 0.001) and the composite outcome consisting of myocardial infarction, ischemic stroke, HF, and death from CVD (adjusted HR [95% CI], 1.23 [1.07–1.40], P  = 0.003). Mediation effect in the association between thicker EAT and higher risk of HF was observed with NT-proBNP (HR [95% CI], 0.95 [0.92–0.98], P  = 0.011) and GLS (HR [95% CI], 1.04 [1.01–1.07], P  = 0.032). Conclusions EAT thickness was correlated with inflammation and fibrosis-related circulating biomarkers, cardiac concentric change, myocardial strain impairment, incident HF risk, and overall CVD risk. NT-proBNP and GLS might partially mediate the effect of thickened EAT on the risk of HF. EAT could refine the assessment of CVD risk and become a new therapeutic target of cardiometabolic diseases. Trial registration URL: https://clinicaltrials.gov . Identifier: NCT00005121.

Background The association between urbanization and myocardial infarction in China was not fully understood. We aim to evaluate the association between urbanization level and the risk of myocardial infarction. Methods Participants’ data from China Health and Nutrition Survey were analyzed. The survey is an ongoing open cohort with a multistage, random cluster process to draw a sample of over 30,000 individuals in 15 provinces and municipal cities. A multi-component score, urbanization index, was used to measure urbanization level. Urbanization index was categorized by cut-off values of 40, 60, and 80. Baseline characteristics were presented as percentage for categorical variables, and mean or median for continuous variables depending on normality. The association of urbanization index and myocardial infarction risk was evaluated longitudinally by a multilevel mixed-effects parametric survival model with urbanization index as a time-dependent variable using Stata software. Results A total of 16,565 participants without previous myocardial infarction were involved in the cohort. At baseline, urbanization index was positively correlated with myocardial infarction risk factors, including blood pressure, body mass index, diabetes, and stroke. In the univariate model, urbanization index was associated with risk of myocardial infarction in a “U-shape” manner, with the lowest myocardial infarction risk in urbanization index ranging from 40 to 60 (Hazard Ratio 0.55 and p =  0.013). However, in the multivariate model adjusting for myocardial infarction risk factors and other confounders, urbanization index ≥ 40 was consistently associated with lower MI risks (Hazard Ratio 0.46 and p =  0.002 for urbanization index 40–60; Hazard Ratio 0.56 and p =  0.021 for urbanization index 60–80; and Hazard Ratio 0.44 and p =  0.002 for urbanization index ≥ 80). Conclusions Our study indicated that urbanization of living communities was associated with a reduced risk of myocardial infarction.

With the rapid growth of elevator installations, conventional scheduled maintenance struggles to meet the dual demands of ensuring operational safety and cost control. This study proposes an innovative on-demand maintenance method that aligns with the Chinese policy directives on elevator maintenance reform. First, we conduct a historical fault cause analysis to identify the root causes of elevator entrapment incidents. Next, we establish an entrapment prediction model based on our historical data. Then, we design an elevator entrapment risk index report according to the prediction results. Finally, we formulate an on-demand maintenance plan that combines insights from the report with the conclusions of the cause analysis. Field implementation and comparative experiments demonstrate that the proposed on-demand maintenance method outperforms the scheduled one. The result shows significant reductions in accident and maintenance workload, justifying the practical value of this approach for the industry.

The effects of long-term levels of body mass index (BMI), blood pressure (BP), plasma lipids and fasting blood glucose (FBG) on the cardiac structure and function in later life in general population are to evaluate. We included adult participants without heart failure from Framingham Heart Study. The respective averages over a span of 30-36 years of seven parameters were pooled into linear regression models simultaneously to evaluate their associations with subsequent left atrial internal dimension (LAID), left ventricular mass index (LVMi), internal dimension (LVID), ejection fraction (LVEF), global longitudinal strain (GLS) and mitral inflow velocity to early diastolic mitral annular velocity (E/é). In 1838 participants (56.0% female, mean age 66.1 years), per 1-standard deviation (SD) increment of mean BMI correlated with larger LAID and LVID (β 0.05~0.17, standard error [SE] 0.01 for all), greater LVMi (β [SE], 1.49 [0.46]), worse E/é (β [SE], 0.28 [0.05]). Per 1-SD increment of mean systolic BP correlated with greater LVMi (β [SE], 4.70 [0.69]), LVEF (β [SE], 0.73 [0.24]), E/é (β [SE], 0.52 [0.08]), whereas increase of mean diastolic BP correlated with smaller LVMi (β [SE], -1.61 [0.62]), LVEF (β [SE], -0.46 [0.22]), E/é (β [SE], -0.30 [0.07]). Per 1-SD increment of mean high density lipoprotein cholesterol (HDL-c) correlated with smaller LVID (β [SE], -0.03 [0.01]) and better systolic function (LVEF, β [SE], 0.63 [0.19]; GLS, β [SE], -0.20 [0.10]). The variabilities of BMI, BP and HDL-c also correlated with certain cardiac measurements. In long-term, BMI affected the size and mass of heart chambers, systolic and diastolic BP differently influenced left ventricular mass and function, higher HDL-c linked to better systolic function. Clinical trial registration: URL: https://clinicaltrials.gov . Identifier: NCT00005121.

Background Recent studies have reported the effects of metabolic syndrome (MetS) and its components on atrial fibrillation (AF), but the results remain controversial. Therefore, we performed a meta-analysis to evaluate the relationship between MetS and AF risk. Methods Studies were searched from the Cochrane library, PubMed, and Embase databases through May 2020. Adjusted hazard ratios (HRs) and its corresponding 95% confidence intervals (CIs) were extracted and then pooled by using a random effects model. Results A total of 6 observational cohort studies were finally included. In the pooled analysis, MetS was associated with an increased risk of AF (HR 1.57; 95% CI 1.40–1.77; P  < 0.01). And the components of MetS including abdominal obesity (HR 1.37; 95% CI 1.36–1.38; P  < 0.01), elevated blood pressure (HR 1.56; 95% CI 1.46–1.66; P  < 0.01), elevated fasting glucose (HR 1.18; 95% CI 1.15–1.21; P  < 0.01) and low high density cholesterol (HDL) (HR 1.18; 95% CI 1.06–1.32; P  < 0.01) was also associated with an increased risk of AF, while high triglyceride (HR 0.99; 95% CI 0.87–1.11, P  = 0.82) was not. Conclusions Our present meta-analysis suggested that MetS, as well as its components including abdominal obesity, elevated blood pressure, elevated fasting glucose and low HDL cholesterol were associated with an increase in the risk of AF.

Background Obesity is a well-defined risk factor for heart failure with preserved ejection fraction (HFpEF), but it is associated with a better prognosis in patients with diagnosed HFpEF. The paradoxically poor prognosis in nonobese patients with HFpEF may be driven by a subset of high-risk patients, which suggests that the nonobese HFpEF subpopulation is heterogeneous. Methods Latent class analysis (LCA) was adopted to identify the potential subgroups of 623 nonobese patients enrolled in the TOPCAT trial. The baseline characteristics of the identified nonobese subgroups were compared with each other and with the obese patients. The risks of all-cause, cardiovascular, and noncardiovascular mortality, and an HF composite outcome were also compared. Results Two subgroups of nonobese patients with HFpEF (the physiological non-obesity and the pathological non-obesity) were identified. The obese patients were younger than both nonobese subgroups. The clinical profile of patients with pathological non-obesity was poorer than that of patients with physiological non-obesity. They had more comorbidities, more severe HF, poorer quality of life, and lower levels of physical activity. Patients with pathological non-obesity showed low serum hemoglobin and albumin levels. After 2 years of follow-up, more patients in the pathological group lost ≥ 10% of body weight compared with those in the physiological group (11.34% vs. 4.19%, P = 0.009). The prognostic implications of the two subgroups were opposite. Compared to patients with obesity, patients with physiological non-obesity had a 47% decrease in the risk of HF composite outcome (hazard ratio [HR] 0.53, 95% confidence interval [CI] 0.40–0.70, P <0.001) and a trend of decreased all-cause mortality risk (HR 0.75, 95% CI 0.55–1.01, P =0.06), while patients with pathological non-obesity had a 59% increase (HR 1.59, 95% CI 1.24–2.02, P <0.001) in all-cause mortality risk. Conclusions Two subgroups of nonobese patients with HFpEF with distinct clinical profiles and prognostic implications were identified. The low BMI was likely physiological in one group but pathological in the other group. Using a data-driven approach, our study provided an alternative explanation for the “obesity paradox” that the poor prognosis of nonobese patients with HFpEF was driven by a pathological subgroup.

Smart grazing is a relatively difficult field of digital agriculture. Restricted by the geographical conditions of pastures, poor network infrastructure and low economic output, conventional IoT systems are difficult to apply in the field of grazing. In this paper, we propose the Space-Air-Ground integrated Grazing IoT(SAG-GIoT) system based on the background of yak grazing production in the Qinghai-Tibet Plateau, and define three smart grazing management application scenarios: (1) daily grazing supervision, (2) UAV grazing, (3) searching for yaks. To this end, we have designed the three-tier technical architecture of SAG-GIoT, and developed collar, base station and grazing management system. We designed the all-terrain network service scheme with the BeiDou Satellite-Base Station Sender(BDS-BSS) and Small Base Stations(SBSs), and verified the daily grazing supervision test in long-term. UAV grazing test was carried out in pasture, and a flexible communication networking was realized through the UAV Based Sation(UAV-BS). With the guidance of UAV searching and APP positioning, taking Handled Base Stations(HBSs) in hand, we quickly and accurately find the lost yaks. SAG-GIoT system is characterized as low cost, flexible deployment and global service, and has broad application prospects. Article highlights SAG-GIoT system boosts yak herding efficiency on the Tibetan Plateau, which reduces the risk of livestock loss. Drones and satellite networks solve the problem of signal coverage in vast pastoral areas, which is expected be a universal network for wild. This system is efficient and feasible, with further cost reduction, it is expected to be widely applied and promoted in pastoral areas.