Background and Aim:Serum uric acid (SUA) has long been linked to elevated blood pressure (BP) in observational clinical studies. Nonetheless, data regarding the correlation between SUA and BP are controversial in randomized controlled trials and mendelian randomization research. Furthermore, it is yet unknown if there is a reciprocal relationship between SUA and BP. This study was conducted to explore the temporal relationship between SUA and BP and related risk factors. Methods:In this cohort study, 27,581 participants free of hypertension and cardiovascular disease from 2010 to 2016 in the Kailuan study were included. Cross-lagged studies with repeated evaluation of BP and SUA were applied to identify the temporal relationship between SUA and BP. The brachial-ankle pulse wave velocity (baPWV) and high-sensitivity C-reactive protein (hs-CRP) were conducted to evaluate the mediation impact on the correlation between SUA and BP among 6761 participants via mediation analysis. Results:The cross-lagged path coefficient of baseline SUA and follow-up systolic BP (β2) was 0.06 (95% CI, 0.03-0.08) in the participants with the age of ≤ 45 (n = 12,244), which was greater versus the coefficient of baseline systolic BP and follow-up SUA (β1) 0.04 (95% CI, 0.01-0.07; p < 0.001), in contrast to the participants with the age of > 45 (n = 15337). The positive correlation between SUA and BPs was mediated by baPWV. Conclusion:SUA may be a precursor to raised BP in young men, vascular stiffness mediated the positive correlation between BP and SUA. Trial Registration:ChiCTR-TNC-11001489.

Abstract BACKGROUND To investigate the association between cumulative cardiac metabolic index (cumCMI) exposure and cardiovascular disease (CVD) risk. METHODS The study was based on 87 967 participants of the Kailuan study who underwent at least two health examinations between 2006 and 2010. Time-weighted average cumCMI was calculated, and participants were categorized into four groups based on cumCMI quartiles: Q1 (cumCMI<0.327), Q2 (cumCMI 0.327–<0.483), Q3 (cumCMI 0.483–<0.755), and Q4 (cumCMI ≥ 0.755). Cox proportional hazard models were used to assess the relationship between cumCMI and the risk of CVD and its subtypes, with stratification by age and gender. Based on the Prediction for Atherosclerotic Cardiovascular Disease Risk in China (China-PAR) model, the values of cumCMI and other related indicators in predicting the risk of CVD were evaluated using C-statistic, integrated discrimination improvement, and net reclassification index. In the sensitivity analysis, the Cox proportional hazards analyses were repeated after excluding individuals who experienced endpoint events within 2 years of follow-up, and those who took antihypertensive, antidiabetic, and lipid-lowering medications at baseline, as well as replacing low-density lipoprotein cholesterol (LDL-C) with cumulative LDL-C (cumLDL-C) as a covariate. Fine-Gray competing risk models were used, with non-CVD mortality considered a competing event, to assess the potential risk of disease mortality from competing events. RESULTS During a mean follow-up of (10.41 ± 2.51) years, 6337 individuals experienced CVD events. With the increase of cumCMI quartile, the cumulative incidence of CVD increased (the cumulative incidence in the Q1 to Q4 group was 5.20%, 6.54%, 7.89%, and 9.18%, respectively, χ2 = 289.789, P<0.001). Multivariate Cox regression analysis showed that after adjusting for other confounding factors, compared with Q1 group, Q2, Q3, and Q4 groups exhibited 21% (HR = 1.21, 95% CI 1.12–1.30), 38% (HR = 1.38, 95% CI: 1.28–1.49), and 58% (HR = 1.58, 95% CI: 1.47–1.70) higher risks, respectively. Stratified analyses indicated a stronger association between elevated cumCMI and CVD risk in populations aged <60 years and females, with the Q4 group showing 91% (HR = 1.91, 95% CI: 1.69–2.16) and 64% (HR = 1.64, 95% CI: 1.33–2.03) higher risk relative to Q1 group, respectively. Sensitivity analysis yielded consistent results. Prediction analysis based on the China-PAR model indicated that cumCMI outperforms other single indicators in predicting CVD risk. CONCLUSIONS High cumCMI levels are significantly associated with the risk of cardiovascular disease and can effectively predict the risk of CVD.

BACKGROUND:The long-term association of central obesity with brain structural integrity remains poorly understood. This study aimed to investigate the longitudinal association between cumulative Weight-adjusted-waist Index (WWI) exposure and multi-modal neuroimaging markers of brain health. METHODS:This prospective community-based cohort study included 935 participants from the META-KLS Study. Cumulative WWI was calculated as the time-weighted average over 12 years prior to MRI acquisition. Neuroimaging outcomes included regional gray matter volume, white matter hyperintensity (WMH), and diffusion tensor imaging (DTI) metrics. Generalized linear models, restricted cubic splines, and mediation analyzes were performed. RESULTS:Elevated cumulative WWI was associated with adverse brain structural outcomes, particularly in females. In women, higher WWI was linked to extensive WMH burden (pFDR = 0.002), widespread microstructural disintegration (pFDR = 0.023), and specific atrophy in the orbital frontal cortex. A J-shaped dose-response relationship was identified for white matter injury, suggesting a tipping point for metabolic resilience. In exploratory mediation analyzes, FBG, SBP, and hs-CRP statistically accounted for 14.7%, 11.3%, and 11.3% of the association between cumulative WWI and WMH burden, respectively, while SBP accounted for 17.8% of the association with global MD. CONCLUSION:Cumulative WWI serves as a potential predictor of adverse brain structural outcomes, particularly manifesting as white matter injury and atrophy in women. Early monitoring of WWI offers a vital window for targeted metabolic interventions to preserve brain structural integrity.

OBJECTIVE:Accurate assessment of gradual age-related weight gain, a common phenomenon, is crucial for identifying brain health risks. This study investigated the associations between long-term trajectories in obesity indices and brain structure and cognition. METHODS:This study included 1114 participants from the Kailuan cohort with ≥ 3 follow-up visits during 2006-2018. The trajectories of body mass index (BMI), waist circumference (WC), and waist-to-hip ratio (WHR) were identified using group-based trajectory modelling. Cognition was assessed using the Montreal Cognitive Assessment. Associations of trajectories in obesity indices with neuroimaging metrics and cognition were examined using generalized linear models. Mediation analyses were performed to assess the associations between trajectories in obesity indices, neuroimaging metrics and cognition. RESULTS:Participants with high-stable WC trajectory were associated with lower grey matter volume (GMV) (β = -0.331; 95% CI: -0.522 to -0.139) and higher white-matter hyperintensity (WMH) (β = 0.423; 95% CI: 0.166 to 0.680). The high-stable BMI trajectory showed similar associations. The high-stable WC and WHR trajectories were associated with lower cognition (β = -0.909; 95% CI: -1.701 to -0.116; β = -0.543; 95% CI: -1.034 to -0.052). GMV atrophy and high WMH statistically partially explained the association between high-stable WC and WHR trajectories and cognitive decline. CONCLUSIONS:Persistent central obesity is associated with adverse brain structural changes, and WC and WHR trajectories are associated with cognitive decline. Preventing persistent central obesity may help preserve brain health and cognition.

To examine how distinct cardiovascular health (CVH) trajectories before age 50, estimated by Life’s Essential 8 (LE8), a composite measure comprising four behavioral and four biological components, relate to incident cardiovascular disease (CVD), all-cause mortality, and CVD-free survival in a Chinese population, from a predictive, preventive, and personalized medicine (PPPM) perspective. We included 39,305 CVD-free participants (77.3

Background:Research on biological age focused on the optimization and upgrading of aging clocks, which can now prospectively predict a variety of diseases. The biological age (BA) based on clinical parameters has shown predictive value for cardiovascular disease. However, evidence linking BA and its trajectories with heart failure (HF) remained limited. This study aimed to construct a clinical-parameter-based BA and to investigate its association, along with BA trajectories, with incident heart failure. Methods:This study utilized data from the Kailuan Study, which included 76,908 Chinese adults who underwent their first health examination between 2006 and 2007. A deep neural network model was employed to estimate BA based on 32 clinical indicators. Participants were stratified into three groups-decelerated aging, accelerated aging, and normal aging-according to their baseline BA values. Six distinct aging trajectories were subsequently identified using data from the first three follow-up examinations. Cox proportional hazard models were applied to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the associations between aging status or BA trajectories and HF incidence. Results:Participants exhibiting accelerated aging demonstrated a 30% higher risk of HF (HR: 1.30; 95%CI: 1.19-1.43) compared to those with normal aging. Conversely, those following a high-stable trajectory demonstrated the highest risk of HF (HR: 1.79; 95%CI: 1.48-2.17). Additionally, when compared to the high-stable trajectory, the high-descending trajectory was linked to a significantly lower risk of HF (HR: 0.74; 95%CI: 0.60-0.91). Conclusions:Accelerated biological aging significantly increased the risk of HF, whereas decelerated biological aging was linked to a reduced risk of HF. Individuals who consistently exhibited a higher level of biological aging were at the greatest risk for HF.

BACKGROUND:Arterial stiffness (AS), a key cardiovascular disease (CVD) risk factor, arises from structural stiffening due to arterial remodeling and load-dependent stiffening from elevated blood pressure (BP). However, their contributions to CVD risk and the mediating role of hypertension remain uncertain. We aimed to quantify the associations of AS components with incident CVD and assess hypertension's mediating effects. METHODS:Among 12,684 Kailuan cohort participants, AS (measured via brachial-ankle pulse wave velocity [baPWV]) and hypertension were assessed at baseline (2010-2014). The exposures were four AS components: measured, total, structural, and load-dependent stiffness. Total stiffness was derived from measured baPWV and concurrent BP. Structural stiffness was calculated by adjusting total stiffness to a reference BP (120/80 mmHg) using participant-specific models, with load-dependent stiffness defined as the residual. Cox models evaluated associations between AS components and incident CVD. Mediation analysis decomposed each component's total effect into direct and hypertension- mediated indirect effects. RESULTS:Over a median follow-up of 11.35 years, 803 CVD events occurred. Each 1-SD increase in AS components was associated with higher CVD risk, with adjusted hazard ratios (95% CIs) of 1.21 (1.14, 1.29) for measured, 1.20 (1.13, 1.28) for total, 1.17 (1.10, 1.25) for structural, and 1.20 (1.11, 1.30) for load-dependent stiffness. Hypertension mediated 48.7%, 50.6%, 24.0%, 75.9% of these associations for measured, total, structural, and load-dependent stiffness, respectively. CONCLUSIONS:Load-dependent stiffness appears to act mainly via hypertension, whereas structural stiffness may reflect BP-independent vascular damage. Thus, combining BP control with vascular protection strategies may help prevent CVD.

BACKGROUND:Limited evidence exists regarding the relationship between long-term exposure to low concentrations of low-density lipoprotein cholesterol (LDL-C) and brain structural integrity. This study aimed to examine the associations of cumulative low LDL-C exposure with a series of neuroimaging metrics. METHODS:This study included 987 participants (median age 55 years) from a population-based cohort study in China. Serum circulatory LDL-C concentrations were assessed biennially from 2006 to 2018. Prolonged LDL-C exposure was calculated using a time-weighted average (TWA) approach during that period. Brain MRI examinations were performed during 2020-2022. We used generalized linear model to investigate the multivariate-adjusted associations of TWA LDL-C levels with MRI markers of brain tissue volume, white matter microstructural integrity, and white matter hyperintensity (WMH). RESULTS:After full adjustments, TWA LDL-C concentrations of 70-100 mg/dL and less than 70 mg/dL were associated with lower fractional anisotropy value and higher mean diffusivity, axial diffusivity, and radial diffusivity value compared to LDL-C concentrations of 100-130 mg/dL. These associations were particularly prominent in male participants and older participants who were over 50 years. No association was found between relatively lower LDL-C levels and brain tissue volumes or WMH. CONCLUSION:LDL-C concentrations of 70-100 mg/dL and <70 mg/dL are associated with impaired microstructural integrity of brain white matter. TRIAL REGISTRATION:https://clinicaltrials.gov/ , NCT05453877.

BACKGROUND AND PURPOSE:Using the clinical obesity concept recently proposed by the Lancet Diabetes & Endocrinology Commission, this study evaluated the impact of clinical obesity on new-onset atrial fibrillation (AF) in the general population. METHODS:Individuals who underwent first health examinations from June 2006 to October 2007 in Kailuan were included. Based on body mass index (BMI), waist circumference (WC), waist-to-height ratio (WHtR), waist-to-hip ratio (WHR), and presence of obesity-related organ/tissue dysfunction, participants were divided into no obesity, preclinical obesity, and clinical obesity groups. RESULTS:A total of 98 730 participants free from AF at baseline were identified. Of these, 1343 developed new-onset AF over a median follow-up of 16.97 years. The AF incidence densities were 0.67, 0.68, and 1.25 per 1000 person-years in the no obesity, preclinical, and clinical obesity groups, respectively. Compared to the no obesity group, the clinical obesity (HR: 1.29, 95% CI: 1.12-1.47) group showed increased risks of new-onset AF. Clinical obesity remained associated with higher new-onset AF risk in participants aged < 45 years (HR: 2.34, 95% CI: 1.42-3.86) and 45- < 60 years (HR: 1.40, 95% CI: 1.14-1.71). In men, clinical obesity was associated with 35% higher risks of new-onset AF (HR: 1.34, 95% CI: 1.16-1.55). No significant association was observed between clinical obesity and new-onset AF in participants with a history of using anti-hypertensive agents (HR: 0.98, 95% CI: 0.73-1.30). CONCLUSIONS:Clinical obesity is an independent risk factor for new-onset AF, with age- and sex-specific associations, while metabolic-targeted therapies were associated with attenuated obesity-associated new-onset AF risk.

BACKGROUND:Exposure to metals has been found to be harmful to health. However, there is currently a lack of evidence on the effect of metals on cerebral small vessel disease (CSVD). METHODS:Based on the Multi-modality MEdical imaging sTudy bAsed on KaiLuan Study, we did a cross-sectional study with 1206 participants. CSVD burden was assessed via scores from four markers: lacunes, white matter hyperintensities, cerebral microbleeds, and enlarged perivascular spaces. We measured 17 plasma metals, used ordered/binary logistic models to test their associations with CSVD burden/presence, and Quantile g-computation model to estimate multi-metal combined effects. RESULTS:Plasma concentrations of Cadmium (Cd), Cesium (Cs), Copper (Cu), and Lead (Pb) were positively associated with total CSVD burden, whereas no metals were associated with the presence of CSVD. A significant mixture association of multiple metals with total CSVD burden was observed [OR (95 % CI)= 1.18 (1.04, 1.34)], with positive weights contributed by Cd (16.6 %), Cs (15.7 %), Pb (14.4 %), and Cu (13.8 %). CONCLUSIONS:Our study indicated that plasma metals, especially Cd, Cs, Cu, and Pb, are positively correlated with CSVD, providing epidemiological evidence to support the further exploration of metals' potential role as risk factors for CSVD.

This study aimed to investigate the association between the C-reactive protein-triglyceride glucose index (CTI) and risk of new-onset myocardial infarction (MI). We conducted a prospective cohort study among participants enrolled in the Kailuan Study in Tangshan City, Hebei Province, China, who underwent the physical examination between June 2006 and October 2007 (n = 101,510). After applying inclusion and exclusion criteria, 94,509 participants were included in the final analysis.The subjects were stratified into four groups according to baseline CTI quartiles: Q1 (CTI < 7.89), Q2 (7.89 ≤ CTI < 8.54), Q3 (8.54 ≤ CTI < 9.19), and Q4 (CTI ≥ 9.19). New-onset myocardial infarction was the main endpoint of the follow-up, which lasted until December 31, 2021.Hazard ratios (HR) and its 95% confidence interval (CI) were calculated using the multivariate-Cox proportional hazards regression model. The cumulative incidence function was constructed with the Kaplan-Meier method, and log-rank tests were performed to assess between-group differences. During a median follow-up of 15.01 (14.65, 15.20) years, 2,062 new-onset myocardial infarctions were documented. As CTI levels increased, the cumulative incidence rates of MI in the Q1 to Q4 groups were 0.86%, 1.60%, 2.12%, and 3.16%, respectively. After adjusting for relevant confounders, Cox proportional hazards regression analysis showed that compared with the Q1 group, the HR (95% CI) for new-onset myocardial infarction in the Q2 to Q4 groups was 1.42 (95% CI 1.21-1.67), 1.69 (95% CI 1.45-1.98), and 2.04 (95% CI 1.74-2.40), respectively. Each 1-unit increment in CTI was associated with a 29% increase in the risk of new-onset MI. Elevated CTI levels are independently associated with a higher risk of new-onset MI.

AIMS:To investigate sex-stratified associations between 4-year weight loss and risk of incident atrial fibrillation (AF) in a prospective cohort study and the potential benefits of sustained weight management. MATERIALS AND METHODS:We analysed 60 402 participants from the Kailuan Study free of AF, with body mass index (BMI) and waist circumference (WC) measured in 2006-2007 and 2010-2011. Reductions in BMI, body weight, and WC were used to define weight loss. Cox proportional hazards models assessed the association between weight loss and incident AF, adjusting for relevant covariates. RESULTS:During a median follow-up of 13.0 years (interquartile range: 12.5-13.3), 582 participants developed AF (484 men, 98 women). In men, BMI reduction >2.5 kg/m2 (hazard ratio [HR] 0.663, 95% confidence interval [CI] 0.467-0.940), body weight loss >5 kg (HR 0.662, 95% CI 0.468-0.936), and WC reduction >4 cm (HR 0.768, 95% CI 0.601-0.982) were associated with a lower risk of incident AF. In women, WC reduction >4 cm (HR 0.499, 95% CI 0.279-0.892) was associated with a lower risk. Similar patterns were observed among participants with overweight or obesity. Formal tests for sex interaction were not statistically significant. CONCLUSIONS:Reductions in BMI, body weight, and WC were associated with lower risk of incident AF, particularly in overweight or obese participants. The magnitude of association differed by anthropometric measure and sex, with BMI change showing stronger associations in men and WC change in women. Anthropometric changes may aid risk stratification and inform prevention efforts in higher-risk groups.

BACKGROUND:Patients with metabolic dysfunction-associated steatotic liver disease (MASLD) are at increased risk of both hepatic and extrahepatic adverse outcomes. However, the evidence regarding lean MASLD and its prognosis remains controversial. OBJECTIVE:To comprehensively investigate the long-term prognosis of lean patients with MASLD versus non-lean MASLD in Western and Asian populations. DESIGN:This prospective multicohort study included 153 192 patients with MASLD from UK Biobank (UKB), 29 700 from Kailuan cohort and 3329 from China Kadoorie Biobank (CKB). Lean MASLD was defined as body mass index (BMI)<23 kg/m² in Kailuan and CKB and <25 kg/m² in UKB. Primary endpoints were liver-related events (LREs), all-cause mortality, liver-related mortality (LRM), cardiovascular disease (CVD) mortality, CVD, hepatocellular carcinoma (HCC) and extrahepatic cancer. RESULTS:Overall, 181 191 non-lean and 5030 lean patients with MASLD were included. During a median of 14.2-year follow-up (median 14.1, 14.8 and 13.4 years in UKB, Kailuan and CKB), 2501 incident LREs, 22 482 all-cause deaths, 28 722 incident CVD cases, 326 HCC and 25 258 extrahepatic cancer cases were identified, with 375 LRM and 4511 CVD deaths. Pooled analysis of three cohorts showed lean MASLD had higher risks of LREs (HR=2.14; 95% CI 1.27 to 3.62), all-cause mortality (HR=1.26; 95% CI 1.14 to 1.39), LRM (HR=2.31; 95% CI 1.54 to 3.46) and CVD mortality (HR=1.22; 95% CI 1.05 to 1.41). By contrast, lean MASLD exhibited comparable HCC risk (HR=1.76; 95% CI 0.84 to 3.71) and extrahepatic cancer risk (HR=1.14; 95% CI 0.88 to 1.48), but reduced CVD risk (HR=0.89; 95% CI 0.83 to 0.95) versus non-lean MASLD. CONCLUSION:Lean patients with MASLD have worse liver outcomes and greater risk of all-cause mortality, but similar risk of HCC and extrahepatic cancer, and lower CVD risk.

OBJECTIVE:To evaluate cardiovascular benefits associated with sustained intensive and moderate interventions targeting body mass index (BMI), systolic blood pressure (SBP), fasting blood glucose (FBG) level, and total cholesterol (TC) concentration. METHODS:Using longitudinal data (from June 2006-October 2007 to December 2017) of 94,661 cardiovascular disease (CVD)-free participants aged 30 years and older from the Kailuan cohort, we emulated a target trial to assess the long-term effectiveness of intensive (BMI <25 kg/m2, SBP <120 mm Hg, FBG <5.6 mmol/L, TC <5.2 mmol/L) and moderate (BMI <30 kg/m2, SBP <140 mm Hg, FBG <7.0 mmol/L, TC <6.2 mmol/L) interventions on 10-year risk of incident CVD. The target trial emulation framework with the parametric g-formula was used to simulate counterfactual outcomes under dynamic interventions, accounting for time-varying confounders and competitive events. RESULTS:Compared with the natural course CVD risk of 6.48%, intensive interventions yielded a 49% decrease in relative risk (risk ratio, 0.51; 95% CI, 0.49 to 0.54), translating to approximately 3 fewer CVD cases per 100 individuals during 10 years (absolute risk reduction, -3.15%; 95% CI, -3.36% to -2.98%), which extended the restricted mean CVD-free time from 9.32 to 9.51 years. Of all the individual risk factors, SBP control yielded the largest benefits. Notably, even moderate interventions produced a 25% relative reduction in CVD risk, with the average proportion intervened on decreasing from 74.8% to 37.6%. Greater absolute risk reductions were observed in male participants and adults aged 60 years and older. CONCLUSION:Long-term interventions addressing cardiometabolic risk factors have considerable public health implications for primary prevention of CVD in China and other Western Pacific countries, where suboptimal cardiometabolic risk profiles remain prevalent.

BACKGROUND:Long-term blood pressure variability (BPV) is associated with cognitive decline, yet the underlying mechanisms have not been fully elucidated. PURPOSE:To investigate the associations between long-term BPV and hippocampal subfield volume and cognitive function and to assess the mediation effect of hippocampal subfield volume. STUDY TYPE:Prospective. POPULATION:One thousand three hundred sixty-six adults attended at least 3 surveys between 2006 and 2020 as part of the Kailuan Study. FIELD STRENGTH/SEQUENCE:3T; 3D T1-weighted sequence (T1WI). ASSESSMENT:Cognitive function was evaluated by Montreal Cognitive Assessment (MoCA) at the last (7th) survey visit and brain MRI acquired. The hippocampus was segmented into 12 subfields via FreeSurfer software: molecular layer, cornu ammonis (CA)1, CA2-3, CA4, subiculum, presubiculum, parasubiculum, hippocampal amygdalar transition area (HATA), dentate gyrus (DG), fimbria, hippocampal tail, and hippocampal fissure. BPV was defined as the standard deviation of manual blood pressure (BP) readings acquired at each survey visit. Associations between BPV, hippocampal subfield volume, and cognitive function were assessed. STATISTICAL TESTS:Associations were evaluated using generalized linear models. To explore whether hippocampal subfield volume mediated the association between BPV and cognitive function, mediation analysis was employed. RESULTS:Higher systolic BPV (SBPV) was significantly associated with lower volumes in CA1, CA2-3, molecular layer, and HATA (β = -8.99, -3.15, -7.18, and -1.27, respectively). Elevated diastolic BPV (DBPV) was significantly associated with lower molecular layer volume (β = -5.71). SBPV and DBPV were significantly negatively associated with MoCA scores (β = -0.24 and -0.20, respectively). Decreased volumes in the molecular layer, CA4, CA2-3, CA1, subiculum, DG, fimbria, and hippocampal tail were significantly associated with lower MoCA scores (β = -0.32, -0.29, -0.25, -0.28, -0.26, -0.31, -0.53, and -0.26, respectively). The association between SBPV and MoCA scores was mediated by molecular layer volume (proportion: 9.45%). DATA CONCLUSIONS:Elevated BPV was associated with hippocampal subfield atrophy and cognitive decline. The association between SBPV and cognitive decline appears to be mediated by molecular layer volume. EVIDENCE LEVEL:3. TECHNICAL EFFICACY:3.

BACKGROUND:Hypertension and diabetes mellitus are both known risk factors for atrial fibrillation (AF). Whether coexisting hypertension exacerbates AF risk among individuals with diabetes remains unclear. This study aims to investigate the association between hypertension and incident AF in this population. METHODS:We studied participants in the prospective Kailuan Study, including 18,084 adults diagnosed with diabetes between 2006 and 2011 and free of AF at baseline. Hypertension was defined by a previous diagnosis, use of antihypertensive medications, or systolic/diastolic blood pressure ≥140/90 mm Hg. Incident AF was identified via biennial electrocardiograms and hospital records. Cox proportional hazards models adjusted for demographic, lifestyle, metabolic, and clinical covariates were used to estimate hazard ratios (HRs). RESULTS:Over a median follow-up of 14.8 years (interquartile range 12.7-16.8), 275 participants with diabetes developed AF, and 5,265 died from any cause. Hypertension was associated with a higher risk of AF (adjusted HR, 1.48; 95% confidence interval [CI], 1.05-2.07) compared to those without hypertension. Compared to participants with normal blood pressure, the adjusted HRs for AF were 1.54 (95% CI, 1.11-2.13) for grade 1 hypertension and 1.61 (95% CI, 1.06-2.44) for grade 2 hypertension. Among those with hypertension, target organ damage-particularly prior myocardial infarction or ischemic stroke-further elevated AF risk (HR, 2.66; 95% CI, 1.26-5.60). CONCLUSIONS:Hypertension independently increases AF risk in individuals with diabetes, especially with higher blood pressure levels and target organ damage. Early hypertension control is crucial for the prevention of AF in this high-risk population.

OBJECTIVE:Individuals with both diabetes and hypertension face a heightened risk of all-cause death. We aimed to validate the DHAM score's performance in predicting 5-year overall mortality in two prospective cohorts. METHODS:The internal validation cohort comprised 3291 patients with diabetes and hypertension drawn from the 1999-2014 cycles of the National Health and Nutrition Examination Survey database. The external validation cohort comprised 2478 patients from the 2008-2015 China Kailuan cohort. The DHAM score was constructed from eight predictors (age, sex, education, marriage, smoking, cardiovascular disease, serum albumin, and urea nitrogen). Renal dysfunction was determined by an estimated glomerular filtration rate < 60 mL/min/1.73 m2 computed via the Chronic Kidney Disease Epidemiology Collaboration equation. RESULTS:The C-index was 0.758 (95% CI: 0.743-0.833) in the NHANES database and 0.741 (95% CI: 0.731-0.790) in the Kailuan cohort. A DHAM score > 148 independently predicted 5-year all-cause death in NHANES (adjusted-HR 10.03, 95% CI: 3.37-18.83, p < 0.001); after recalibration, a score > 152 independently predicted mortality in Kailuan (adjusted-HR 9.24, 95% CI: 4.71-16.84, p < 0.001). The patients were further stratified by DHAM score and renal function into three risk groups. Intermediate- and high-risk categories showed higher 5-year all-cause death rates than low-risk categories across both cohorts (log-rank p < 0.001). CONCLUSION:The DHAM score had a robust prognostic value for 5-year all-cause death among individuals with both diabetes and hypertension. Higher DHAM score combined with renal dysfunction could identify patients at highest risk of all-cause death. TRIAL REGISTRATION:Chinese Registry of Clinical Trials: ChiCTR2000029767.

Objective Evidence on the association of levels of serum uric acid (SUA) with muscle mass has been inconsistent and limited to that from studies with a cross-sectional design. This study investigated the longitudinal association of baseline and changes in SUA levels with low muscle mass and distinct trajectories of muscle mass. Methods Data were taken from the Kailuan study (an ongoing Chinese population-based cohort study), in which 87,284 and 66,129 participants respectively had records of baseline SUA levels and changes in SUA levels from baseline to the second follow-up visit. The primary outcome was incident low muscle mass, and the secondary outcome was muscle mass trajectory, which was identified by group-based trajectory modeling. Cox regressions and multinominal logistic regressions were performed to assess the aforementioned associations. Results During a median follow-up of 13.05 years, a total of 5916 (6.78%) cases of incident low muscle mass occurred, and three trajectories of muscle mass were identified. The risk of incident low muscle mass decreased by 28% (hazard ratio [HR] 0.72; 95% confidence interval [CI] 0.66–0.78) in the Q4 group of baseline SUA, 23% (HR 0.77; 95% CI 0.71–0.85) in the stable high SUA, and 22% (HR 0.78; 95% CI 0.70–0.87) in the Q4 group of changes in SUA, compared with their counterparts. Additionally, these participants were associated with 53%, 50%, and 57% higher risks of following a low-stable pattern of muscle mass, with relative risks (95% CI) of 0.47 (0.39–0.56), 0.50 (0.41–0.60), and 0.43 (0.37–0.50), respectively. Conclusions Higher SUA levels were longitudinally associated with a lower incidence of low muscle mass; however, causality cannot be inferred.

Background As a series of metabolic abnormalities, metabolic syndrome (MetS) is closely linked to lifestyle. When lifestyle changes occur, the status of MetS is also likely to alter. Given the high prevalence of MetS in China, a comprehensive understanding of how lifestyle and its changes affect the prognosis of MetS can aid in better prevention and treatment of MetS in order to reduce the disease burden. Methods Based on the Kailuan Study, 58,749 eligible individuals were included. The dynamic patterns were defined by the status of MetS in 2006 and 2010 as follows: MetS free, MetS developed, MetS stable, and MetS recovery. Drinking, smoking, physical activity, and salt intake were included to construct the healthy lifestyle score (HLS). And the difference of HLS between 2008 and 2006 was considered as the changes of lifestyle. Multivariate logistic regression was used to calculated the odds ratio (OR) and 95% confidence interval (CI) to analyze the impact of HLS and changes in HLS on the development and recovery of MetS. Results Among individuals without MetS at baseline, for per 1 increment in the HLS, the risk of developing MetS was reduced by 5% (OR = 0.95, 95% CI: 0.93, 0.97). Similarly, for per 1 increment in the HLS change, the risk of developing MetS was decreased by 8% (OR = 0.92, 95% CI: 0.90, 0.95). For those with MetS at baseline, the possibility of recovery from MetS was increased by 8% (OR = 1.08, 95% CI: 1.04, 1.12) with per 1 increment in the HLS. Furthermore, the likelihood of recovering from MetS was increased by 11% (OR = 1.11, 95% CI: 1.06, 1.15). Conclusion Adopting a healthy lifestyle or a shift from an unhealthy to a healthy lifestyle can reduce individuals’ risk of developing MetS and increase the likelihood of patients with MetS transitioning to a status free of MetS. These findings highlight the importance of healthy lifestyle in the prevention and treatment of MetS.