Silica nanoparticles (SiNPs), as one of the most widely produced nanomaterials globally, have garnered widespread attention for their potential toxicity. Epidemiological and experimental evidence have illuminated that exposure to SiNPs can lead to cardiovascular toxicity, though the precise underlying mechanisms remain unclear. We previously identified PKA as a crucial regulator in SiNPs-elicited myocardial injury. Considering this, we further conducted validation in an animal model and also an in-depth investigation into the mechanisms involved. Our data manifested that the pharmacological activation of PKA via intraperitoneal administration of Forskolin greatly mitigated SiNPs-induced abnormalities in histology and function of the rat heart, along with lessening cardiac oxidative stress and mitochondrial damage. Concomitantly, copper overload was present in the rat heart and cardiomyocytes with SiNPs administration. Notably, PKA inhibition could worsen this phenomenon, whilst PKA activation alleviated it. The mechanistic investigation hinted at the PKA/DRP1/ATP7B signaling to modulate mitochondrial dysfunction and copper overload in cardiomyocytes and ultimately apoptosis caused by SiNPs.

ABSTRACT Adherence to antihypertensive medications is essential for blood pressure (BP) control, influencing long‐term outcomes in hypertensive patients. This study examines the association between visit‐to‐visit variability in BP and heart rate (HR) and its effect on adherence to beta‐blocker therapy among outpatients. Conducted across 160 hospitals in China from January 1, 2011, to December 31, 2011, this study included 9225 hypertensive outpatients prescribed metoprolol succinate. BP and HR variability were assessed over three visits (baseline, 1‐month, and 2‐month follow‐up) using standard deviation (SD) and mean‐independent parameters. Nonadherence was defined as medication discontinuation or treatment regimen changes by the 2‐month follow‐up. Among the 9037 patients analyzed, the mean age was 58.85 years (±12.54), and 52.9% were male. Visit‐to‐visit variability in the rate–pressure product (RPP; SBP×HR) was a significant predictor of nonadherence, with an odds ratio (OR) of 1.26 (95% confidence interval [CI]: 1.04–1.53, p < 0.05) for the top‐decile SD of RPP, independent of mean RPP. Variability in diastolic blood pressure (DBP) and pulse pressure (PP) were also associated with nonadherence, with ORs of 1.65 (95% CI: 1.35–2.00, p < 0.001) for DBP and 1.66 (95% CI: 1.39–1.99, p < 0.001) for PP, independent of their mean values. Patients with fluctuations in PP or HR had a higher risk of nonadherence compared to those with consistent reductions in these measures. Visit‐to‐visit variability in RPP, DBP, and PP is a significant predictor of nonadherence to beta‐blockers, regardless of mean levels. Addressing this variability is critical for improving adherence to antihypertensive treatments and optimizing patient outcomes.

The massive global output and extensive application of silica nanoparticles (SiNPs) raise great human health concerns, especially in the lungs since the respiratory tract is a major portal for NPs entry. Emerging evidence has revealed that SiNPs cause pulmonary impairments, but the underlying mechanism remains elucidated. In this study, we clarify the role of ferroptosis in SiNPs-induced pulmonary toxicity and elucidate its molecular mechanism. First, the Wistar rats were administered to SiNPs (10 mg/kg·bw) with or without ferrostatin-1 (a well-known inhibitor of ferroptosis, shorted as Fer-1,1.0 mg/kg·bw). Results revealed that SiNPs induced impairments in lung function and histopathology by inducing ferroptosis, and the use of ferrostatin-1 alleviated the onset of ferroptosis and lung injury by SiNPs. In particular, the excessive activation of NCOA4 was involved in the ferroptotic process in response to SiNPs. In vitro, SiNPs generated intracellular Fe2+ accumulation, ROS generation, and GPX4 depletion in the human bronchial epithelial cells (16HBE). By contrast, the inhibition of NCOA4 using the RNAi technique protected cells against these phenomena by SiNPs, hinting that SiNPs-induced ferroptosis was dependent on NCOA4-mediated ferritinophagy. Also, the inhibition of ferroptosis or NCOA4-mediated ferritinopathy could protect lung cells/tissue from apoptosis. In conclusion, our data indicated that ferroptosis via the NCOA4-mediated ferritinopathy pathway was a novel and critical mechanism of SiNP-induced lung injury. Of note, we highlight the therapeutic potential of suppressing ferritinopathy or ferroptosis for the management of SiNPs' toxicity.

>Wellens’ syndrome is defined by specific T-wave inversions in the precordial leads of the electrocardiogram （ECG）, which are indicative of acute anterior myocardial ischemia caused by severe proximal stenosis of the left anterior descending （LAD）artery. If not promptly treated, approximately 75%of patients with Wellens’ syndrome may experience extensive anterior wall myocardial infarction or sudden cardiac death within days to weeks. [1,2] Although the characteristic ECG changes associated with Wellens’syndrome are highly suggestive of LAD occlusion, there are rare instances in which similar ECG alterations are observed in the absence of LAD stenosis, a phenomenon referred to as pseudo-Wellens’ syndrome. The precise pathophysiological mechanisms underlying this syndrome remain unclear. Here, we present a patient with a myocardial bridge who presented a typical Wellens’ECG pattern.

Although ample evidence indicated the pulmonary toxicity of silica nanoparticles (SiNPs), the persistence or reversibility of such injury, along with the intricate molecular networks involved, remains limited. This study investigated the toxicity and recovery effects of SiNPs on rats in the exposure (3-month via intratracheal instillation) and recovery (6-week) stages. Histopathological changes and collagen deposition in lung tissues were clearly observed following SiNPs exposure, accompanied by elevated hydroxyproline. After a 6-week recovery, these pathological alterations showed remarkable improvement, alongside with the restoration of pulmonary reactive oxygen species (ROS) and cytokines. Proteomic analysis indicated that the activation of immune responses in the serum was crucial for the recovery from lung damage caused by SiNPs instillation. Based on protein-protein interaction (PPI) network analysis, predictive modeling and validation, Hck in the lungs and serum complement component (i.e., C1qc) were identified as potential regulatory molecules, responsible for the reversibility of SiNPs-induced lung damage. In parallel to pulmonary inflammation upon SiNPs stimuli, Hck expression was elevated. In turn, the restored Hck in the recovery period contributed to the mitigation of lung damage. The findings firstly elucidate the reversibility of SiNPs-induced lung damage from a proteomic perspective, providing new insights to fully understand nanotoxicity and assess nanosafety.

Background:Non-invasive computed tomography angiography (CTA)-based fractional flow reserve (CT-FFR) could become a gatekeeper to invasive coronary angiography. Deep learning (DL)-based CT-FFR has shown promise when compared to invasive FFR. To evaluate the performance of a DL-based CT-FFR technique, DeepVessel FFR (DVFFR). Methods:This retrospective study was designed for iScheMia Assessment based on a Retrospective, single-center Trial of CT-FFR (SMART). Patients suspected of stable coronary artery disease (CAD) and undergoing both CTA and invasive FFR examinations were consecutively selected from the Beijing Anzhen Hospital between January 1, 2016 to December 30, 2018. FFR obtained during invasive coronary angiography was used as the reference standard. DVFFR was calculated blindly using a DL-based CT-FFR approach that utilized the complete tree structure of the coronary arteries. Results:Three hundred and thirty nine patients (60.5 ±10.0 years and 209 men) and 414 vessels with direct invasive FFR were included in the analysis. At per-vessel level, sensitivity, specificity, accuracy, positive predictive value (PPV) and negative predictive value (NPV) of DVFFR were 94.7%, 88.6%, 90.8%, 82.7%, and 96.7%, respectively. The area under the receiver operating characteristics curve (AUC) was 0.95 for DVFFR and 0.56 for CTA-based assessment with a significant difference (P < 0.0001). At patient level, sensitivity, specificity, accuracy, PPV and NPV of DVFFR were 93.8%, 88.0%, 90.3%, 83.0%, and 95.8%, respectively. The computation for DVFFR was fast with the average time of 22.5 ± 1.9 s. Conclusions:The results demonstrate that DVFFR was able to evaluate lesion hemodynamic significance accurately and effectively with improved diagnostic performance over CTA alone. Coronary artery disease (CAD) is a critical disease in which coronary artery luminal narrowing may result in myocardial ischemia. Early and effective assessment of myocardial ischemia is essential for optimal treatment planning so as to improve the quality of life and reduce medical costs.

The relationship of fine particulate matter (PM2.5) exposure and insulin resistance remains inclusive. Our study aimed to investigate this association in the project of Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR). Specifically, we examined the associations between long-term PM2.5 exposure and three surrogate indicators of insulin resistance: the triglyceride-glucose index (TyG), TyG with waist circumference (TyG-WC) and metabolic score for insulin resistance (METS-IR). Additionally, we explored potential effect modification of dietary intake and components. Generalized estimating equations were used to evaluate the associations between PM2.5 and the indicators with an unbalanced repeated measurement design. Our analysis incorporated a total of 162,060 observations from 99,329 participants. Each 10 μg/m3 increment of PM2.5 was associated with an increase of 0.22 % [95 % confidence interval (CI): 0.20 %, 0.25 %], 1.60 % (95 % CI: 1.53 %, 1.67 %), and 2.05 % (95 % CI: 1.96 %, 2.14 %) in TyG, TyG-WC, and METS-IR, respectively. These associations were attenuated among participants with a healthy diet, particularly those with sufficient intake of fruit and vegetable, fish or tea (pinteraction < 0.0028). For instance, among participants with a healthy diet, TyG increased by 0.11 % (95 % CI: 0.08 %, 0.15 %) per 10 μg/m3 PM2.5 increment, significantly lower than the association observed in those with an unhealthy diet. The findings of this study emphasize the potential of a healthy diet to mitigate these associations, highlighting the urgency for improving air quality and implementing dietary interventions among susceptible populations in China.

Objective: To analyze the clinical effect of percutaneous coronary intervention in the treatment of chronic coronary syndrome. Methods: 120 cases of chronic coronary syndrome patients who received inpatient treatment in a hospital from July 2023 to June 2024 were selected as the object, and were divided into the control group and the observation group using the mean score method, each with 60 cases, the control group was treated with conventional medications (aspirin, carbamazepine, β-receptor blockers, angiotensin-converting enzyme inhibitors, statin and other medications), and the observation group was treated with percutaneous The observation group implemented percutaneous coronary intervention based on this treatment, comparing the therapeutic effects of the two groups. Results: The treatment efficiency of the observation group (98.33%) was significantly higher than that of the control group (86.67%), and the difference was statistically significant (P < 0.05); before treatment, the IVPWTd and LVEDd indexes of the patients in the control group and the observation group were (10.39 ± 0.86) mm, (55.36 ± 5.67) mm and (10.41 ± 0.78) mm, (56.01 ± 6.80) mm, respectively. The difference was not statistically significant (P > 0.05); after 3 weeks of treatment, all the indexes of the two groups decreased significantly, respectively (9.76 ± 0.62) mm, (53.28 ± 5.63) mm and (8.56 ± 0.49) mm, (49.65 ± 5.47) mm, and the observation group was significantly lower than the control group, and the difference was statistically significant (P < 0.05). In the control group, 3 cases of arrhythmia and 2 cases of coronary artery spasm occurred during the treatment period, and 1 case each of residual cardiac insufficiency, acute thrombosis, chronic renal impairment, and cardiogenic death, with a total incidence rate of 15%, while in the observation group, only 1 case of arrhythmia and 1 case of coronary artery spasm occurred, with a total incidence rate of 3.33%, and the difference between the groups was statistically significant (P < 0.05). Conclusion: Percutaneous coronary intervention for the treatment of chronic coronary syndrome combined with renal disease is effective, can significantly improve the level of patients’ left ventricular function and reduces the risk of related complications, and is recommended to be popularized and applied in the clinic.

Along with the growing production and application of silica nanoparticles (SiNPs), increased human exposure and ensuing safety evaluation have progressively attracted concern. Accumulative data evidenced the hepatic injuries upon SiNPs inhalation. Still, the understanding of the hepatic outcomes resulting from SiNPs exposure, and underlying mechanisms are incompletely elucidated. Here, SiNPs of two sizes (60 nm and 300 nm) were applied to investigate their composition- and size-related impacts on livers of ApoE-/- mice via intratracheal instillation. Histopathological and biochemical analysis indicated SiNPs promoted inflammation, lipid deposition and fibrosis in the hepatic tissue, accompanied by increased ALT, AST, TC and TG. Oxidative stress was activated upon SiNPs stimuli, as evidenced by the increased hepatic ROS, MDA and declined GSH/GSSG. Of note, these alterations were more dramatic in SiNPs with a smaller size (SiNPs-60) but the same dosage. LC-MS/MS-based quantitative proteomics unveiled changes in mice liver protein profiles, and filtered out particle composition- or size-related molecules. Interestingly, altered lipid metabolism and oxidative damage served as two critical biological processes. In accordance with correlation analysis and liver disease-targeting prediction, a final of 10 differentially expressed proteins (DEPs) were selected as key potential targets attributable to composition- (4 molecules) and size-related (6 molecules) liver impairments upon SiNPs stimuli. Overall, our study provided strong laboratory evidence for a comprehensive understanding of the harmful biological effects of SiNPs, which was crucial for toxicological evaluation to ensure nanosafety.

Purpose: To investigate the impact of dapagliflozin treatment on blood glucose control, cardiac function, and myocardial injury markers in patients with type 2 diabetes and heart failure. Methods: In a retrospective analysis of clinical data for 132 patients with type 2 diabetes and heart failure admitted to Beijing Tongren Hospital, China from January 2020 to June 2021, these patients were stratified into two groups (66 patients each). Control group received conventional pharmacotherapy and study group received additional treatment with dapagliflozin. Both treatment courses lasted for 6 months. The levels of blood glucose control, cardiac function, and myocardial injury markers before and after 6 months of treatment were compared between the two groups, as well as safety during treatment. Results: After 6 months of treatment, both groups exhibited significant reductions in fasting plasma glucose (FPG), 2-h postprandial glucose (2 h PG), glycated hemoglobin (HbA1c), N-terminal pro-brain natriuretic peptide (NT-proBNP), cardiac troponin I (cTnI), creatine kinase-MB isoenzyme activity (CK-MB), aspartate aminotransferase (AST) levels, left ventricular end-diastolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD), and Minnesota Living with Heart Failure Questionnaire (MLHFQ) score, with study group showing a greater improvement (p < 0.05). Conclusion: Dapagliflozin enhances blood glucose control and cardiac function, improving quality of life in patients with type 2 diabetes and heart failure. Furthermore, Dapagliflozin demonstrates a safe and well-tolerated profile. Future studies will require establishing the mechanism of dapagliflozin action in a larger and more diverse population.

Background Amorphous silica nanoparticles (SiNPs) have been gradually proven to threaten cardiac health, but pathogenesis has not been fully elucidated. Ferroptosis is a newly defined form of programmed cell death that is implicated in myocardial diseases. Nevertheless, its role in the adverse cardiac effects of SiNPs has not been described.Results We first reported the induction of cardiomyocyte ferroptosis by SiNPs in both in vivo and in vitro. The sub-chronic exposure to SiNPs through intratracheal instillation aroused myocardial injury, characterized by significant inflammatory infiltration and collagen hyperplasia, accompanied by elevated CK-MB and cTnT activities in serum. Meanwhile, the activation of myocardial ferroptosis by SiNPs was certified by the extensive iron overload, declined FTH1 and FTL, and lipid peroxidation. The correlation analysis among detected indexes hinted ferroptosis was responsible for the SiNPs-aroused myocardial injury. Further, in vitro tests, SiNPs triggered iron overload and lipid peroxidation in cardiomyocytes. Concomitantly, altered expressions of TfR, DMT1, FTH1, and FTL indicated dysregulated iron metabolism of cardiomyocytes upon SiNP stimuli. Also, shrinking mitochondria with ridge fracture and ruptured outer membrane were noticed. To note, the ferroptosis inhibitor Ferrostatin-1 could effectively alleviate SiNPs-induced iron overload, lipid peroxidation, and myocardial cytotoxicity. More importantly, the mechanistic investigations revealed miR-125b-2-3p-targeted HO-1 as a key player in the induction of ferroptosis by SiNPs, probably through regulating the intracellular iron metabolism to mediate iron overload and ensuing lipid peroxidation.Conclusions Our findings firstly underscored the fact that ferroptosis mediated by miR-125b-2-3p/HO-1 signaling was a contributor to SiNPs-induced myocardial injury, which could be of importance to elucidate the toxicity and provide new insights into the future safety applications of SiNPs-related nano products.

Objective: To analyze the clinical effect of percutaneous coronary intervention in the treatment of chronic coronary syndrome combined with kidney disease. Methods: 150 patients with chronic coronary syndrome combined with renal disease admitted to a hospital from June 2023 to May 2024 were selected, and were divided into the control group and the observation group, 75 cases each, using the mean score method. The control group implemented conventional drug (clopidogrel, aspirin, statins) treatment, and the observation group implemented percutaneous coronary intervention on this basis, comparing the two groups’ treatment effects. Results: The mortality rate (9.33%) and the deterioration rate of renal function (5.33%) of patients in the observation group during the treatment period were significantly lower than those of the control group (21.33%) and (16.00%). The average hospitalization time of patients in the observation group was shorter than that of the control group (15.75 ± 4.24) days. The recurrence rate of angina pectoris of the patients of the observation group in the three months after discharge from the hospital was lower than that of the control group (25.33%) and that of the observation group was lower than that of the control group (6.67%), the difference was statistically significant (P < 0.05). Before treatment, there was no statistically significant difference in the levels of LVEDD, LVESD, and LVEF between the two groups (P > 0.05). After three months of treatment, the LVEDD (52.55 ± 4.02) mm and LVESD (41.44 ± 2.17) mm in the patients of the observation group were lower than those of the control group (57.37 ± 3.74) mm and (46.44 ± 2.59) mm; LVEF (50.78 ± 5.97)% of patients in the observation group was higher than that of (43.06 ± 5.92)% in the control group, and the difference was statistically significant (P < 0.05). Before treatment, there was no statistically significant difference in the levels of CK-MB and cTnI between the two groups (P > 0.05). At 24h and 72h after treatment, the levels of CK-MB and cTnI in patients of the observation group and the control group were (35.21 ± 9.81) U/L, (1.24 ± 0.34) μg/L, (13.19 ± 5.12) U/L, (0.36 ± 0.08) μg/L and (38.79 ± 10.84) U/L, (1.45 ± 0.32) μg/L, (19.87 ± 4.76) μg/L, (0.58 ± 0.11) μg/L, the difference was statistically significant (P < 0.05). Conclusion: Percutaneous coronary intervention is effective in treating chronic coronary syndrome combined with renal disease, which can significantly improve the level of a patient’s cardiac function and reduce the level of CK-MB and cTnI, and is worth being widely used in clinical practice.

Given the inevitable human exposure owing to its increasing production and utilization, the comprehensive safety evaluation of silica nanoparticles (SiNPs) has sparked concerns. Substantial evidence indicated liver damage by inhaled SiNPs. Notwithstanding, few reports focused on the persistence or reversibility of hepatic injuries, and the intricate molecular mechanisms involved remain limited. Here, rats are intratracheally instilled with SiNPs in two regimens (a 3-month exposure and a subsequent 6-week recovery after terminating SiNPs administration) to assess the hepatic effects. Nontargeted lipidomics revealed alterations in lipid metabolites as a contributor to the hepatic response and recovery effects of SiNPs. In line with the functional analysis of differential lipid metabolites, SiNPs activated oxidative stress, and induced lipid peroxidation and lipid deposition in the liver, as evidenced by the elevated hepatic levels of ROS, MDA, TC, and TG. Of note, these indicators showed great improvements after a 6-week recovery, even returning to the control levels. According to the correlation, ROC curve, and SEM analysis, 11 lipids identified as potential regulatory molecules for ameliorating liver injury by SiNPs. Collectively, the work first revealed the reversibility of SiNP-elicited hepatotoxicity from the perspective of lipidomics and offered valuable laboratory evidence and therapeutic strategy to facilitate nanosafety. SiNPs are frequently encountered in the environment, and the liver is vital to SiNPs accumulation and removal after introduction into the body. Here, subchronic exposure to SiNPs induces hepatic oxidative stress and lipid deposition. Nevertheless, these phenomena are greatly alleviated when rats are given a 6-week recovery. Lipidomics analysis reveals 11 lipids as potential mediators to ameliorate liver injury by SiNPs.image

Importance The genetic basis of coronary heart disease (CHD) has expanded from a germline to somatic genome, including clonal hematopoiesis of indeterminate potential (CHIP). How CHIP confers CHD risk in East Asian individuals, especially those with small clones (variant allele fraction [VAF] 0.5%-2%) and different genetic backgrounds, was completely unknown. Objective To investigate the CHIP profile in a general Chinese cohort by deep sequencing and further explore the association between CHIP and incident CHD considering germline predisposition. Design, Setting, and Participants This cohort study used data from 3 prospective cohorts in the project Prediction for Atherosclerotic Cardiovascular Disease Risk in China. Participants without cardiovascular disease or cancer at baseline were enrolled in 2001 and 2008 and had a median follow-up of 12.17 years extending into 2021. Exposures CHIP mutations were detected by targeted sequencing (mean depth, 916×). A predefined CHD polygenic risk score (PRS) comprising 531 variants was used to evaluate germline predisposition. Main Outcomes and Measures The main outcome was first incident CHD. Results Among 6181 participants, the median (IQR) age was 53.83 years (45.35-62.39 years); 3082 participants (49.9%) were female, and 3099 (50.1%) were male. A total of 1100 individuals (17.80%) harbored 1372 CHIP mutations at baseline. CHIP was independently associated with incident CHD (hazard ratio [HR], 1.42; 95% CI, 1.18-1.72; P = 2.82 × 10 −4 ) and presented a risk gradient with increasing VAF ( P = 3.98 × 10 −3 for trend). Notably, individuals with small clones, nearly half of CHIP carriers, also demonstrated a higher CHD risk compared with non-CHIP carriers (HR, 1.33; 95% CI, 1.02-1.74; P = .03) and were 4 years younger than those with VAF of 2% or greater (median age, 58.52 vs 62.70 years). Heightened CHD risk was not observed among CHIP carriers with low PRS (HR, 1.02; 95% CI, 0.64-1.64; P = .92), while high PRS and CHIP jointly contributed a 2.23-fold increase in risk (95% CI, 1.51-3.29; P = 6.29 × 10 −5 ) compared with non-CHIP carriers with low PRS. Interestingly, the diversity in CHIP-related CHD risk within each PRS group was substantially diminished when removing variants in the inflammatory pathway from the PRS. Conclusions This study revealed that elevated CHD risk attributed to CHIP was nonnegligible even for small clones. Inflammation genes involved in CHD could aggravate or abrogate CHIP-related CHD risk.

Epidemiological data indicate atmospheric particulate matter, especially fine particulate matter (PM2.5), has many negative effects on human health. Of note, people spend about 90% of their time indoors. More importantly, according to the World Health Organization (WHO) statistics, indoor air pollution causes nearly 1.6 million deaths each year, and it is considered as one of the major health risk factors. In order to obtain a deeper understanding of the harmful effects of indoor PM2.5 on human health, we used bibliometric software to summarize articles in this field. In conclusion, since 2000, the annual publication volume has increased year by year. America topped the list for the number of articles, and Professor Petros Koutrakis and Harvard University were the author and institution with the most published in this research area, respectively. Over the past decade, scholars gradually paid attention to molecular mechanisms, therefore, the toxicity can be better explored. Particularly, apart from timely intervention and treatment for adverse consequences, it is necessary to effectively reduce indoor PM2.5 through technologies. In addition, the trend and keywords analysis are favorable ways to find out future research hotspots. Hopefully, various countries and regions strengthen academic cooperation and integration of multi-disciplinary.

Objective: To analyze the effects of a general medicine management model in the treatment of chronic coronary syndrome. Methods: The study included 100 patients with chronic coronary syndrome admitted to the hospital between April 2022 and May 2023. Patients were divided into an observation group and a control group to compare the outcomes of the general medicine-based management model with those of the conventional management model. Results: The incidence of adverse cardiovascular events in the observation group was significantly lower than in the control group (P < 0.05). Anxiety and depression scores in the observation group were also significantly lower than those in the control group (P < 0.05). Quality-of-life scores and patient satisfaction in the observation group were significantly higher than those in the control group (P < 0.05). Conclusion: Implementing a general medicine-based management model for patients with chronic coronary syndrome effectively reduces the incidence of adverse cardiovascular events, significantly improves patients’ emotional well-being and quality of life, and has notable clinical significance for wider adoption.

Background: With rapid socioeconomic development and transition, associations between socioeconomic status (SES) and hypertension remained uncertain in China. We aimed to examine the health effects of SES on hypertension incidence and explore the sex differences among Chinese adults. Methods: We included 53 891 participants without hypertension from the China-PAR (Prediction for Atherosclerotic Cardiovascular Disease Risk in China) project. SES was evaluated by education level, occupation prestige, and household monthly per capita income, and categorized into low, medium, and high groups. Hazard ratios and their 95% CIs were calculated using Cox proportional hazards regression models. Results: Compared with high SES, participants with medium SES (hazard ratio, 1.142 [95% CI, 1.068–1.220]) or low SES (hazard ratio, 1.166 [95% CI, 1.096–1.241]) had increased risks of incident hypertension in multivariate analyses. Interactions between SES and sex on hypertension were observed, with more pronounced adverse effects of lower SES among women. The corresponding hazard ratios (95% CIs) for low SES group were 1.270 (1.155–1.397) for women and 1.086 (0.999–1.181) for men. Effects of occupation prestige on hypertension were the strongest among SES factors. Conclusions: Our study provided the compelling evidence from China that lower SES was associated with incident hypertension and women were more susceptible. These findings will have substantial implications on future hypertension prevention and management, especially among women. Sex-specific approaches are warranted to reduce socioeconomic disparities.

BackgroundThe effect of long-standing prediabetes or its transition on incident cardiovascular disease (CVD) is unclear. This study aimed to evaluate the association of changes in fasting blood glucose (FBG) status with the risk of developing CVD. MethodsThis research included 12 145 Chinese adults aged 35-74 years and free from diabetes mellitus (DM) at baseline. Study participants were cross-classified into six categories according to glucose at the first (1998-2001) and the second visit after 8 years: normal fasting glucose (NFG; 50-99 mg/dl), impaired FBG (IFG; 100-125 mg/dl), and DM. Cox proportional hazard regression model was used to estimate the hazard ratio (HR) and 95% confidence interval (CI) for CVD associated with transition of glucose status. ResultsDuring a median follow-up of 5.5 years, 373 incident CVD cases occurred. Compared with participants remaining persistent NFG, a higher risk of developing CVD was identified among those remaining persistent IFG, progressing to DM from NFG or from IFG, with the multivariate-adjusted HR (95% CI) of 1.792 (1.141, 2.816), 1.723 (1.122, 2.645) and 1.946 (1.120, 3.381), respectively. Furthermore, when stratified by glucose status at baseline, persistent IFG and progression from IFG to DM still increased CVD risk in comparison with reversion from IFG to NFG, with the multivariate-adjusted HR (95% CI) of 1.594 (1.003, 2.532) and 1.913 (1.080, 3.389). ConclusionsParticipants with long-standing IFG and progressing to DM had a higher risk of developing CVD. Further well-designed studies are warranted to assess the association of other phenotypes or prediabetes duration with CVD.