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BackgroundStroke remains a significant global health challenge, especially in low- and middle-income countries, despite advances in treatment and prevention. Understanding stroke trends is crucial for guiding prevention and healthcare strategies.MethodsWe analysed global data from the Global Burden of Disease Study 2021 on stroke incidence, prevalence, disability-adjusted life years and mortality from 1990 to 2021. The study focused on the major subtypes of stroke—ischaemic stroke (IS), intracerebral haemorrhage and subarachnoid haemorrhage—examining the effects of age, sex and sociodemographic index (SDI) on stroke outcomes. Decomposition analysis assessed the contributions of population growth, ageing and other factors to stroke burden. The Nordpred Prediction Model was used to forecast stroke trends from 2022 to 2046.ResultsFrom 1990 to 2021, global stroke incidence and deaths increased by 70.20% and 32.17%, respectively, driven by population ageing (45.3%) and growth (29.1%). However, age-standardised incidence and mortality rates declined by 21.78% and 39.10%, reflecting improvements in healthcare and risk factor control. IS saw the largest increase in crude incidence (87.97%), with regional disparities, especially in low-SDI countries. By 2046, global stroke incidence and mortality are projected to rise by 20.3% and 35.7%, primarily in low- and middle-SDI countries.ConclusionsThe global stroke burden is rising, particularly in low-SDI regions, due to ageing and population growth. Declines in age-standardised rates emphasise the importance of healthcare improvements. Region-specific strategies are needed to address the rising burden and reduce disparities in stroke outcomes.

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.

Long-acting nitrates are widely prescribed in coronary artery disease (CAD), yet their association with long-term outcomes remains controversial. Whether left ventricular ejection fraction (LVEF) modifies this relationship has not been well characterized. We conducted a single-center retrospective cohort study using the Guizhou Provincial People's Hospital CAD database. Adults (≥18 years) who underwent coronary angiography between July 2012 and September 2016 and met angiographic criteria for CAD (≥50% stenosis in ≥1 proximal epicardial coronary artery) were eligible if LVEF and discharge medications were available. Patients were stratified by LVEF (<45%, 45%-55%, >55%) and by discharge prescription of any nitrate (mononitrate or dinitrate). The primary endpoint was all-cause death. The secondary endpoint was major adverse cardiovascular events (MACE), defined as a composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke. Kaplan-Meier methods and multivariable Cox regression were used to evaluate associations. Among 2,404 patients followed for 27.2 ± 13.5 months, 1,153 (48.0%) were discharged on nitrates. In the overall cohort, discharge on nitrates was not associated with all-cause death or MACE. In contrast, among patients with LVEF < 45%, nitrates at discharge were linked to higher cumulative incidences of all-cause death and MACE (log-rank  = 0.024 and 0.029, respectively) and remained independently associated after adjustment [all-cause death: hazard ratio (HR) 2.14, 95% confidence interval (CI) 1.15-3.96; MACE: HR 1.91, 95% CI 1.07-3.43]. No significant associations were observed in the LVEF 45%-55% or >55% strata. In this CAD cohort, nitrates were commonly prescribed at discharge. An adverse association with long-term outcomes was confined to patients with reduced LVEF, supporting cautious use in this subgroup and highlighting the need for prospective confirmation.

Several published studies have disagreements on whether the use of antidepressants is associated with increased risk of arrhythmias. In this study, we performed this meta-analysis to assess the association of antidepressants with cardiac arrhythmias in patients who require antidepressants. The PubMed and Embase databases were systematically searched until December 2021 to find studies that investigated the association between antidepressant use and cardiac arrhythmias. Studies that assessed the effects of any antidepressant on arrhythmias in patients who require antidepressants compared with those who require no antidepressants were included. We used a random-effects model to pool the adjusted risk ratios (RRs) and 95% confidence intervals (CIs). The stability of the results was examined by omitting an individual study at a time. A total of 3,396 studies were screened and 6 studies with 2,626,746 participants were finally included in this meta-analysis. When compared with no antidepressants, the use of antidepressants was significantly associated with an increased risk of atrial fibrillation (RR = 1.37, 95% CI: 1.16-1.61). However, there was no difference in the risk of ventricular arrhythmias or sudden cardiac death (RR = 1.33, 95% CI: 0.88-2.01) between the two studied groups. In the subgroup analysis, tricyclic antidepressants (RR = 1.12, 95% CI: 0.89-1.41), selective serotonin reuptake inhibitors (RR = 1.46, 95% CI: 0.63-3.38), and selective serotonin reuptake inhibitors (RR = 0.99, 95% CI: 0.97-1.01) did not increase the risk of ventricular arrhythmias and/or sudden cardiac death. Recently published data suggested that the use of antidepressants did not increase the risk of ventricular arrhythmias or sudden cardiac death. Antidepressants were associated with an increased risk of atrial fibrillation but that still needs further confirmation.

Notoginsenoside R1 (NGR1), the primary bioactive compound found in Panax notoginseng, is believed to have antihypertrophic and antiapoptotic properties, and has long been used to prevent and treat cardiovascular diseases. However, its potential role in prevention of diabetic cardiomyopathy remains unclear. The present study aimed to investigate the mechanism of NGR1 action in high glucose-induced cell injury. H9c2 cardiomyocytes were cultured in a high-glucose medium as an in-vitro model, and apoptotic cells were visualized using TUNEL staining. Expression of Nrf2 and HO-1 was measured using Western blotting or reverse transcription-quantitative PCR (RT-qPCR). The Nrf2 small interfering (si) RNA was transfected into cardiomyocytes using Opti-MEM containing Lipofectamine ® RNAiMAX. NGR1 protected H9c2 cardiomyocytes from cell death, apoptosis and hypertrophy induced by high glucose concentration. Expression of auricular natriuretic peptide and brain natriuretic peptide was remarkably reduced in NGR1-treated H9C2 cells. Western blot analysis showed that high glucose concentration markedly inhibited AMPK, Nrf2 and HO-1, and this could be reversed by NGR1 treatment. However, the cardioprotective effect of NGR1 was attenuated by compound C, which reverses Nrf2 and HO-1 expression levels, suggesting that AMPK upregulates Nrf2 and HO-1 gene expression, protein synthesis and secretion. Transfection of H9C2 cells with Nrf2 siRNA markedly reduced the cardioprotective effect of NGR1 via reduced expression of HO-1. These results indicated that NGR1 attenuated high glucose-induced cell injury via AMPK/Nrf2 signaling and its downstream target, the HO-1 pathway. We conclude that the cardioprotective effects of NGR1 result from upregulation of AMPK/Nrf2 signaling and HO-1 expression in cardiomyocytes. Our findings suggest that NGR1 treatment might provide a novel therapy for diabetic cardiomyopathy.

Aims Liver fibrosis scores (LFSs) are non‐invasive and effective tools for estimating cardiovascular risks. To better understand the advantages and limitations of currently available LFSs, we determined to compare the predictive values of LFSs in heart failure with preserved ejection fraction (HFpEF) for primary composite outcome, atrial fibrillation (AF), and other clinical outcomes. Methods and results This was a secondary analysis of the TOPCAT trial, and 3212 HFpEF patients were enrolled. Five LFSs, namely, non‐alcoholic fatty liver disease fibrosis score (NFS), fibrosis‐4 score (FIB‐4), BARD, aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio, and Health Utilities Index (HUI) scores were adopted. Cox proportional hazard model and competing risk regression model were performed to assess the associations between LFSs and outcomes. The discriminatory power of each LFS was evaluated by calculating the area under the curves (AUCs). During a median follow‐up of 3.3 years, a 1‐point increase in the NFS [hazard ratio (HR) 1.10; 95% confidence interval (CI) 1.04–1.17], BARD (HR 1.19; 95% CI 1.10–1.30), and HUI (HR 1.44; 95% CI 1.09–1.89) scores was associated with an increased risk of primary outcome. Patients with high levels of NFS (HR 1.63; 95% CI 1.26–2.13), BARD (HR 1.64; 95% CI 1.25–2.15), AST/ALT ratio (HR 1.30; 95% CI 1.05–1.60), and HUI (HR 1.25; 95% CI 1.02–1.53) were at an increased risk of primary outcome. Subjects who developed AF were more likely to have high NFS (HR 2.21; 95% CI 1.13–4.32). High levels of NFS and HUI scores were a significant predictor of any hospitalization and hospitalization for heart failure. The AUCs for the NFS in predicting primary outcome (0.672; 95% CI 0.642–0.702) and incident of AF (0.678; 95% CI 0.622–0.734) were higher than other LFSs. Conclusions In light of these findings, NFS appears to have superior predictive and prognostic utility compared with AST/ALT ratio, FIB‐4, BARD, and HUI scores. Clinical trial registration: (https://clinicaltrials.gov). Unique identifier: NCT00094302.

Abstract Background/Aims: Cyr61-cysteine-rich protein 61 (CCN1/CYR61) is a multifunctional matricellular protein involved in the regulation of fibrogenesis. Animal experiments have demonstrated that CCN1 can inhibit cardiac fibrosis in cardiac hypertrophy. However, no study has been conducted to assess the relation between serum CCN1 and prognosis of acute heart failure (AHF). Methods: We measured the serum CCN1 levels of 183 patients with AHF, and the patients were followed up for 6 months. The associations between CCN1 levels and some clinical covariates, especially left ventricular ejection fraction (LVEF), estimated glomerular filtration rate (eGFR), atrial fibrillation and age, were estimated. The AHF patients were followed up for 6 months. The endpoint was all-cause mortality. Kaplan-Meier curve analysis and multivariable Cox proportional hazards analysis were employed to evaluate the prognostic ability of CCN1. We used calibration, discrimination and reclassification to assess the mortality risk prediction of adding CCN1. Results: Serum CCN1 concentrations in AHF patients were significantly increased compared with those in individuals without AHF (237 pg/ml vs. 124.8 pg/ml, p< 0.001). CCN1 level was associated with the level of NT-proBNP (r=0.349, p< 0.001) and was not affected by LVEF, eGFR, age or atrial fibrillation in AHF patients. Importantly, Kaplan-Meier curve analysis illustrated that the AHF patients with serum CCN1 level > 260 pg/ ml had a lower survival rate (p< 0.001). Multivariate Cox hazard analysis suggests that CCN1 functions as an independent predictor of mortality for AHF patients (LgCCN1, hazard ratio 5.825, 95% confidence interval: 1.828-18.566, p=0.003). In addition, the inclusion of CCN1 in the model with NT-proBNP significantly improved the C-statistic for predicting death (0.758, p< 0.001). The integrated discrimination index was 0.019 (p< 0.001), and the net reclassification index increased significantly after addition of CCN1 (23.9%, p=0.0179). Conclusions: CCN1 is strongly predictive of 6-month mortality in patients with AHF, suggesting serum CCN1 as a promising candidate prognostic biomarker for AHF patients.

BackgroundSeveral published studies have examined the association of coffee consumption with atrial fibrillation (AF) risk, but their findings are still controversial. Therefore, we performed a systematic review and dose–response meta-analysis of prospective studies to determine the relationship between coffee consumption and the risk of incident AF.MethodsWe systematically retrieved the PubMed and Embase databases until October 2021 for pertinent studies that reported the association of coffee consumption (caffeinated or decaffeinated coffee) with AF risk. A cubic spline random-effects model was used to fit the potential dose–response curve. The effect estimates were expressed as adjusted risk ratios (RRs) and 95% CIs.ResultsA total of 10 prospective studies (11 cohorts) involving 30,169 AF events and 723,825 participants were included. In the dose–response analysis, there was a linear inverse association between coffee intake and risk of AF although not statistically significant ( P non–linearity = 0.25). Compared with participants with no coffee consumption, the RRs (95% CI) of AF risk estimated directly from the dose–response curve were 1.01 (0.98–1.03), 1.00 (0.97–1.04), 0.99 (0.92–1.02), 0.95 (0.89–1.01), 0.94 (0.87–1.01), 0.89 (0.79–1.02), and 0.87 (0.76–1.02) for 1–7 cups of coffee per day, respectively. One cup per day increased in coffee consumption was associated with a 2% reduced risk of AF (RR = 0.98, 95% CI: 0.97–1.00, P = 0.02).ConclusionsOur evidence from this meta-analysis suggested that coffee consumption had a trend toward reducing the risk of AF in a dose–response manner. Further studies could be conducted to reinforce our findings.

BackgroundCurrent guidelines recommend the utilization of direct-acting oral anticoagulants (DOACs) in patients with non-valvular atrial fibrillation (AF). However, the optimal anticoagulation strategy for AF patients with bioprosthetic heart valves (BPHV) remains controversial. Therefore, we conducted this meta-analysis to explore the effect of DOACs versus vitamin K antagonists (VKAs) in this population.MethodsWe systematically searched the PubMed and Embase databases until November 2021 for studies reporting the effect of DOACs versus VKAs in AF patients with BPHV. Adjusted risk ratios (RRs) and 95% confidence intervals (CIs) were pooled using the random-effects model with an inverse variance method.ResultsWe selected four randomized clinical trials and seven observational studies (2236 DOAC- and 6403 VKAs-users). Regarding the effectiveness outcomes, there were no significant differences between DOACs and VKAs in stroke or systemic embolism (RR = 0.74, 95%CI: 0.50–1.08), ischemic stroke (RR = 1.08, 95%CI: 0.76–1.55), all-cause death (RR = 0.98, 95%CI: 0.86–1.12), and cardiovascular death (RR = 0.85, 95%CI: 0.40–1.80). In terms of the safety outcomes, DOACs was associated with lower risks of major bleeding (RR = 0.70, 95%CI: 0.59–0.82) and intracranial bleeding (RR = 0.42, 95%CI: 0.26–0.70), but the risks of any bleeding (RR = 0.85, 95%CI: 0.65–1.13) and gastrointestinal bleeding (RR = 0.92, 95%CI: 0.73–1.17) are not significantly different when compared with VKAs. The subgroup analysis with follow-up as a covariate revealed that the DOACs had lower risks of SSE (RR = 0.59, 95%CI: 0.37–0.94) and major bleeding (RR = 0.69, 95%CI: 0.58–0.81) in patients with a mean follow-up of more than 24 months, but no statistical differences were found in patients with the follow-up less than 24 months (SSE: RR = 1.10, 95%CI: 0.92–1.32; major bleeding: RR = 0.91, 95%CI: 0.42–2.01).ConclusionsIn AF with BPHV, patients on DOACs experienced a reduced risk of major bleeding and intracranial bleeding compared with VKAs, while the risks of stroke, cardiovascular death, and all-cause mortality were similar.

Objective: To explore the effect of the 6-minute walk test (6MWT) guided by non-invasive cardiac output on the rehabilitation of patients with knee osteoarthritis following artificial total knee arthroplasty. Methods: About 66 patients with knee osteoarthritis planned to undergo artificial total knee arthroplasty were included from March 2019 to October 2019, and randomly assigned to the intervention group or control group. Under the guidance of a clinical rehabilitation physician, orthopedic physician, and cardiologist, a home rehabilitation exercise program based on 6MWT and non-invasive cardiac output was formulated for patients with knee osteoarthritis. The participants of the intervention group conducted full rehabilitation training supervision and guidance through the WeChat platform to ensure their rehabilitation pieces of training were completed safely and effectively. As for the control group, patients were just given rehabilitation training manuals at the time of discharge and completed the training by themselves. Results: At 6 months post-operatively, 6-minute walk distance (413.88 ± 44.61 vs. 375.00 ± 40.53 m, P < 0.05), active metabolic equivalent (4.13 ± 0.29 vs. 3.88 ± 0.27, P < 0.05), stroke volume after 6MWT (114.97 ± 12.05 vs. 98.38 ± 16.43 ml, P < 0.05), and cardiac output (11.92 ± 1.68 vs. 9.79 ± 1.82 l/min, P < 0.05) of the intervention group were significantly higher than those of the control group. The symptom evaluation scores of the intervention group were also better than those of the control group. Conclusions: The multidisciplinary post-operative rehabilitation exercise training program is beneficial to the recovery of lower limb function and the improvement of exercise capacity after knee replacement, and it also helps to improve the non-invasive hemodynamic indicators related to the cardiac function of the patient. Clinical Trial Registration: http://www.chictr.org.cn/index.aspx .