Hypertension is a major driver of atherosclerotic cardiovascular disease (ASCVD), many hypertensive patients harbor occult subclinical coronary atherosclerosis (SCA). The monocyte to high-density lipoprotein cholesterol ratio (MHR), a novel biomarker integrating inflammation and lipid metabolism, has emerged as a potential risk indicator. However, its value in identifying coronary artery characteristics in asymptomatic hypertensive populations remains unclear. We aimed to investigate the association between MHR and subclinical coronary atherosclerosis characteristics in asymptomatic hypertensive patients.

We conducted a cross-sectional study enrolling 283 hypertensive patients who underwent coronary computed tomography angiography (CCTA) at Shenzhen Traditional Chinese Medicine Hospital between January 2019 and September 2024. Patients were categorized into quartiles (Q1-Q4) based on MHR levels. CCTA was used to evaluate coronary artery calcium score (CACS) and plaque characteristics (non-calcified, calcified, mixed). Multivariable logistic regression, restricted cubic spline (RCS), and receiver operating characteristic (ROC) curve analyses were performed.

There was a significant difference in the prevalence of non-calcified plaques across MHR quartiles (P < 0.001). After fully adjusting for confounders including age, gender, smoking, BMI, TG, LDL-C, serum creatinine, statin use and diabetes, patients in the highest MHR quartile (Q4) had a 5.97-fold higher risk of having non-calcified plaques compared to those in Q1 (OR = 5.97, 95% CI: 2.63-14.1, P < 0.001; P for trend < 0.001). RCS analysis revealed a significant non-linear positive association between MHR and non-calcified plaque risk (P for nonlinearity = 0.007), characterized by an initial increase, a subsequent transient decline, and a marked rise at higher MHR values. The area under the ROC curve (AUC) for MHR in identifying non-calcified plaques was 0.700. Subgroup analyses revealed no significant interaction between MHR and age, sex, diabetes, smoking status, BMI category, or statin use (P for interaction > 0.05).

Elevated MHR is independently and non-linearly associated with the presence of non-calcified plaques in hypertensive patients. Given that non-calcified plaques represent an active, lipid-driven inflammatory state, MHR may serve as a simple and cost-effective adjunctive biomarker to help identify individuals with a higher burden of such plaques in asymptomatic hypertensive patients. However, its role in clinical risk stratification requires validation in prospective studies.

Medical students are exposed to chronic stress, unhealthy lifestyle habits, and emerging cardiometabolic risks, which are usually related to their nutritional status and quality of life (QoL). This study aimed to assess the relationship between overweight or obesity, elevated blood pressure, and QoL among medical students in Poland, and to identify its determinants over a 2-year longitudinal period.

A total of 887 first-year medical students from the Medical University of Silesia in Katowice were enrolled in the prospective POLLEK study, with 705 students followed up in their second year. Anthropometric measurements, blood pressure assessments, and QoL evaluation using the WHOQOL-BREF questionnaire were performed at both time points. Logistic regression and chi-square tests were applied to identify predictors of lower QoL and elevated blood pressure across BMI categories.

The prevalence of overweight or obesity increased slightly from 12.9% in the first year to 13.6% in the second year, and was statistically significant higher among male students. A small but statistically significant increase in BMI and blood pressure values was observed over the follow-up period. The highest rates of elevated blood pressure were found among obese students at both time points (p < 0.0001). Overall QoL scores did not differ significantly across BMI categories. Logistic regression identified poor financial situation (OR = 1.669-1.910) and a history of chronic disease (OR = 2.153-2.228) as independent predictors of lower QoL in both years of observation.

Overweight or obesity among medical students slightly increased over 2 years of follow-up and was associated with elevated blood pressure and unfavorable lifestyle patterns. The primary determinants of reduced QoL were financial hardship and chronic diseases rather than BMI itself. We believe that the early preventive interventions addressing weight disorders and health-promoting behaviors should be useful in the improvement of the situation.

Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are common intermediate hyperglycaemic states, yet most cohorts have compared diabetes with non-diabetes, or have relied on fasting glucose alone, so the stroke risk gradient across the full glucose tolerance spectrum and the relative prognostic value of fasting versus postload glycaemia remain unresolved. Evidence is particularly scarce for low-income rural Chinese populations, in whom vascular risk factors cluster while chronic-disease management and screening resources are limited. This study aimed to investigate the associations of glucose tolerance status with incident first-ever post-baseline stroke and all-cause mortality among low-income rural adults in China.

This population-based prospective cohort study included 2,087 adults from a low-income rural community in northern China who underwent a baseline examination including a 75-g oral glucose tolerance test (OGTT) in 2019. Among them, 2,057 participants with valid baseline examination dates were included in the time-to-event analyses, contributing 13,074.9 person-years for stroke and 13,477.4 person-years for mortality over a mean follow-up of 6.4 years. Baseline glucose tolerance status was classified as normal glucose tolerance (NGT), IFG, IGT, or diabetes according to the WHO/IDF criteria. Incident first-ever post-baseline stroke was defined as the first stroke event occurring after the 2019 baseline examination; participants with a stroke before baseline were excluded from this analysis, and all-cause mortality was recorded during follow-up. Incidence rates were calculated per 1,000 person-years and were additionally standardised for age and sex by the direct method. Cox proportional hazards regression models were used to estimate HRs and 95% CIs. The primary multivariable model (Model 2) was adjusted for sex, age group, smoking, drinking and eGFR; metabolic syndrome was added only in Model 3 and examined separately, because it shares glycaemic components with the exposure. In addition, fasting glucose and 2-h postload glucose were analysed as continuous variables in separate models, so that fasting and postload glycaemia could be compared without inducing collinearity. Proportional hazards were assessed using scaled Schoenfeld residuals, and multiple-imputation, Fine-Gray competing-risk and prespecified subgroup analyses were performed as sensitivity analyses.

During follow-up, 121 participants developed incident first-ever post-baseline stroke and 68 died from any cause, corresponding to overall incidence rates of 9.25 and 5.05 per 1,000 person-years, respectively. For incident stroke, the incidence rates were 7.55, 5.40, 12.74, and 14.06 per 1,000 person-years in the NGT (n = 1,324; 63.4%), IFG (n = 86; 4.1%), IGT (n = 449; 21.5%), and diabetes (n = 228; 10.9%) groups, respectively; for all-cause mortality the corresponding rates were 4.68, 1.77, 6.27 and 6.05 per 1,000 person-years. In crude analyses, both IGT (HR 1.69, 95% CI 1.11-2.55, *P* = 0.013) and diabetes (HR 1.85, 95% CI 1.12-3.06, *P* = 0.016) were associated with a higher risk of incident first-ever stroke compared with NGT. In the primary multivariable model (Model 2), both IGT (HR 1.58, 95% CI 1.03-2.41, *P* = 0.036) and diabetes (HR 1.69, 95% CI 1.02-2.81, *P* = 0.043) remained associated with incident stroke, whereas IFG did not (HR 0.78, 95% CI 0.25-2.51, *P* = 0.682). Adding metabolic syndrome (Model 3) attenuated both estimates and rendered diabetes non-significant (IGT: HR 1.55, 95% CI 1.01-2.39, *P* = 0.046; diabetes: HR 1.63, 95% CI 0.96-2.79, *P* = 0.071). No glucose tolerance subtype was significantly associated with all-cause mortality in any model. In continuous analyses modelled separately, both fasting glucose (HR 1.18 per 1 mmol/L, 95% CI 1.01-1.38, *P* = 0.035) and 2-h postload glucose (HR 1.07 per 1 mmol/L, 95% CI 1.02-1.13, *P* = 0.008) were associated with incident stroke; per standard deviation the postload association was the stronger of the two (HR 1.23, 95% CI 1.05-1.42 versus HR 1.17, 95% CI 1.01-1.35). Neither measure was associated with mortality.

Three conclusions follow. First, in this specific setting - a low-income rural Chinese community with clustered vascular risk factors and limited screening capacity - both IGT and diabetes were associated with an increased risk of incident first-ever stroke, whereas isolated IFG was not. Second, postload glycaemia carried more prognostic information for stroke than fasting glycaemia: the postload association was the stronger of the two per standard deviation, and only the postload phenotype (IGT) showed an excess risk in the categorical analysis, while the continuous fasting association appeared to be driven largely by participants in the diabetes range rather than by isolated fasting hyperglycaemia. Third, for grassroots public-health practice these findings identify IGT as a candidate phenotype for earlier vascular risk assessment; whether adding postload measurement to existing screening improves outcomes remains to be tested directly.

Cardiovascular disease (CVD) remains the leading cause of death worldwide, particularly among older adults. The glycated hemoglobin A1c-to-high-density lipoprotein cholesterol (HbA1c/HDL-C) ratio is an emerging biomarker reflecting glucolipid metabolic derangement. However, prospective evidence regarding its association with incident CVD among community-dwelling older adults in southwestern China remains limited.

This study aimed to investigate the association between the HbA1c/HDL-C ratio and incident CVD, characterize its dose-response relationship, and evaluate its incremental predictive value beyond conventional cardiovascular risk factors in an older adult population.

This prospective cohort study included 1,875 community-dwelling adults aged ≥60 years without baseline CVD from the Early Screening and Intervention Program for High-Risk Populations of Cardiovascular and Cerebrovascular Disease Risk Factors in Wanzhou District. Participants were followed during 2024. The HbA1c/HDL-C ratio was calculated from baseline measurements and analyzed both continuously and as quartiles. Incident CVD events were ascertained using a dual-source validation approach that combined standardized questionnaire data with linkage to the regional surveillance system. Multivariable Cox proportional hazards models, restricted cubic spline (RCS), time-dependent area under the receiver operating characteristic curve (AUC), C-statistic and decision curve analysis (DCA) were fitted to estimate the association between HbA1c/HDL-C and CVD risk. Subgroup, sensitivity analyses were performed to verify robustness.

During a median follow-up of 5.08 years, 207 participants developed incident CVD, with a cumulative incidence of 11.04%. After fully adjusting for confounding factors, participants in the highest quartile (Q4) of the HbA1c/HDL-C ratio exhibited a significantly elevated risk of incident CVD compared with the lowest quartile (Q1) (HR = 2.111, 95%CI: 1.276-3.170, P = 0.003), whereas the linear trend across quartiles did not reach statistical significance (P _{for trend} = 0.068). RCS analysis revealed a nonlinear dose-response relationship (P _{for overall} < 0.001, P _{for nonlinear} = 0.017), with a data-driven inflection point at an HbA1c/HDL-C ratio of 4.83 (95%CI: 3.55-6.06). Below this threshold, each unit increment was associated with a 44.10% increase in CVD risk (HR = 1.441, 95%CI: 1.138-1.825, P = 0.002). Incorporation of the HbA1c/HDL-C ratio into a conventional risk factor model enhanced the time-dependent AUC (test-set C-statistic: 0.795 vs. 0.777). DCA demonstrated enhanced net benefit, particularly during mid-to-long-term follow-up. Subgroup and sensitivity analyses verified the robustness.

After multivariable Cox regression adjustment, participants in the highest quartile (Q4) of the HbA1c/HDL-C ratio showed a significant association with incident CVD, while the linear trend across Q1 to Q4 was borderline significant. RCS analysis further identified a nonlinear dose-response relationship between HbA1c/HDL-C ratio and incident CVD. Given its accessibility, low cost, and ease of calculation, the HbA1c/HDL-C ratio may serve as a complementary indicator for community-based CVD risk stratification, particularly in resource-constrained primary care settings. The apparently stronger association observed should be considered exploratory and requires confirmation in larger prospective cohort studies.

Systemic inflammation after acute ischemic stroke is usually assessed using admission biomarkers, which may not distinguish transient stress from sustained immune-inflammatory activation. We examined whether serial immune-inflammatory recovery trajectories were associated with early neurological deterioration (END) and 90-day functional outcome.

This single-center retrospective cohort included 760 adults with acute ischemic stroke identified from a hospital stroke database. NLR, SII, SIRI, and hs-CRP measured at admission, 24 h, 72 h, and day 7 were log-transformed and standardized, and equally weighted values were averaged at each observed time point. Latent class mixed models with 2-5 classes were compared without using outcome information, and a five-class solution was selected before association and prediction analyses. The primary outcome was 90-day mRS 3-6. END was defined as an NIHSS increase of ≥2 points within 72 h; the landmark END analysis excluded END within 24 h and tested 0-24 h immune change for END from 24 to 72 h.

The five LCMM classes comprised 182 low-stable, 223 transient moderate, 161 delayed recovery, 122 persistent high, and 72 extreme persistent high patients. Among 751 patients with 90-day outcome data, the observed rate of mRS 3-6 increased from 21.5 to 30.6%, 44.2, 71.9, and 98.6% across these classes. After adjustment, persistent high (OR 2.46, 95% CI 1.31-4.61; p = 0.005) and extreme persistent high inflammation (OR 20.24, 95% CI 2.48-165.26; p = 0.005) were associated with mRS 3-6; a bias-reduced sensitivity estimate for the extreme class remained large (OR 13.61, 95% CI 2.34-79.26). Ordinal analysis showed progressively worse mRS for delayed recovery (common OR 2.73), persistent high (4.18), and extreme persistent high (6.72). The 0-24 h composite immune-change metric was not associated with landmark END (OR 1.12, 95% CI 0.92-1.36; p = 0.265). Adding LCMM-5 to the clinical model increased AUC from 0.828 to 0.841, but did not clearly outperform adding admission NLR/SII.

Longitudinal classification identified five immune-inflammatory recovery trajectories with a marked gradient in 90-day disability. Persistent-high and extreme persistent-high classes retained independent associations with poor functional outcome.

To explore the correlation of serum brain-derived neurotrophic factor (BDNF), matrix metalloproteinase-9 (MMP-9), and glutamate (Glu) changes with functional recovery after repetitive transcranial magnetic stimulation (rTMS) in acute ischemic stroke (AIS) patients, so as to provide biological evidence for rTMS efficacy evaluation.

A retrospective study was conducted on 149 patients with AIS, who were assigned to a control group (n = 89, conventional comprehensive treatment) or an rTMS group (n = 60, combined rTMS intervention) based on their actual treatment, both for 4 weeks. The two groups were comparable at baseline in age (60.90 ± 2.92 vs. 61.28 ± 3.26 years), gender distribution (54 males vs. 40 males), and admission NIHSS scores [median (IQR): 10.0 (9.0-12.0) vs. 11.0 (9.0-12.0)] (all P > 0.05). In the rTMS group, rTMS was initiated within 72 h after stroke onset; the control group did not receive rTMS intervention. Serum levels of BDNF, MMP-9, and Glu were measured before and after treatment in both groups. Neurological and motor functions were assessed using the National Institutes of Health Stroke Scale (NIHSS) and the Fugl-Meyer Assessment (FMA). Pearson correlation was used to analyze the relationships between biomarker changes and functional improvements in the rTMS group, and adverse events were compared between groups.

After 4 weeks, the rTMS group showed significantly greater increase in BDNF and decreases in MMP-9 and Glu than controls (P < 0.05), along with lower NIHSS and higher FMA scores (P < 0.05). Changes in all three biomarkers significantly correlated with NIHSS reduction and FMA improvement (P < 0.001). Adverse events were similar between groups (P > 0.05).

: rTMS combined with conventional therapy may be associated with greater improvement in neurological and motor function in AIS, potentially via regulating BDNF, MMP-9, and Glu. These biomarkers may serve as candidate indicators for treatment response. However, given the observational nature of this study, these findings should be interpreted with caution and require confirmation in future randomized controlled trials.

Ruptured basilar artery dissecting aneurysms (BADAs) are rare and associated with high risks of rebleeding, brainstem ischemia, and death. Evidence specific to the basilar artery remains limited, and experience derived from vertebral artery dissections may not be directly transferable because the basilar trunk supplies numerous critical pontine perforators and generally cannot be sacrificed.

To describe the real-world management of a consecutive cohort of ruptured BADA and compare long-term clinical outcomes after primary flow diverter (FD)-based versus conventional endovascular treatment.

This retrospective single-center cohort study included consecutive patients with angiographically confirmed ruptured BADA who underwent endovascular treatment between February 2015 and April 2024. Patients were classified according to the index endovascular treatment as the FD group or the conventional endovascular treatment group. The primary outcome was favorable functional outcome (mRS 0-2) at the last follow-up. Secondary outcomes included mortality, retreatment, complications, and descriptive radiological outcomes.

Twenty-two patients were included: 5 received FD-based treatment as the index strategy and 17 received conventional endovascular treatment. Fusiform morphology was more frequent in the FD group (80.0% vs. 23.5%, p = 0.039), while aneurysm maximum diameter was numerically larger (median 19.0 vs. 6.0 mm, p = 0.078). At the last follow-up, 4 of 5 patients (80.0%) in the FD group and 9 of 17 patients (52.9%) in the conventional group had a favorable outcome (p = 0.360). Mortality was 20.0 and 47.1%, respectively (p = 0.360).

Primary FD-based reconstruction was feasible in selected ruptured BADA, particularly in anatomically complex or fusiform lesions. Given the small sample, non-randomized treatment selection, and absence of statistically significant between-group differences, these findings support individualized treatment and do not establish superiority of either strategy.

The factors governing the presence and severity of orthostatic hypotension (OH) in multiple system atrophy (MSA) may differ. We investigated factors independently associated with OH and severe OH in MSA, and assessed the consistency of these associations across subtypes.

We examined the clinical data of 242 MSA patients who had blood pressure evaluations to assess OH. We analyzed the clinical data of MSA patients with and without OH, as well as those with mild and severe OH, focusing on clinical characteristics and brain MRI features to identify factors associated with OH presence and severe OH.

OH was present in 136 patients (56.2%). MSA-C subtype (OR = 2.42, 95% CI = 1.33-4.43, p = 0.004), probable MSA (OR = 2.68, 95% CI = 1.49-4.80, p = 0.001), and higher UMSARS-I scores (OR = 1.10, 95% CI = 1.03-1.17, p = 0.005) were independently associated with the presence of OH. Among OH-positive patients, male (OR = 2.57, 95% CI = 1.21-5.44, p = 0.014) and higher NMSS scores (OR = 1.06, 95% CI = 1.02-1.11, p = 0.009) were independently associated with severe OH, whereas MSA subtype was not. Subgroup analyses showed directionally consistent associations for male sex and NMSS across MSA-C and MSA-P subgroups. The association between NMSS and severe OH was statistically significant in the MSA-C subgroup (OR = 1.09, 95% CI = 1.03-1.15, p = 0.004), whereas the remaining subgroup estimates did not reach statistical significance. No neuroimaging marker was associated with OH.

Factors associated with OH presence differed from those associated with severe OH in MSA. MSA-C subtype, diagnostic certainty, and UMSARS-I score were associated with OH presence, whereas male sex and NMSS burden were associated with severe OH.

Early risk stratification is critical for critically ill patients with ischemic stroke. The prognostic value of the lactate-to-albumin ratio (LAR) remains unclear in this population.

This single-center retrospective cohort study enrolled adult ICU patients with ischemic stroke from West China Hospital. LAR was calculated using the first lactate and albumin values on ICU admission. Log-transformed LAR was adopted as the main exposure, and the primary outcome was in-hospital mortality. Multivariable logistic regression, ROC analysis, quartile stratification, subgroup, and sensitivity analyses were performed among 749 patients with complete exposure and outcome data, of whom 576 had complete covariate data and comprised the primary multivariable regression cohort.

A total of 749 patients were included, with an in-hospital mortality rate of 30.7%. In complete-case multivariable analysis (N = 576; deaths = 172), log-transformed LAR was independently associated with in-hospital mortality (OR = 1.44, 95%CI: 1.09-1.91, p = 0.010) after full adjustment. Each two-fold increase in LAR was associated with a 29% increase in mortality odds. The highest LAR quartile had a significantly higher mortality risk than the lowest quartile (OR = 2.16, 95%CI: 1.21-3.92). LAR showed modest predictive ability (AUC = 0.628). When modeled as a raw continuous LAR, the direction of association remained consistent but did not reach conventional statistical significance (OR 1.23; 95% CI 0.97-1.56; p = 0.083). Moreover, no significant interaction or non-linearity was found.

Elevated LAR is independently linked to higher in-hospital mortality among critically ill ischemic stroke patients. It may serve as a simple adjunctive marker for early risk stratification.

Ageing biomarkers quantify molecular, physiological or functional features that vary between individuals as they age and may improve prediction of health outcomes beyond chronological age. Recently, plasma proteomics have been used to estimate the biological ages of 11 human organs. Although accelerated organ ageing is associated with higher mortality risk, systematic benchmarking against established ageing biomarkers is lacking. Here, we pursued two complementary aims. First, we benchmarked proteomic organ clocks against multimodal ageing biomarkers for associations with 16-year all-cause mortality in the Lothian Birth Cohort 1936 (LBC1936) using Cox regression (861 participants; 444 deaths). Biomarkers included the epigenetic clock GrimAge2, telomere length, physical function (grip strength, walk time and respiratory function), neuroimaging and cognitive measures. Among proteomic clocks, accelerated liver (HR_perSD [95% CI] = 1.43 [1.30-1.58]), immune (1.42 [1.29-1.57]) and heart (1.38 [1.25-1.53]) ageing were most strongly associated with increased mortality risk. However, older epigenetic age, smaller total brain and grey matter volumes, reduced respiratory function and poorer cognition showed stronger associations with mortality (HR_perSD = 1.44-1.62). Second, survival analyses of 9703 plasma protein targets identified 368 candidates associated with mortality, with high-risk proteins enriched for immune functions, and low-risk proteins involved in genomic stability and cellular maintenance. GDF15 (HR_perSD [95% CI] = 1.56 [1.42-1.72]), WFDC2 (1.47 [1.33-1.62]) and TIMP1 (1.45 [1.29-1.62]) were the leading proteomic candidates associated with mortality. This study provides a systematic, cross-modal benchmarking of proteomic organ clocks against established ageing biomarkers and identifies proteins and biological functions associated with mortality risk.