BACKGROUND:Depression is common in the general population and may occur more frequently in individuals with rheumatoid arthritis (RA). This study examined the association between RA and depressive symptoms in a population-based cohort from Salzburg, Austria. METHODS:Data were obtained from the Paracelsus 10,000 cohort, comprising 9401 participants. RA was determined according to the EULAR/ACR classification criteria and verified through structured baseline interviews and medical documentation. Depressive symptoms were assessed using the Beck Depression Inventory-II (BDI-II). Depression was defined as a BDI-II score >13, according to national guidelines. Logistic regression analyses were used to estimate the association between RA and depression, and linear regression analyses assessed differences in continuous BDI-II scores. Models were adjusted sequentially for demographics, socioeconomic, and clinical covariates. RESULTS:Among 293 participants with RA and 9108 without RA, elevated depressive symptoms were present in 20% and 9%, respectively. RA was associated with higher odds of elevated depressive symptoms in unadjusted analyses (OR 2.48, 95% CI 1.84-3.35; p < 0.001), after adjustment for age and sex (OR 2.39, 95% CI 1.76-3.23; p < 0.001), and in fully adjusted models (OR 2.10, 95% CI 1.52-2.89; p < 0.001). Median BDI-II scores were higher in participants with RA compared to those without RA (6 [IQR 2-11] vs. 3 [IQR 0-7]; p < 0.001). In linear regression analyses, RA was associated with a mean increase of 3.40 BDI-II points (95% CI 2.65-4.14; p < 0.001), exceeding the minimal clinically important difference. CONCLUSION:In this population-based cohort, RA was statistically associated with higher depressive symptoms after adjustment for demographic, socioeconomic and clinical covariates. Given the cross-sectional design, causal inferences cannot be drawn. These findings support routine depression screening and integrated care for patients with RA. Moreover, the bidirectional link between rheumatic and psychiatric conditions highlights that psychiatrists should consider underlying rheumatic disease in patients presenting with depression, fatigue or unexplained pain.

Background and Aim Steatotic liver disease (SLD) affects over 30% of adults and is classified into metabolic dysfunction-associated (MASLD), alcohol-related (ALD), and metabolic dysfunction and alcohol-associated (MetALD) subtypes. Cardiovascular disease is the leading cause of death in SLD, yet the differential atherosclerotic risk across subtypes remains uncertain. Methods and Results We conducted a cross-sectional analysis of 7,820 participants from the population-based Paracelsus 10,000 cohort. SLD was defined by the Fatty Liver Index according to international consensus criteria. Atherosclerosis was assessed by carotid ultrasonography (n=7,820), coronary artery calcium (CAC) scoring by computed tomography (n=1,434), and polygenic risk scores (PGS, n=1,652). Primary outcomes were carotid plaque presence and CAC burden (Agatston score). Multivariable logistic regression adjusted for age, sex, and SCORE2 cardiovascular risk. We identified 5,448 controls (69.7%), 2,098 MASLD (26.8%), 201 ALD (2.6%), and 73 MetALD (0.9%). Carotid plaque prevalence increased stepwise: 30% in controls, 47% in MASLD, 53% in MetALD, and 62% in ALD (p<0.001). High-risk CAC (Agatston >300) was present in 4% of controls, 7% of MASLD, and 18% of both MetALD and ALD (p<0.001). Unadjusted odds ratios for plaque were 2.10 (95% CI, 1.89-2.33) for MASLD, 2.69 (1.69-4.28) for MetALD, and 3.86 (2.89-5.16) for ALD. After SCORE2 adjustment, associations attenuated and lost statistical significance. CAD-PGS differed modestly across subtypes (p=0.019) and inclusion further attenuated associations. Conclusions All SLD subtypes were associated with increased atherosclerotic burden, with ALD showing the highest risk. Associations were attenuated after adjustment for established cardiovascular risk factors, indicating shared cardiometabolic rather than liver-specific pathways.

Objective Patients with inflammatory bowel disease (IBD) have an increased risk of cardiovascular and cerebrovascular events, but the underlying mechanisms remain unclear. We aimed to assess subclinical carotid atherosclerosis in IBD in a large population-based cohort. Methods We performed a cross-sectional analysis of the Paracelsus 10 000 cohort in Salzburg, Austria. Adults aged 40–77 years underwent standardised clinical evaluation, laboratory testing and bilateral carotid ultrasonography. The primary endpoint was carotid plaque burden; secondary endpoints included plaque presence, intima–media thickness, carotid stenosis, coronary artery calcium and polygenic risk scores. Multivariable ordered logistic regression models were adjusted for age, sex and comprehensive cardiovascular risk measures including Systematic Coronary Risk Evaluation 2 and Life’s Essential 8. Results Among 9723 participants, 70 had IBD and 9653 served as controls. Patients with IBD had higher levels of high-sensitivity C reactive protein (median 0.15 vs 0.12 mg/dL; p=0.039) and lower ferritin levels (86 vs 117 ng/mL; p=0.018). Carotid plaque prevalence (40% vs 38%; p=0.79) and plaque burden distribution (p=0.82) were similar between groups. Intima–media thickness, carotid stenosis, coronary artery calcium score categories and polygenic risk scores were also comparable. In multivariable analysis, IBD was not associated with higher plaque burden (adjusted OR 1.49; 95% CI 0.88 to 2.55; p=0.139). Conclusions In this population-based cohort, IBD was not associated with increased subclinical carotid atherosclerosis. These findings suggest that cardiovascular risk in IBD may not be fully explained by atherosclerotic burden alone and may involve inflammation-related and prothrombotic mechanisms beyond atherosclerosis.

Serum uric acid has been consistently associated with cardiovascular risk, yet whether this relationship reflects independent vascular pathology or cardiometabolic risk clustering remains unresolved. We examined associations of serum uric acid and hyperuricemia with imaging-defined subclinical coronary and carotid atherosclerosis in a large population-based cohort. We analyzed data from the Paracelsus 10,000 study, a population-based cohort of adults aged 40–77 years recruited from the Austrian national population registry. Coronary artery calcium (CAC) was assessed by computed tomography in 1561 participants with available cardiac computed tomography and polygenic risk score data; carotid plaque burden was assessed by ultrasonography in 8970 participants. Associations were evaluated using ordinal logistic regression — with CAC categorized by Agatston score (0, 1–99, 100–299, ≥ 300) and carotid plaque burden categorized by total plaque area — with sequential adjustment for cardiovascular risk score (SCORE2), metabolic syndrome, polygenic cardiovascular risk, lipoprotein(a) and systemic inflammation. Higher serum uric acid levels were strongly associated with greater CAC burden in unadjusted analyses (OR 1.60 per 1 mg/dL, 95

Objectives: EuroSCORE II is widely used to predict perioperative and 30-day mortality in cardiac surgery, yet data on its ability to predict long-term outcomes remain limited. This study investigates whether EuroSCORE II is associated with one-year and long-term mortality in a heterogeneous population undergoing major cardiac surgery with cardiopulmonary bypass. Methods: A retrospective cohort study was conducted including 2179 patients who underwent elective or urgent cardiac surgery with cardiopulmonary bypass between 2017 and 2021 at the University Hospital Salzburg. Data were extracted from the Salzburg Intensive Care database (SICdb) and supplemented with mortality information from Statistik Austria. EuroSCORE II values were compared between survivors and non-survivors. Kaplan-Meier analyses, Cox regression and logistic regression with ROC analysis were performed to evaluate the predictive association of EuroSCORE II with mortality. Results: EuroSCORE II was significantly higher in patients who died within one year and in those who died during a mean follow-up period of 1152.67 ± 521.39 days. Patients who survived at least one year had a median EuroSCORE II of 2.2, whereas those who died within one year had a median of 7.0. Cox regression demonstrated a hazard ratio of 1.062 for one-year mortality and 1.058 for long-term mortality. Kaplan-Meier curves showed significantly reduced survival with increasing EuroSCORE II quartiles. Logistic regression for one-year mortality yielded an AUC of 0.773, indicating good discriminative ability. Conclusions: EuroSCORE II is significantly associated with long-term mortality after major cardiac surgery, demonstrating good discriminatory performance. These findings support its potential utility not only as a short-term but also as a long-term prognostic indicator in cardiac surgery populations.

The red cell distribution width (RDW) measures erythrocyte size variability and is linked to increased mortality in various diseases, including cardiovascular, kidney, and liver conditions. In critically ill patients, particularly those with sepsis, RDW is a prognostic marker. While its role in cardiac surgery patients is well established, its value in surgical patients is less well explored. This study investigates whether a single postoperative RDW measurement predicts short- and long-term mortality surgical intensive care unit (ICU) patients. This retrospective cohort study analyzed data from 2312 surgery patients admitted to a surgical ICU over 2 years. The RDW was measured within 2 h of surgery and analyzed as a continuous and binary variable (threshold 15). Mortality at 30 days and 1 year was assessed using univariable and multivariable logistic regression and Cox regression models, adjusting for factors like the simplified acute physiology score 3 (SAPS3), lactate levels, age, sex, and comorbidities. Interaction analyses evaluated the impact of cofactor on RDW’s mortality prediction. Of 2312 patients, 1687 (73.0

Background:Older adults represent an increasing proportion of intensive care unit admissions, but the relationship between country-level human development and outcomes after critical illness remains incompletely understood. Methods:We conducted a secondary analysis of three prospective multicentre registries, VIP1, VIP2, and COVIP, including acutely admitted older ICU patients with available Clinical Frailty Scale assessment, country-level Human Development Index (HDI), and 30-day vital status. VIP1 and VIP2 enrolled patients aged ≥80 years, whereas COVIP enrolled patients aged ≥70 years. The primary exposure was exceptionally high human development, defined as HDI ≥ 0.90 versus <0.90. The primary outcome was 30-day mortality. Associations were assessed using logistic regression with robust standard errors clustered by country, adjusting for age, sex, SOFA score, frailty, admission diagnosis, organ support modalities, and treatment-limitation decisions. Exploratory mediation analyses examined selected ICU management variables as potential pathways linking HDI to mortality. Results:Among 9920 patients included in the primary analysis, 8324 (83.9%) were treated in countries with HDI ≥ 0.90 and 1596 (16.1%) in countries with HDI < 0.90. Thirty-day mortality was lower in high-HDI countries than in lower-HDI countries (40.0% vs. 53.3%). In unadjusted analysis, HDI ≥ 0.90 was associated with lower 30-day mortality (OR 0.58; 95% CI 0.38-0.90; P = 0.016). This association persisted after multivariable adjustment (adjusted OR 0.49; 95% CI 0.31-0.80; P = 0.004) and was similar after additional adjustment for study cohort (aOR 0.49; 95% CI 0.31-0.77; P = 0.002) and ICU bed capacity (aOR 0.50; 95% CI 0.29-0.86; P = 0.013). When modelled continuously, higher HDI was associated with lower mortality after full adjustment (OR 0.33 per 0.10-unit increase; 95% CI 0.19-0.56; P < 0.001). Exploratory mediation analyses suggested that lower use of invasive mechanical ventilation in high-HDI countries may partially contribute to the observed association (NIE OR 0.86; 95% CI 0.83-0.89). Mediation analyses involving treatment-limitation decisions were more difficult to interpret because these decisions are closely linked to prognosis, clinical trajectory, and end-of-life practice. Conclusions:In this large European cohort of older critically ill patients, treatment in countries with exceptionally high human development was associated with lower 30-day mortality. The association persisted after adjustment for patient-level severity, frailty, treatment limitation, organ support, study cohort, and ICU bed capacity. These findings suggest that country-level development and ICU management patterns, particularly invasive ventilation practices, may contribute to outcome differences. Because this was an observational secondary analysis using country-level exposure data, causal interpretation should remain cautious.

Background:Barrett's esophagus (BE) is the main precursor of esophageal adenocarcinoma (~2% prevalence in Western adults). Steatotic liver disease (SLD), affecting ~25% of adults, is linked to systemic inflammation, but its relationship with BE is unclear. Methods:In the population-based Salzburg Colon Cancer Prevention Initiative (2007-2020), we analyzed 5507 asymptomatic screening participants. SLD was diagnosed by ultrasound and classified as MASLD or MetALD; BE was confirmed endoscopically and histologically. Associations were assessed using multivariable logistic regression adjusting for demographic, metabolic, and clinical factors. Results:SLD was present in 2550 participants and clustered with diabetes and metabolic syndrome. BE was found in 62 individuals (1.0% without SLD, 1.5% with MASLD, 1.1% with MetALD; P = 0.28). After adjustment, MASLD (OR 1.28; 95% CI 0.74-2.21) and MetALD (OR 0.66; 95% CI 0.16-2.85) were not significantly associated with BE. Female sex was protective (OR 0.26; 95% CI 0.13-0.50), while hiatal hernia increased BE risk (OR 2.05; 95% CI 1.16-3.60). Conclusion:In this population-based cohort, MASLD and MetALD were not clearly associated with BE. Current data do not support incorporating SLD status into BE screening algorithms, although modest risk increases cannot be ruled out.

Open access intensive care unit (ICU) databases, including MIMIC-III, MIMIC-IV, the eICU Collaborative Research Database (eICU-CRD), AmsterdamUMCdb, HiRID-high time resolution ICU data set, and the Salzburg Intensive Care Database (SICdb), have fundamentally transformed critical care research over the past decade. Despite their widespread use, no comprehensive bibliometric analysis has systematically mapped the scientific output generated by studies relying on these resources. A structured search was conducted in PubMed and Web of Science covering 2018 to 2025, retrieving original articles citing at least one of six defined open access ICU databases in title or abstract. Database selection followed the methodology of two prior systematic reviews of publicly available adult ICU datasets. Structured fields covering database used, machine learning (ML) methods, study design, clinical outcomes, AUROC values and patient counts were extracted via a semi-automated AI pipeline (DeepSeek API, multi-label JSON schema). The extraction pipeline was validated against a manually coded reference sample of 110 publications. Bibliometric analyses used R (bibliometrix v4.0.1) and Python. Citation counts, open-access status and SCImago journal quartile were retrieved via OpenAlex and SCImago to characterise the visibility and venue quality of the corpus. Four network analyses were performed: database-to-ML-method co-occurrence, country-to-database, international collaboration, and clinical topic co-occurrence networks. A total of 4,648 publications were included. Annual publication counts increased 45-fold from 42 (2018) to 1,907 (2025), accelerating markedly after 2021 following the release of MIMIC-IV. MIMIC-IV dominated database attributions (54.6

BACKGROUND:Evidence on sex-related mortality differences in critically ill older adults is inconsistent, and frailty is rarely incorporated despite its major prognostic relevance in geriatric intensive care. METHODS:We performed a pooled analysis of acute ICU admissions from three prospective multinational cohorts within the Very Old Intensive Care Patients project: VIP1 and VIP2, which enrolled patients aged 80 years or older, and COVIP, which enrolled patients aged 70 years or older with COVID-19. Frailty was assessed before the acute illness using the Clinical Frailty Scale. The primary endpoint was 30-day mortality. Associations between sex and mortality were examined using robust Poisson regression adjusted for age, frailty, Sequential Organ Failure Assessment score, organ support, and treatment limitations, with Bayesian models used to estimate posterior probabilities of clinically relevant effect sizes. RESULTS:Among 10,363 acute ICU admissions, 43% were women. Women were older and more often frail, whereas men more frequently received invasive mechanical ventilation, vasopressors, and renal replacement therapy. Crude 30-day mortality was higher in men than in women (44%vs. 40%). Frailty was a strong independent predictor of mortality, with each 1-point increase in the Clinical Frailty Scale associated with an 8% increase in adjusted mortality risk (incidence-rate ratio 1.08, 95% CI 1.06-1.10). After multivariable adjustment for frailty and clinical covariates, male sex remained associated with a small residual increase in 30-day mortality (incidence-rate ratio 1.08; 95% CI 1.01-1.15). This association was attenuated with greater illness severity and more intensive organ support. Bayesian analyses yielded adjusted posterior median incidence-rate ratios of 1.04 to 1.06, and the probability of at least 10% excess mortality in men was low after adjustment (2% to 13%). CONCLUSIONS:In older critically ill adults, pre-admission frailty is a major driver of mortality. After explicit adjustment for frailty and illness severity, male sex was associated with only a small residual increase in 30-day mortality. Bayesian analyses suggest that large clinically meaningful sex-based mortality differences are unlikely after accounting for case mix and treatment intensity.

BACKGROUND:Helicobacter pylori (H. pylori) infection has been associated with insulin resistance and metabolic syndrome, particularly in East Asian populations. Whether these associations are independent or explained by socioeconomic and lifestyle confounding remains unclear. We examined this relationship in a large European cohort using rigorous confounder adjustment and Bayesian sensitivity analyses. METHODS:This cross-sectional study included 4,681 asymptomatic adults (2007-2020), with H. pylori status determined by gastric biopsy. The primary outcome was insulin resistance (HOMA-IR > 2.5); secondary outcomes included HOMA2 model parameters and metabolic syndrome (ATP III criteria). Poisson regression estimated incidence rate ratios (IRR) with sequential adjustment for age, sex, education, alcohol, smoking, and diet. Bayesian analyses quantified the probability of clinically meaningful effects. RESULTS:Of 4,681 participants (median age 57; 52% male), 868 (18.5%) were H. pylori-positive. Infected individuals had lower education, higher BMI, and higher alcohol consumption. Crude insulin resistance prevalence was higher in H. pylori-positive participants (31% vs. 27%; P = 0.015). In unadjusted regression, H. pylori was associated with insulin resistance (IRR 1.15, 95% CI 1.01-1.32), but this association disappeared after full adjustment (IRR 1.12, 95% CI 0.95-1.31; P = 0.176). No association with metabolic syndrome was found (IRR 1.03; P = 0.681). Bayesian analysis showed an 87.9% probability of practical equivalence, arguing strongly against a clinically meaningful independent effect. CONCLUSIONS:The association between H. pylori and insulin resistance is fully explained by socioeconomic and lifestyle confounding. H. pylori acts as a marker of adverse metabolic risk rather than a causal factor, and eradication cannot be recommended for metabolic syndrome prevention.

BACKGROUND & AIMS:Recent reclassification of steatotic liver disease (SLD) distinguishes metabolic dysfunction-associated steatotic liver disease (MASLD) from MetALD, a newly defined entity combining MASLD with alcohol consumption. Since the mechanisms linking alcohol consumption in the context of SLD to cardiovascular disease (CVD) - the leading cause of SLD mortality - remain elusive, we investigated how metabolic dysregulation and alcohol intake synergistically promote atherosclerosis. METHODS:Low-density lipoprotein receptor-deficient (Ldlr-/-) mice were fed a high-fat, high-cholesterol (HFC) diet with regular or ethanol-containing drinking water (10-20% v/v). Germ-free and antibiotic-treated Ldlr-/- mice were used to assess the contribution of ethanol-induced dysbiosis. Associations between alcohol consumption and cardiometabolic risk were assessed in two human cohorts (n = 5,115, n = 2,515). RESULTS:Ethanol intake in HFC diet-fed Ldlr-/- mice exacerbated hepatic steatosis and systemic dyslipidemia, despite only modest elevations in systemic ethanol levels (p values ≤0.05). Liver transcriptomic profiling revealed ethanol-induced alterations in lipid metabolism and enhanced proinflammatory signatures, accompanied by increased recruitment of Ly6Chigh monocytes to the liver (p = 0.0121) and elevated levels in the circulation (p = 0.0043). Correspondingly, ethanol-consuming HFC diet-fed Ldlr-/- mice developed enlarged aortic root lesions (p = 0.0105). Neither germ-free conditions nor antibiotic treatment mitigated CVD progression. Metabolomic profiling revealed hyperuricemia in ethanol-exposed HFC diet-fed Ldlr-/- mice, which was associated with upregulation of inflammasome-related genes in the liver, along with an increase in hepatic NLRP3 protein expression (p values ≤0.05). Notably, human data mirrored these findings, demonstrating a dose-dependent association between alcohol intake, dyslipidemia, monocytosis, hyperuricemia, and increased cardiovascular risk (p values ≤0.05). CONCLUSION:Our findings identify alcohol as an important immunomodulatory lifestyle factor that contributes to elevated cardiovascular risk. IMPACT AND IMPLICATIONS:Alcohol consumption, even at moderate levels, contributes to cardiovascular risk, particularly in individuals with steatotic liver disease (SLD). Combining murine models with human cohort data, we show that alcohol intake in SLD is associated with coordinated immune-metabolic alterations, including dyslipidemia, monocytosis, hyperuricemia, and enhanced NLRP3 inflammasome signaling, collectively indicating an elevated cardiovascular risk profile. These findings are relevant to hepatology and cardiovascular medicine, linking alcohol consumption to measurable systemic pathways beyond liver injury. Clinically, systematic assessment of alcohol intake and incorporation into cardiovascular risk evaluation may improve risk stratification and support closer surveillance and preventive strategies in patients with SLD.

AIMS:Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality. SCORE2 may underestimate risk in those classified as low-to-moderate risk. Polygenic risk scores (PGSs) capture genetic predisposition to CVD and could enhance traditional models. This study examines whether integrating PGS with SCORE2 improves the prediction of significant subclinical coronary atherosclerosis, defined as coronary artery calcium (CAC) > 100. METHODS AND RESULTS:We analysed data from 1420 participants in the Paracelsus 10 000 cohort with available PGS, SCORE2, and CAC measurements. Predictive performance was compared across SCORE2 alone, PGS alone, and their combination, assessed using the Akaike information criterion and area under the receiver operating characteristic curve (AUC). Decision curve analysis was performed to evaluate clinical utility. Polygenic risk score improved the prediction of CAC > 100 beyond SCORE2 alone, increasing the AUC from 0.662 to 0.738 in women and from 0.659 to 0.714 in men, with substantial net reclassification index (NRI: women 0.649, men 0.450). The addition of PGS, particularly in the highest quintiles, significantly enhanced classification accuracy for CAC > 100. Decision curve analysis demonstrated that using PGS as a continuous variable provided the highest net benefit at lower threshold probabilities, supporting its role in refining risk stratification, especially in low-to-moderate risk populations. CONCLUSION:Polygenic risk score enhances SCORE2-based prediction of significant CAC. These findings highlight the potential of PGS to refine cardiovascular risk stratification, supporting targeted screening and prevention. Prospective validation, assessment of long-term cardiovascular outcomes, and cost-effectiveness analysis are warranted to guide clinical implementation.