Background Recent studies have suggested a protective effect of finerenone on renal function and reduced the risk of cardiovascular events in patients with CKD and type 2 diabetes. However, its role in IgA nephropathy remains unknown. This study aimed to evaluate its efficacy against IgA nephropathy. Methods A total of 18 IgAN patients with full supportive therapy, including RAS blockade as much as allowed or tolerated, blood pressure control and steroids and/or other immunosuppressive agents. Analyzed at 2, 4, 6 and 8 months after finerenone therapy. Results Eighteen IgA nephropathy patients were enrolled in this study, after 6.78 ± 3.47 months follow-up, a significant reduction was observed in protein-to-creatinine ratio with a 28.48% (p = 0.003), 13.12% (p = 0.17), 31.33% (p = 0.003), 39.69% (p = 0.02), respectively, at 2, 4, 6 and 8 months of treatment with finerenone compared to baseline. The eGFR was relatively stable during follow-up. Conclusions The protein-to-creatinine ratio was significantly reduced after finerenone treatment in IgA nephropathy patients with full supportive therapy, and the eGFR was stable during follow-up.

Diabetes mellitus (DM) is a globally prevalent metabolic disorder with rising incidence. Diabetic peripheral neuropathy (DPN), the most common microvascular complication in DM, disrupts autonomic nervous system regulation of cardiac and circulatory functions, thereby increasing susceptibility to cardiovascular and cerebrovascular events. Elucidating the relationship between diabetic DPN and cardiovascular complications is critical for optimizing holistic management of diabetic patients. This study aimed to investigate the correlation between DPN and cardiovascular events in patients attending the Diabetes Clinic of Rafsanjan University of Medical Sciences, Iran. In this cross-sectional study, 260 patients with type 2 diabetes mellitus (T2DM), diagnosed per the American Diabetes Association (ADA) 2023 criteria, were enrolled via convenience sampling. The patients with cardiovascular complications group comprised 121 patients with T2DM and documented cardiovascular events, while the control group included 138 patients with T2DM and no cardiovascular history. Data on demographic characteristics, body mass index (BMI), blood pressure, clinical laboratory parameters, and neuropathy severity (assessed via the Michigan Neuropathy Screening Instrument [MNSI]) were collected. Statistical analysis was performed using SPSS version 22. The patients with cardiovascular complications had significantly higher neuropathy scores (p = 0.039), longer diabetes duration (p < 0.05), greater prevalence of hypertension (p < 0.001), and elevated serum creatinine (p = 0.020) compared to those without cardiovascular complications. In multivariable logistic regression, severe diabetic neuropathy (score > 4) was associated with increased odds of cardiovascular complications in the unadjusted model (OR = 1.73, 95% CI: 1.03-2.91) and after adjustment for demographic and lifestyle factors (adjusted OR = 2.07, 95% CI: 1.07-3.97; p = 0.030). A significant crude association was also observed for each one-unit increase in continuous neuropathy score (OR = 1.09, 95% CI: 1.01-1.18; p = 0.021). A significant association was found between peripheral neuropathy and increased odds of cardiovascular disease in T2DM patients. This underscores the potential role of neuropathy as a marker for cardiovascular risk. Further longitudinal studies are warranted to explore the mechanistic interplay between neuropathy progression and cardiovascular outcomes.

Xanthine oxidase inhibitors (XOis) are commonly used to treat gout and hyperuricemia. Beyond urate-lowering effects, XOis may influence cardiovascular outcomes via oxidative stress pathways. Prior evidence, including post hoc analyses of the CARES trial, suggests increased mortality after XOi discontinuation, raising concern for a potential "withdrawal syndrome." However, evidence from real-world outpatient populations is limited. This study aims to evaluate whether the recent discontinuation of XOi therapy is associated with an increased risk of acute cardiovascular events in patients with gout. We conducted a retrospective cohort study using the Merative MarketScan database. Adults with gout initiating allopurinol or febuxostat were included. Discontinuation was defined as no XOi supply in the prior 90days during the 121- to 180-day window post-initiation. The primary outcome was hospitalization or outpatient diagnosis of acute myocardial infarction or ischemic stroke. Cox proportional hazards models with stabilized inverse probability weights were used to estimate hazard ratios (HRs), adjusting for demographic and clinical covariates. Among 508,872 patients initiating XOi therapy, 23.6% discontinued therapy within the first 121- to 180-day post-initiation timeframe. Discontinuers were younger with fewer comorbidities at baseline. After weighting, groups were well balanced. XOi discontinuation was associated with a modest but statistically significant increased risk of acute cardiovascular events (HR, 1.05; 95% CI, 1.01-1.09; p = 0.019). The magnitude of the effect increases among patients with preexisting hypertension diagnoses (HR, 1.13; 95% CI, 1.03-1.23; p = 0.006). In this large real-world cohort, early discontinuation of XOi therapy was linked to a small but significant elevation in cardiovascular risk. These findings support prior signals of potential harm from XOi withdrawal, particularly among patients with cardiovascular disease, and highlight the importance of sustained therapy adherence. Key Points • Xanthine oxidase inhibitor (XOi) discontinuation was associated with a modest but significant increase in acute cardiovascular events in a large national cohort of patients with gout. • Even early discontinuation after XOi initiation may increase cardiovascular risk, underscoring the importance of treatment persistence. • Adherence to XOi therapy may be an important factor in reducing cardiovascular risk among gout patients.

The junctional protein associated with coronary artery disease predicts adverse cardiovascular events in patients with acute coronary syndromes at high residual risk.

ST-elevation myocardial infarction (STEMI) remains a major health concern despite advances in care. Indoxyl sulfate (IS) and p-cresyl-sulfate (p-CS) are gut-derived uremic toxins linked to higher morbidity and mortality in patients with chronic kidney disease (CKD). IS has been identified as an independent predictor of major adverse cardiovascular events (MACE) after STEMI, but data on p-CS are lacking. This study assessed the predictive value of IS and p-CS in STEMI patients with preserved renal function (cohort # NCT03070496). Plasma IS and p-CS were measured in 260 patients with STEMI who underwent primary coronary angiography. Samples collected 4 h after inclusion were analyzed using ultra-performance liquid chromatography with fluorescence detection. Optimal cut-offs were determined by the Youden index, and associations with MACE were evaluated by log-rank tests and Cox regression. Among 234 analyzed patients, 11.5% experienced MACE within one year. IS and p-CS levels were higher in the MACE group (IS: 3.14 vs. 2.19 µmol/L, p &lt; 0.05; p-CS: 6.76 vs. 2.70 µmol/L, p &lt; 0.01). Elevated p-CS independently predicted MACE (HR 3.79, 95% CI 1.29–11.17, p &lt; 0.05), whereas IS lost significance after adjusting for kidney function. In STEMI patients, plasma p-CS is a stronger independent predictor of MACE than IS, highlighting its potential role in the gut–heart axis.

BackgroundPercutaneous coronary intervention (PCI) is the primary revascularization method for acute myocardial infarction (AMI); however, patients remain at significant risk of developing left ventricular remodeling (LVR), which is closely associated with major adverse cardiovascular events (MACE). This study evaluated cystatin C (CysC) as a potential biomarker for LVR and MACE after PCI in AMI patients.MethodsA total of 168 AMI patients who underwent PCI were followed for 6 months. Transthoracic echocardiography was performed at admission and 6-month follow-up. The endpoints were LVR and MACE. Multivariable logistic regression analysis was used to identify factors associated with LVR, while Cox proportional hazards regression was employed for time-to-MACE analysis. Variables with P < 0.1 in univariate analyses were included in multivariate models. Stepwise forward selection was applied to construct the final models, with adjustment for potential confounders.Results22% of patients developed LVR and 18.6% experienced MACE. Multivariate regression analysis identified CysC as independently associated with both LVR and MACE after PCI. The AUC for CysC in predicting LVR and MACE was 0.757 and 0.707, respectively. Adding CysC to conventional risk prediction models improved their discriminatory accuracy. Internal validation using bootstrap sampling (1,000 replications) confirmed model reliability. Kaplan–Meier analysis stratified by CysC tertiles demonstrated a significant association between increasing CysC levels and higher incidence of MACE (log-rank P = 0.002).ConclusionCysC was independently associated with LVR and MACE after PCI in patients with AMI, highlighting its potential value as a biomarker for early identification of high-risk patients and guiding targeted therapeutic interventions.

CD36-mediated fatty acid metabolic reprogramming activates synovial fibroblasts and promotes rheumatoid arthritis progression.

The monocyte-to-high-density lipoprotein cholesterol ratio (MHR) is an emerging biomarker associated with inflammation and oxidative stress, being linked to cardiovascular events in patients with chronic kidney disease or those with diabetes. Given that monocyte activation plays a central role in the pathogenesis of thrombosis in antiphospholipid syndrome (APS), and that HDL-cholesterol suppresses monocyte activation, we aimed to investigate whether MHR could serve as a predictor for recurrent thrombotic events in APS patients. This retrospective longitudinal study included 107 patients diagnosed with APS at Hokkaido University Hospital. The MHR at the time of APS diagnosis was calculated and compared between patients with and without subsequent thrombotic recurrence. Among patients who experienced recurrence, MHR values were compared between two time intervals prior to the event: 0-6 months and 6-36 months. The median [IQR] age at diagnosis was 46 [31-56] years, with a median follow-up duration of 14.4 [11.6-17.8] years. Thrombotic events recurred in 31 patients, including 22 arterial and 9 venous events. The MHR at diagnosis did not significantly differ between patients with and without recurrence (5.0 [3.4-8.0] vs 5.3 [3.5-8.6], p = 0.57). However, among patients with recurrent thrombosis, average MHR values during the 0-6 months preceding the event were significantly higher than those measured 6-36 months prior (6.1 [4.3-8.3] vs 5.1 [3.8-8.6], p = 0.04). Our findings suggest that MHR increases in the 6 months preceding recurrent thrombotic events in APS patients, indicating that it may serve as a dynamic, time-sensitive biomarker for predicting thrombotic recurrence in thrombotic APS.

Aim: Anticholinergic burden (ACB) is associated with profound clinical and economic burden; however, anticholinergic medications are often prescribed for overactive bladder (OAB). This analysis assessed risk of adverse health outcomes and costs associated with ACB among patients with OAB. Materials & methods: Adults with ≥1 pharmacy claim for ≥1 OAB anticholinergic medication and continuous coverage for ≥6months before and after the first prescription fill date for OAB anticholinergic medication (index) from January 2010 to November 2021 in the Optum Research Database were included. Daily ACB scores were calculated postindex. The impact of ACB on risk of certain adverse health outcomes was examined using Cox proportional hazards regression with categorical and piecewise linear specifications for ACB. Time-varying total ACB association with healthcare costs was evaluated with marginal structural models. Results: Overall, 428,142 patients were included in the analysis; mean (SD) age was 65.2 (14.9) years. Mean (SD) preindex ACB was 0.53 (1.44) points/day. Postindex, OAB medications accounted for 61.0% (95% CI: 60.9%-61.1%) of total ACB. Adjusted hazard ratios for urinary tract infection (UTI), urinary retention, delirium/drowsiness, cognitive impairment, falls/fractures and cardiovascular events were >1 (vs 0 points/day) and increased with ACB. A 1-point/day increase in ACB was associated with increased risk of UTI, urinary retention, delirium/drowsiness, cognitive impairment, falls/fractures and cardiovascular events for patients with ACB ≤8 points/day preindex. Increasing ACB was associated with increased all-cause total healthcare costs and costs related to cognitive impairment and falls/fractures. Conclusion: The association between increased ACB and greater risk of certain adverse health outcomes and costs supports the reassessment of anticholinergic medication use for patients with OAB.

To reduce the risk of recurrent cardiovascular events in patients with established cardiovascular disease (CVD), guidelines recommend adopting a more plant-based diet. The EAT-Lancet diet, which focuses on plant-based foods, is associated with a lower risk of CVD in apparently healthy people. However, the relationship in patients with established CVD is unclear. Therefore, the aim of this research was to quantify the relationship between the EAT-Lancet Healthy Reference Diet (HRD) and risk of recurrent CVD in patients with established CVD. Patients with established CVD from the Utrecht Cardiovascular Cohort-Second Manifestations of ARTerial disease were studied. Dietary intake was measured using a food frequency questionnaire and the relationship between the EAT-Lancet HRD (score from 0 to 140 points) and non-fatal myocardial infarction and stroke was assessed using Cox regression adjusted for age, sex, educational background, lifestyle factors, and energy intake. During a follow-up of 24,212 person-years 209 non-fatal vascular events occurred. The median score for the EAT-Lancet HRD was 57 out of 140 points (IQR: 41-68). After adjustment for confounders, a diet more in line with the EAT-Lancet HRD was associated with a lower risk of non-fatal vascular events (HR 0.87 (95% CI 0.79-0.96) per 10-point increase); stroke (HR 0.76 (95% CI 0.63-0.91) per 10-point increase); and a trend towards lower risk of myocardial infarction (HR 0.90 (95% CI 0.81-1.02) per 10-point increase). In patients with established CVD, a dietary pattern more in line with the EAT-Lancet HRD is associated with a lower risk of non-fatal stroke and myocardial infarction.

The stress hyperglycemia ratio (SHR) is a novel biomarker that reflects true acute hyperglycemia and has been associated with adverse outcomes and an increased risk of cardiovascular events in patients with myocardial infarction (MI). However, the relationship between SHR and different culprit plaque phenotypes in acute myocardial infarction (AMI) remains unexplored. This study aims to investigate the association between SHR and clinical outcomes in AMI patients stratified by plaque phenotype. Between March 2017 and January 2020, a total of 1698 AMI patients were prospectively enrolled. Of these, 364 underwent optical coherence tomography (OCT) to assess culprit lesion morphology. SHR was calculated using the formula: [admission blood glucose (mmol/L)]/[1.59 × HbA1c (%)-2.59]. The primary endpoint was the occurrence of major adverse cardiovascular events (MACEs), defined as a composite of all-cause death, recurrent MI, ischemic stroke, and rehospitalization due to heart failure. Overall, patients were divided into two groups according to quartile of SHR (Q1-Q3 vs. Q4). After a median follow-up of 4years, elevated SHR was independently associated with an increased risk of MACEs after adjustment (HR: 1.14, 95% CI 1.05-1.24, p = 0.002). In patients with plaque rupture (PR), SHR remained a significant predictor of MACEs after adjustment (HR: 2.09, 95% CI 1.17-3.73, p = 0.013). In contrast, among patients with plaque erosion (PE), no significant difference in MACEs was observed across SHR-based groups (HR: 1.49, 95% CI 0.66-3.38, p = 0.342). This study demonstrates that AMI patients with elevated SHR (> 1.2) experience significantly worse clinical outcomes compared to those with lower SHR (≤ 1.2). The prognostic value of SHR was particularly evident in patients with PR rather than those with PE, suggesting its utility for risk stratification and guiding precision management in patients with PR.

Ischemia-modified albumin and cardiovascular risk in obstructive sleep apnea and acute coronary syndrome. Long term follow-up after treatment from the ISAACC study.

Cardiovascular prognosis in people with drug-resistant hypertension, defined by office and home blood pressure, has not been fully evaluated. This Japan Morning Surge-Home Blood Pressure study data analysis evaluated the cardiovascular event rate in patients with drug-resistant hypertension defined using office and home blood pressure. The incidence of cardiovascular events (stroke, coronary artery disease, congestive heart failure, aortic dissection) in participants with true resistant hypertension (office blood pressure ≥140/90 mm Hg and home blood pressure ≥135/85 mm Hg during treatment with ≥3 antihypertensives, including a diuretic) was determined and compared with other hypertension subgroups. During mean 6.2 years' follow-up in 4278 participants (mean age, 64.9±10.9 years; 46.9% male), cardiovascular events included stroke (n=96), coronary artery disease (n=125), congestive heart failure (n=42), aortic dissection (n=8), and sudden death (n=15). The incidence of cardiovascular events in patients with home blood pressure monitoring-confirmed resistant hypertension was 34.7 per 1000 person-years (significantly higher than in those with well-controlled hypertension on ≥3 drugs including a diuretic; 11.9 per 1000 person-years [P<0.001]). In the home blood pressure monitoring-confirmed resistant hypertension group, cardiovascular event incidence was highest in those with versus without cardiovascular disease history (39.4 versus 22.7 per 1000 person-years). These data showed that home blood pressure-confirmed resistant hypertension was associated with a high incidence of cardiovascular events over time, especially in the presence of a cardiovascular disease history. The relevance of home blood pressure monitoring for defining resistant hypertension and treatment strategies, especially compared with ambulatory blood pressure monitoring, remains to be determined. URL: https://www.umin.ac.jp/ctr; Unique identifier: UMIN000000894.

The effects of low-dose colchicine on the progression of aortic valve stenosis: Rationale, design, and baseline characteristics of the Colchicine and Inflammation in Aortic Stenosis (CHIANTI) trial.

Protein-energy wasting (PEW) is a strong indicator of adverse outcomes such as all-cause death and cardiovascular events. Although this association has been established in dialysis patients, it has not been clearly demonstrated in those with non-dialysis-dependent chronic kidney disease (NDD-CKD). This study aimed to evaluate the association between PEW and all-cause death or cardiovascular events in patients with NDD-CKD. We investigated the association between PEW and adverse outcomes in patients with NDD-CKD through a prospective cohort study of 1,847 patients (median follow-up: 6.94 years). The definition of PEW followed the International Society of Renal Nutrition and Metabolism criteria: serum albumin <3.8 g/dL, body mass index <23.0 kg/m2, skeletal muscle mass <19.7 kg in women, <26.9 kg in men, and protein intake <0.6 g/kg/day. During follow-up, 129 deaths and 264 composite outcomes (all-cause death or cardiovascular events) occurred. In Cox regression analysis, all-cause death and composite outcomes were significantly increased in patients with two or more PEW parameters. All-cause death was significantly increased in patients with two PEW parameters (hazard ratio [HR], 2.78; 95% confidence interval [CI], 1.61-4.08; p < 0.001) or ≥3 PEW parameters (HR, 3.78; 95% CI, 1.81-7.89; p < 0.001). Composite outcomes were also significantly increased in patients with two PEW parameters (HR, 2.16; 95% CI, 1.51-3.11; p < 0.001) or ≥3 PEW parameters (HR, 2.30; 95% CI, 1.30-4.07; p = 0.004). PEW was a strong indicator of all-cause death and composite outcomes among NDD-CKD patients.

Glycemic variability (GV) reflects glucose fluctuations, and increased GV is associated with adverse cardiovascular outcomes. We systematically evaluated the association between GV, measured by the mean amplitude of glycemic excursions (MAGE) and standard deviation (SD), and cardiovascular risk in patients with pre-existing cardiovascular disease (CVD). We searched PubMed, Embase, Scopus, Web of Science, and CENTRAL through May 2025 for studies on GV and cardiovascular outcomes in patients with established cardiovascular disease. Random-effects models with Knapp-Hartung adjustment were used to pool the risk ratios (RRs) and 95% confidence intervals (CIs). Subgroup, sensitivity, and meta-regression analyses were used to explore heterogeneity. The risk of bias was assessed using the ROBINS-I tool. Seventeen studies comprising 6,096 patients were included. In the categorical analysis, higher MAGE (RR: 2.18; 95% CI: 1.70, 2.80; I² = 15.6%) and SD (RR: 1.94; 95% CI: 1.32, 2.87; I² = 55.9%) were associated with increased risk of major adverse cardiovascular events (MACE). Continuous MAGE was also associated with MACE (RR: 1.66; 95% CI: 1.28, 2.14; I² = 65.65%), while continuous SD showed a non-significant association. The adjusted analyses for MAGE reinforced these findings. The MAGE cut-off thresholds significantly moderated the effect sizes in the meta-regression analysis. Subgroup analyses showed between-group differences in SD according to diabetes status and in MAGE according to country and follow-up duration. The certainty of evidence (GRADE) was very low for all contrasts. In outcome-specific analyses, both MAGE and SD were associated with acute heart failure and myocardial infarction, but not cardiovascular mortality. GV, particularly when assessed using MAGE, is a significant predictor of cardiovascular risk in patients with pre-existing CVD. While these findings support its prognostic utility, limitations such as the observational design and residual confounding warrant cautious interpretation. Further studies should establish standardized thresholds and dose-response relationships. PROSPERO CRD420251002622.

Introduction. Cardiac magnetic resonance (CMR) is the gold standard for assessing myocardial remodeling after myocardial infarction. Particular attention is paid to myocardial tissue characteristics assessed using late gadolinium enhancement (LGE). Textural heterogeneity parameters of LGE are a novel quantitative metric that reflects the structural heterogeneity of left ventricular (LV) myocardial tissue changes. Aim: To investigate the association between textural parameters, assessed by quantitative analysis of signal intensity heterogeneity on late gadolinium enhancement CMR, and the development of major adverse cardiovascular events (MACE) in patients with acute myocardial injury. Material and methods. This retrospective study included 108 patients admitted to the emergency cardiology department with a diagnosis of primary ST-elevation or non-ST-elevation myocardial infarction (STEMI or NSTEMI). A composite primary endpoint was established, which included the following clinical outcomes: cardiovascular death, all-cause death, non-fatal myocardial infarction, and non-fatal acute stroke. Inclusion criteria were: 1) performance of contrast-enhanced CMR within 4–7 days of hospitalization; 2) CMR findings consistent with acute ischemic injury of the LV; and 3) satisfactory image quality. CMR criteria for acute ischemic injury included: a high-intensity signal on T2-weighted images (T2WI) with co-localized LGE in a segment(s) demonstrating an ischemic pattern of contrast distribution. Quantitative CMR analysis was performed using the dedicated post-processing software CVI42 (Circle Cardiovascular Imaging, Canada). Myocardial texture analysis was conducted using the 3D Slicer application, version 5.2.2 (The Slicer Community, USA). For the analysis, LGE images were used. From each slice, textural features of signal intensity (SI) heterogeneity were extracted separately for the following regions of interest (ROIs): the LV myocardial injury zone, intact myocardium, and the entire LV (comprising both injured and intact myocardium). Results. The mean age of the patients was 59.56 ± 10.7 years, with 75% (n = 81) being male. STEMI was present in 89.3% of the entire cohort. The follow-up period was 1095 ± 23 days. Follow-up data were obtained for all 108 patients (100% of the sample). Based on the occurrence of the primary endpoint, two groups were formed: the group without cardiovascular events (“–MACE”) and the group that reached the endpoint (“+MACE”). Analysis of LV myocardial tissue characteristics assessed in the LGE phase revealed no significant differences between the study groups for almost all parameters, with the exception of the global LV SI elevation on T2-WI, which was significantly lower in the “+MACE” group. Quantitative analysis of SI heterogeneity across the entire LV using textural features revealed differences in first-order statistics, with higher values of these indices in the “+MACE” group. Patients who experienced a MACE during the follow-up period were characterized by a more asymmetric and complex signal texture, featuring abrupt variations in gray-level intensity, higher gray-level irregularity, shorter lengths of homogeneous areas and run lengths, and a predominance of small heterogeneous areas. Analysis of the intact myocardium in the LV also demonstrated higher heterogeneity and gray-level irregularity, with a high number of small heterogeneous regions. Conclusion. Heterogeneity parameters assessed by CMR reflect the changes occurring in the LV myocardium after MI, are associated with cardiac functional indices, and may be considered prognostic factors for an adverse clinical course. Given the limitations of this study, further research is needed to investigate the relationship between LV tissue characteristics on CMR, entropy, and adverse outcomes after acute myocardial injury.

Type 2 diabetes mellitus (T2DM) is a major risk factor for atherosclerosis and cardiovascular events (CVEs), partly due to increased platelet activation and inflammation. Neutrophil-derived cathepsin G (CatG), a prothrombotic protease, may play a role in this process by promoting platelet aggregation. However, its association with CVEs in T2DM has not been previously explored. This study aimed to evaluate whether circulating CatG levels independently predict CVEs in patients with T2DM. We included 485 T2DM patients from two prospective cohorts (PLINIO and ATHERO-AF studies). The primary outcome was a composite of cardiovascular death, non-fatal coronary and cerebrovascular events, and peripheral artery events. Cardiovascular death, all-cause death, non-fatal coronary and cerebrovascular events were tested as secondary outcomes. Multivariate Cox-regression was used to assess associations between the top (V) CatG quintile and outcomes. A subgroup analysis was conducted in 312 patients with available neutrophil count data and after a propensity score matching, to test the correlation between CatG and plasma soluble P-selectin (sP-selectin), an in vivo marker of platelet activation. During the follow-up yielding for 2,437.6 person-years, 86 CVEs occurred. Patients developing CVEs had higher CatG (2.9 [1.9-4.4]ng/mL vs. 2.1 [1.6-2.6]ng/mL; p < 0.001) compared to CVEs-free patients. The CVEs incidence rate in patients in the V CatG quintile was 10.4% per year (V quintile versus each other quintile: p < 0.001). V CatG quintile associated with increased CVEs (adjusted Hazard Ratio (aHR) 6.081 [95% confidence interval (CI) 3.887-9.514], p < 0.001) and its component incidence, including cardiovascular mortality or non-fatal coronary events or all-cause mortality. The association between higher CatG levels and CVEs remained significant after adjustment for neutrophil count (aHR 4.051 [95% CI 2.098-7.820], p < 0.001). Neutrophil count was also independently associated with CVEs (aHR 1.177 [95% CI 1.009-1.372], p = 0.038). Finally, in the propensity score matching analysis CatG independently correlated with sP-selectin (Beta: 0.443; p < 0.001). Circulating CatG is an independent predictor of cardiovascular events in T2DM, suggesting a novel biomarker linking inflammation to athero-thrombosis. NCT01882114, NCT04036357.

Association between waist-to-height ratio and cardiovascular events in patients with chronic obstructive pulmonary disease: the mediating effect of prognostic nutritional index.

Acute coronary syndrome (ACS) is a major cause of morbidity and mortality worldwide. Identifying biomarkers that predict outcomes is essential for guiding management. This study evaluated whether elevated serum uric acid (SUA) is associated with increased risks of major adverse cardiovascular events (MACE), recurrent myocardial infarction (re-MI), and all-cause mortality (ACM) in patients with ACS. This retrospective cohort study enrolled 829 inpatients with ACS admitted to a tertiary referral hospital in Taiwan from 2015 to 2019. Patients were divided into normal (< 7.25mg/dL, n = 566) and high (≥ 7.25mg/dL, n = 263) SUA groups based on a receiver operating characteristic-derived cutoff for whole cohort. All patients received standard ACS care, and SUA levels were retrospectively analyzed. The primary outcome was MACE, defined as ACM, re-MI, and target lesion/vessel revascularization (TLR/TVR), assessed up to 60 months. Kaplan-Meier survival analysis, logistic regression, and Cox proportional hazards regression were applied. The overall incidences of MACE (19.54%), re-MI (2.90%), and ACM (4.46%) were higher in the high SUA group compared with the normal SUA group (MACE: 26.62% vs. 16.25%, p = 0.0005; re-MI: 6.08% vs. 1.41%, p = 0.0002; ACM: 7.22% vs. 3.18%, p = 0.0087). No significant difference was observed in TLR/TVR (overall 11.94%; 11.48% vs. 12.93%, p = 0.5508). Kaplan-Meier analysis at 60 months demonstrated higher event-free rates for MACE, re-MI, and ACM in the normal SUA group (log-rank p = 0.0117, 0.0006, and 0.0261, respectively). Multivariable logistic regression showed that SUA ≥ 7.25mg/dL was associated with increased odds of MACE (odds ratio = 1.639, 95% confidence interval [CI] = 1.084-2.477, p = 0.0191). Cox regression revealed higher hazards of MACE (hazard ratio [HR] = 1.399, 95% CI = 1.024-1.191, p = 0.0350), re-MI (HR = 3.758, 95% CI = 1.605-8.799, p = 0.0023), and ACM (HR = 1.956, 95% CI = 1.019-3.753, p = 0.0438) in the high SUA group after adjustment for age, uremia, use of drug-eluting stent, and number of diseased vessels. Elevated SUA is an independent prognostic marker for increased risks of MACE, re-MI, and ACM in patients with ACS. SUA assessment can enhance risk stratification, helping to identify higher-risk patients who may benefit from more intensive secondary prevention strategies and closer follow-up.