Pulmonary embolism (PE) can be a life-threatening complication following coronary artery bypass grafting (CABG). However, the impact of PE on short-term outcomes such as readmission and mortality remains poorly characterized. The Nationwide Readmission Database 2016 to 2021 was queried to identify patients with isolated CABG who were readmitted with PE within 30 days. International Classification of Diseases (ICD) 10th Revision Clinical Modification and Procedure Coding System codes were used to identify the cohort. Rates and patient characteristics were compared between post-CABG patients with and without PE. Multivariable logistic regression analysis was performed to identify risk factors for PE within 30 days of isolated CABG, as well as risk factors for mortality in these patients. Patients with PE had a higher prevalence of female sex (32.7% vs 30.7%,  = .04) and obesity (25.7% vs 22.3%,  < .001), but lower rates of hypertension and diabetes. Thirty-day mortality was higher in PE patients in univariable (Odds ratio (OR) 1.53, 95% confidence interval (CI) 1.16-2.05,  = .002) and multivariable analyses (OR 1.45, 95% CI 1.00-2.11,  = .04). PE following CABG is associated with increased 30-day readmission and mortality. These findings underscore the need for improved risk stratification, early detection, and targeted prevention strategies in the postoperative period.

Vascular cognitive impairment (VCI) affects 20% to 40% of cardiovascular patients, yet early identification remains challenging. This retrospective study evaluated the predictive value of carotid ultrasound parameters for VCI in 412 patients with cardiovascular risk factors who underwent carotid ultrasound and cognitive assessment between January 2019 and December 2023. Patients were categorized into normal cognition (n = 156), mild cognitive impairment (n = 184), and vascular dementia (n = 72) based on Montreal Cognitive Assessment scores. Carotid intima-media thickness (cIMT) progressively increased from normal cognition (0.89 ± 0.15 mm) to vascular dementia (1.18 ± 0.24 mm,  < .001). After multivariable adjustment, cIMT >1.0 mm (Odds Ratio [OR]: 2.84, 95% CI: 1.76-4.58), carotid stenosis ≥50% (OR: 4.92, 95% CI: 2.31-10.47), and resistive index >0.75 (OR: 3.15, 95% CI: 1.89-5.24) were independently associated with VCI. A combined model incorporating multiple carotid parameters achieved an area under the curve of 0.82 for VCI detection. These findings suggest that carotid ultrasound parameters may help identify cardiovascular patients at elevated risk for cognitive impairment, though external validation is needed before clinical implementation.

Free energy calculations are at the heart of physics-based analyses of biochemical processes. They allow us to quantify molecular recognition mechanisms, which determine a wide range of biological phenomena, from how cells send and receive signals to how pharmaceutical compounds can be used to treat diseases. Quantitative and predictive free energy calculations require computational models that accurately capture both the varied and intricate electronic interactions between molecules as well as the entropic contributions from the motions of these molecules and their aqueous environment. However, accurate quantum-mechanical energies and forces can be obtained only for small atomistic models and not for large biomacromolecules. Here, we demonstrate how to consistently link accurate quantum-mechanical data obtained for substructures to the overall potential energy of biomolecular complexes using machine learning in an integrated algorithm. We do so using a two-fold quantum embedding strategy where the innermost quantum cores are treated at a very high level of accuracy. We demonstrate the viability of this approach for the molecular recognition of a ruthenium-based anticancer drug by its protein target by applying traditional quantum chemical methods. As such methods scale unfavorably with system size, we analyze the requirements for quantum computers to provide highly accurate energies that affect the resulting free energies. Once the requirements are met, our computational pipeline, FreeQuantum, is able to make efficient use of the quantum-computed energies, thereby enabling quantum computing-enhanced modeling of biochemical processes. This approach combines the exponential speedups of quantum computers for simulating interacting electrons with modern classical simulation techniques that incorporate machine learning to model large molecules.

INTRODUCTION: Multipoint pacing (MPP) delivers sequential stimuli from multiple left-ventricular electrodes, potentially improving cardiac resynchronization therapy (CRT) response versus conventional biventricular pacing (BiV). We performed an updated systematic review and meta-analysis to synthesize contemporary evidence. METHODS: Following PRISMA 2020 (PROSPERO CRD420261293273), MEDLINE, EMBASE, and CENTRAL were searched to January 2026 for comparative studies of MPP versus conventional BiV in adults receiving CRT. Primary outcomes were all-cause mortality and heart failure (HF)-related hospitalization. Secondary outcomes included echocardiographic response, NYHA class improvement, and absolute change in left-ventricular ejection fraction (LVEF). Random-effects models produced pooled odds ratios (OR) or mean differences (MD). RESULTS: Eight studies (n = 2430; 1190 MPP, 1240 BiV), including five randomized and three observational studies, were analyzed. All-cause mortality showed no significant difference between groups (OR = 1.46, 95% CI 0.76-2.80; p = 0.25; I = 0%). HF-related hospitalization was significantly reduced with MPP in the largest trial (5.4% vs. 8.9%; p = 0.015), corresponding to a 39% relative risk reduction. MPP was associated with significantly higher echocardiographic response (OR = 0.43, 95% CI 0.29-0.64; p < 0.0001; I = 0%), greater NYHA class improvement (OR = 0.38, 95% CI 0.20-0.73; p = 0.004; I = 3%), and greater absolute LVEF (MD = -4.67, 95% CI -6.70 to -2.64; p < 0.00001; I = 0%). CONCLUSIONS: Compared with conventional CRT, MPP was associated with improved functional and echocardiographic outcomes and reduced HF hospitalization, without a demonstrated mortality benefit. Larger prospective studies with longer follow-up are required to assess long-term prognostic effects.

BACKGROUND: Bachmann's bundle pacing (BBp) improves interatrial conduction, but its clinical impact on atrial function has not fully established. METHODS AND RESULTS: We report eight cases of attempted BBp. Three cases met BBp electrocardiographic criteria with significant P-wave shortening and P-wave amplitude increase in the inferior leads, resulting in improved left atrial (LA) function (increased a' velocity, decreased E/e', and reduced LA diameter) and heart failure stabilization. Conversely, the remaining five cases failing to achieve significant P-wave changes showed no such improvements. CONCLUSIONS: Restoring interatrial conduction through successful BBp may optimize LA performance, potentially offering heart failure stabilization.

BACKGROUND High systolic blood pressure (HSBP) is a major contributor to stroke mortality in China. This study analyzed trends in HSBP-attributable stroke mortality from 1990 to 2021 to elucidate the effects of age, period, and cohort and to project future trends for precision prevention. MATERIAL AND METHODS Using Global Burden of Disease 2021 estimates, temporal trends in age-standardized mortality rates were assessed by Joinpoint regression, age-period-cohort (APC) patterns were evaluated using APC modeling, and mortality trends were projected to 2030 within a Bayesian APC framework incorporating United Nations population projections. Uncertainty was summarized via 95% credible intervals. RESULTS From 1990 to 2021, HSBP-attributable stroke mortality declined overall (average annual percentage change [AAPC] -1.31%, 95% confidence interval [CI] -1.52 to -1.10), with pronounced subtype heterogeneity: ischemic stroke (IS) was relatively stable (AAPC -0.03%, 95% CI -0.29 to 0.24), whereas intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH) substantially declined (AAPC -1.75%, 95% CI -1.97 to -1.52; and -5.03%, 95% CI -5.29 to -4.76, respectively). IS trends diverged by sex, declining in women but increasing in men; mortality steeply increased according to age, with pronounced acceleration after 75 years. Cohort patterns suggested elevated risk in more recent birth cohorts. CONCLUSIONS Our analyses show that HSBP-attributable stroke mortality in China generally declined over the past 3 decades, but trends noticeably diverged among subtypes (ICH substantially declined and SAH most rapidly decreased, whereas IS remained relatively stable), underscoring the need for subtype- and population-specific prevention priorities, including sustained population-wide sodium reduction.

BACKGROUND: Medication prescribing in Long-Term Care Facilities (LTCFs) is characterised by widespread polypharmacy and frequent exposure to potentially clinically relevant drug-drug interactions (DDIs). METHODS: Data from the Italian Prescription Day in LTCFs 2024, a national multicentre point-prevalence study conducted in 82 LTCFs, were analysed. Prescriptions were classified using the Anatomical Therapeutic Chemical system, and DDIs were identified using an international consensus list. Resident-level variables were assessed using validated tools, and associations with DDI burden were examined using univariate mixed-effects Poisson regression models. Facility-level organisational characteristics were described by centre-level DDI burden. RESULTS: The analysis included 3,174 residents (mean age 84.8 years; 74.1% women), with a mean of 7.7 prescribed drugs. Drugs acting on the nervous system, alimentary tract and metabolism, and cardiovascular system were most frequently prescribed; furosemide, paracetamol, pantoprazole, quetiapine, and macrogol were the most commonly used active substances. Overall, 42.2% of residents were exposed to at least one potentially clinically relevant DDI, most commonly involving centrally acting drugs, cumulative anticholinergic burden, serotonergic combinations, and potassium-related interactions. Higher DDI burden was associated with greater pharmacological complexity, depression, sleep disorders, cardiopulmonary disease, and behavioural and psychological symptoms of dementia, whereas older age, severe cognitive impairment, malnutrition, and dysphagia were associated with fewer DDIs. Facility-level and staffing characteristics showed limited differentiation, with assisted living facilities under-represented at higher DDI burden. CONCLUSIONS: Potentially clinically relevant DDIs are common in Italian LTCFs and are primarily associated with resident-level clinical complexity, highlighting targets for medication review and deprescribing to improve medication safety.

BACKGROUND: Pathological cardiac fibrosis arising from acute/chronic myocardial injury drives ventricular remodeling, functional impairment, and elevated mortality through mechanisms lacking effective therapies. Central to fibrogenesis, myofibroblast activation via TGFβ1-Smad3 signaling necessitates targeted therapeutic strategies. METHODS: Anti-fibroblast activation protein (FAP)-functionalized nanoparticles (NPs-SIS3-Ab) were fabricated using PLGA@PDA cores to deliver a Smad3 inhibitor (SIS3). In vitro targeting was assessed through confocal microscopy in TGFβ1-stimulated myofibroblasts. Therapeutic efficacy was evaluated in murine acute myocardial infarction (AMI) and transverse aortic constriction (TAC) models using in vivo imaging system, confocal microscopy, histopathology, transthoracic echocardiography and Western blotting. RESULTS: The NPs-SIS3-Ab nanoparticles demonstrated efficient SIS3 loading, antibody conjugation density, and colloidal stability. Anti-FAP antibody modification enabled specific targeting ability to myofibroblasts both in vitro and in vivo. NPs-SIS3-Ab significantly suppressed TGFβ1-Smad3 pathway activation of myofibroblast in vitro and furthermore, systemic intravenous delivery of NPs-SIS3-Ab markedly inhibited Smad3 phosphorylation, decreased cardiac fibrosis area and more importantly, restored cardiac function both in AMI and TAC models without evident side effects. CONCLUSION: This FAP-targeted nanoplatform achieves precision Smad3 inhibition, demonstrating dual efficacy against acute ischemic and chronic pressure-overload fibrosis while preserving systemic safety. Our findings establish a clinically translatable strategy for modulating pathological fibroblast activity in heart failure.

BACKGROUND: Atherosclerosis is a chronic inflammatory disease initiated by endothelial dysfunction. Junctional adhesion molecule-like protein (JAML) is known to regulate inflammatory responses; however, its function in vascular endothelial cells and atherosclerosis remains unclear. This study aimed to investigate the function of endothelial JAML in atherosclerosis and to uncover the molecular mechanisms involved. METHODS: We generated mice with specific deletion of JAML in endothelial cells and fed them a high-fat diet to induce atherosclerosis, then assessed plaque formation in the aortic root and entire aorta. In parallel, endothelial cells were treated with tumor necrosis factor alpha, and the effects of increasing or silencing JAML on adhesion molecule expression were evaluated, with protein interactions analyzed by co-immunoprecipitation and immunoblotting. RESULTS: JAML exhibited downregulation in endothelial cells within both atherosclerotic lesions and cultured cells subjected to inflammatory stimuli. In mice, the loss of JAML resulted in exacerbated atherosclerotic progression, characterized by larger plaque formation, increased vascular inflammation, and increased macrophage infiltration. Conversely, overexpression of JAML attenuated the expression of adhesion molecules. Mechanistically, JAML was found to promote the degradation of signal transducer and activator of transcription 1 (STAT1) by facilitating its interaction with the E3 ubiquitin ligase tripartite motif-containing 25. This interaction led to ubiquitin-mediated proteolysis of STAT1, independent of alterations in its gene expression levels. CONCLUSIONS: These findings suggest that endothelial JAML holds significant promise as a novel therapeutic target for the prevention and intervention of atherosclerosis.

BACKGROUND: Individuals with excess body weight do not share the same risk for cardiovascular disease (CVD). The phenotype of metabolically healthy obesity (MHO) has drawn the attention of the scientific community due to a potentially reduced CVD risk compared with the phenotype of metabolically unhealthy obesity (MUO). METHODS: A prospective cohort study was conducted involving 3042 participants from the Attica region in Greece. Baseline demographic, clinical, and lifestyle characteristics were assessed, with participants categorized by their obesity and metabolic health status. Cox proportional hazards models were used to analyze the association between obesity/metabolic health status and 20-year CVD incidence, adjusting for relevant covariates. RESULTS: The sample at baseline comprised 38% individuals who were metabolically healthy without obesity (MHWO), 44% individuals who were metabolically unhealthy without obesity (MUWO), 6% individuals with MHO, and 12% individuals with MUO. Over the 20-year follow-up, 718 participants experienced a CVD event; participants with MUO demonstrated the highest incidence rate (61.1%). Cox regression analyses revealed that individuals with MUO had an 85% higher risk of developing CVD compared with individuals having the MHWO phenotype (HR = 1.85, 95% CI = 1.02-3.58). Individuals with MHO had a 39% elevated risk compared with individuals having the MHWO phenotype (HR = 1.39, 95% CI = 1.06-3.42). Groups with MHO and MUO had independently increased CVD risk, even after multivariable adjustment. CONCLUSIONS: Individuals with MUO exhibit the highest risk, but individuals with MHO also have an independently increased CVD risk, emphasizing the significant impact of both obesity and metabolic health status on long-term CVD incidence.

Efficacy of bipolar radiofrequency ablation (BA) is often limited by high impedance between the two ablation catheters in cases of therapy-refractory ventricular tachycardias. Tripolar ablation (TA) is a novel approach, adding a dispersive return electrode to BA. The study aimed to investigate differences in lesion growth and geometry in BA and TA using variable power (20-50W) during power-controlled, irrigated radiofrequency ablation on cross-sections of porcine heart preparations in an ex-vivo model. Using high-resolution imaging at one-second intervals, 1694 measurements in 40 lesions were analyzed regarding lesion geometries and ablation parameters. Baseline impedance was lower in TA (213.1 ± 20.6 Ω vs. 242.7 ± 23.6 Ω, p < 0.001) and distinct differences in lesion geometry were present. Specifically, TA produced deeper and wider lesions at the active catheter compared to the return catheter, resulting in trapezoidal lesions in contrast to rectangular lesions in BA. All lesions reached transmurality; however, lesion width continued to increase in BA and TA after transmurality had been achieved. The majority of steam pops (16/18) occurred above 40W without differences in BA and TA. In cases of high baseline impedance, TA using an additional dispersive return electrode seems effective. In this experimental setup, TA creates trapezoidal lesions in contrast to rectangular lesions in BA without an associated increase in the risk of steam pops.

Heart disease is the leading cause of morbidity and mortality in individuals with diabetes, due largely to risks associated with ischaemic injuries such as myocardial infarction (MI). We use human population genetic data to demonstrate that classical cardiovascular disease risk biomarkers, including common measures of hyperglycaemia, do not fully account for the increased risk of post-MI mortality in patients with diabetes. This study therefore systematically evaluates glycaemic stress underpinning cardiovascular risk in diabetes. Here, we show using in vivo studies in adult male mice and in vitro models that glycaemic variability, rather than sustained hyperglycaemia alone, is a key risk factor for cardiomyocyte dysfunction and increased susceptibility to myocardial injury in diabetes. We further demonstrate that patient plasma assays can elucidate the predictive potential of glycaemic variability as a primary contributor to cardiomyocyte dysfunction and subclinical cardiac injury in diabetes. These findings provide preclinical models for mechanistic and drug discovery studies and inform strategies for managing cardiovascular outcomes in patients with diabetes.

BACKGROUND: Iron metabolism has been associated with cardiovascular diseases, but its relationship with cardiovascular health (CVH) in childhood remains unclear. This study aimed to investigate the associations of iron parameters with CVH using the latest Life's Essential 8 (LE8) framework among Chinese children and adolescents. METHODS: A cross-sectional survey involving 1514 children and adolescents aged 7-18 years was conducted in South China. Iron parameters including serum ferritin (SF) (reflecting iron stores), transferrin saturation (TSAT) (reflecting circulating iron availability), and serum hepcidin (iron regulatory hormone) were measured. CVH was assessed by the American Heart Association's LE8 metrics that comprise three composite scores (CVH, health behavior, and health factor scores), with higher scores indicating better health status. The associations of iron parameters with CVH metrics were examined by regression and restricted cubic spline models. RESULTS: SF was negatively associated with CVH and health factor scores (P=0.034 and 0.003, respectively), whereas TSAT was positively associated with these two scores (P=0.010 and 0.008, respectively). Serum hepcidin exhibited reverse J-shaped associations with CVH and health behavior scores (both P<0.001). The ratio of hepcidin relative to SF showed a positive association with health factor score (P=0.009), while the ratio of hepcidin relative to TSAT displayed a negative association with CVH score (P=0.024). CONCLUSIONS: Reduced iron stores and elevated circulating iron availability, as well as moderate serum hepcidin levels, were associated with better CVH status in Chinese children and adolescents. Moreover, hepcidin expression relative to increased iron stores rather than circulating iron availability may be more favorable to CVH.

Junctophilin-2 (JP2) and junctin (JCN) are key proteins in maintaining calcium homeostasis in cardiomyocytes. Both are reduced in diseased hearts while overexpression of JP2 mitigates heart failure. This study demonstrates that JP2 and JCN are reduced in cardiomyocytes under stress, leading to intracellular calcium dysregulation and subsequent cell death. JP2 binds JCN, thereby blocking muscle ring finger protein-1 (MURF1)-JCN interaction and subsequently preventing MURF1-mediated JCN ubiquitination and degradation in cardiomyocytes. Thus, JP2 overexpression and MURF1 inhibition similarly preserve JCN protein and attenuate myocardial injury and remodeling, and improve myocardial function in preclinical animal models of lipid overload-induced cardiomyopathy and transverse aortic constriction-induced heart failure. Disruption of the JP2-JCN axis represents an important mechanism underlying heart disease and may serve as a potential therapeutic target for cardiac protection.

BACKGROUND: Novel collagen-derived circulating peptides, such as endotrophin, have been proposed as biomarkers of myocardial fibrosis. OBJECTIVES: We aimed to determine the effect of pirfenidone, an antifibrotic agent, on circulating levels of these peptides, and their association with cardiovascular magnetic resonance extracellular volume (ECV). METHODS: In the PIROUETTE (Pirfenidone in Patients with Heart Failure and Preserved Left Ventricular Ejection Fraction) trial, novel collagen-derived circulating peptides (PRO-C3, C3M, CTX-III, endotrophin, PRO-C6, and C6M) were measured at baseline and at prespecified time points in patients with ECV ≥27% randomized (n = 94) to pirfenidone or placebo. Baseline peptide levels were also measured in patients with ECV <27% who were not randomized (n = 13). RESULTS: Treatment with pirfenidone was associated with a significant reduction in log endotrophin (P = 0.034), with a treatment effect seen from 13 weeks. After multivariable adjustment there were significant albeit modest associations between change in myocardial ECV and change in log endotrophin (R: 0.14; P = 0.031), and baseline ECV and baseline log endotrophin (R: 0.30; P = 0.022). Pirfenidone had no effect on the levels of other collagen-derived circulating peptides, and there were no associations between their levels and change in myocardial ECV or baseline ECV. CONCLUSIONS: In patients with heart failure with preserved ejection fraction, treatment with pirfenidone was associated with a sustained reduction in circulating levels of endotrophin from 13 weeks. Circulating endotrophin was also independently associated with both baseline myocardial ECV and change in myocardial ECV. Endotrophin shows high potential as a circulating biomarker reflective of myocardial fibrosis burden and sensitive to change in myocardial fibrosis over time.

BACKGROUND: Cardiovascular disease (CVD) remains the leading global cause of death. While metabolic dysregulation is central to CVD pathogenesis, the extent to which distinct clinical subtypes exhibit unique or shared metabolic signatures remains unclear. OBJECTIVES: The purpose of this study was to systematically characterize metabolomic patterns across a broad spectrum of CVD subtypes and to delineate both shared and subtype-specific metabolic features. METHODS: We analyzed nuclear magnetic resonance-based metabolomic data (325 metabolites) from 244,567 UK Biobank participants, including 27,950 with prevalent CVDs classified into 87 phenotypes (37 classes, 50 subclasses) using International Classification of Diseases-10th Revision codes. Logistic regression, random forest, and XGBoost models assessed cross-sectional metabolite-disease associations. SHapley Additive exPlanations analysis identified key discriminative features. Internal geographic validation used Scotland and Wales cohorts. RESULTS: Metabolomic profiles demonstrated substantial heterogeneity across CVD subtypes. We identified 21 metabolites consistently associated with multiple conditions, including Intermediate-Density Lipoprotein cholesteryl esters, linoleic acid percentage, and small very low_density lipoprotein particles, reflecting shared alterations in lipoprotein metabolism and inflammatory pathways. Cross-sectional discrimination models achieved moderate-to-high performance for prevalent disease status (eg, chronic ischemic heart disease area under the curve = 0.876). Disease similarity clustering revealed reproducible organizational structures: ischemic entities formed tight clusters, hypertensive-renal diseases showed graded patterns, while rheumatic and pulmonary conditions remained distinct. These patterns were confirmed in geographic validation cohorts. CONCLUSIONS: This comprehensive metabolomic atlas reveals both shared and subtype-specific metabolic alterations across prevalent CVD. The identified metabolite set provides a hypothesis-generating framework for understanding cardiovascular metabolic heterogeneity. However, the cross-sectional design and inclusion of treated patients preclude causal or predictive inference, requiring validation in prospective, treatment-naive cohorts.

BACKGROUND: Patients with a coronary artery calcium (CAC) score >300 on dedicated CAC scoring computed tomography (CT) are at equivalent risk of major adverse cardiac events (MACE) as those with established atherosclerotic cardiovascular disease (ASCVD). OBJECTIVES: The aim of the study was to identify the extent of CAC on CT performed for attenuation correction (CTAC) as part of nuclear myocardial perfusion imaging that equates to secondary prevention. METHODS: We retrospectively studied 17,901 patients (48% female, age 64 ± 12 years, body mass index 30 kg/m2 [26-36]) who underwent nuclear myocardial perfusion imaging with CTAC (single photon emission computed tomography/CT or positron emission tomography/CT) at a single center. Prior ASCVD was defined as myocardial infarction (MI), cerebrovascular accident, peripheral artery disease, or prior revascularization. A semiquantitative visually estimated CAC score was obtained by scoring CAC in each coronary artery from 0 (absent) to 3 (severe), yielding a total score of 0 to 12 (zero, mild 1-2, moderate 3-6, and severe ≥7). The primary outcome was the composite of death, MI, or late revascularization. RESULTS: Among 13,852 patients without prior ASCVD (CAC zero 45%, mild 23%, moderate 21%, severe 11%) and 4,049 with ASCVD, 2,006 patients (11%) experienced MACE during a median follow-up of 25 (Q1-Q3: 10-43) months. In multivariable Cox regression, patients with severe calcification had no difference in risk for MACE, MI, or all-cause mortality vs ASCVD patients (P > 0.05). CONCLUSIONS: Patients without prior ASCVD but with severe CAC (score ≥7) on CTAC demonstrated a risk for cardiovascular events and mortality comparable to those with known ASCVD, highlighting the need for more aggressive management in this high-risk primary prevention group.

BACKGROUND: The prevalence of diabetes‑associated Lower Urinary Tract Symptoms (LUTS) is relatively low, and there are limited clinical studies on its associated factors. The present study proposed to investigate the predictive value of various inflammatory indices in patients with diabetes‑associated LUTS. METHODS: Utilizing data from the National Health and Nutrition Examination Survey 2005‒2008, patients were categorized into four groups: normal group, Diabetes Mellitus (DM) group, LUTS group, and diabetes‑associated LUTS group. Inflammatory indices included C-Reactive Protein (CRP), White Blood Cell (WBC) count, Neutrophil-to-Lymphocyte Ratio (NLR), Platelet-to-Lymphocyte Ratio (PLR), Systemic Inflammation Response Index (SIRI), and Systemic Inflammation Index (SII). Multivariate logistic regression and Restricted Cubic Splines (RCS) were employed to evaluate the relationship between inflammatory indices and diabetes‑associated LUTS. RESULTS: A total of 5680 participants were included in the final analysis, comprising 3779 females and 1901 males. The prevalence of diabetes‑associated LUTS was 6.9% in females and 2.2% in males. Diabetes-associated LUTS was associated with older age, lower educational level, hypertension, congestive heart failure, coronary heart disease, emphysema, and higher body mass index and inflammatory indices. Furthermore, multivariate logistic regression analysis revealed that WBC count was a significant factor for both female and male diabetes‑associated LUTS patients, with higher WBC levels correlating with increased diabetes‑associated LUTS risk (females: adjusted Odds Ratio [OR] = 1.115 [1.032‒1.205], p = 0.006; males: OR = 1.207 [1.083‒1.345], p = 0.001). RCS revealed a positive association between WBC count and diabetes‑associated LUTS in female and male participants. CONCLUSION: Inflammatory markers such as CRP and WBC count were higher in the diabetes‑associated LUTS group compared to the other three groups. WBC count is an associated factor for diabetes‑associated LUTS, and incorporating WBC count into clinical assessments can aid in identifying diabetes‑associated LUTS patients, thereby facilitating targeted interventions.