Cardiovascular Disease Biomarkers Research Articles

Incremental role of Cardio-Ankle Vascular Index in predicting ischemic threshold in patients with suspected coronary artery disease

Abstract Background The Cardio-Ankle Vascular Index (CAVI) quantifies arterial stiffness and has emerged as a potential biomarker for cardiovascular disease and its associated risk factors. This study explores the prognostic utility of CAVI in predicting myocardial ischemia in patients with suspected coronary artery disease (CAD). Additionally, it examines the relationship between global longitudinal strain (GLS) and the wall motion score index (WMSI) during both rest and stress echocardiography. Methods We conducted a retrospective analysis of patients with suspected CAD who underwent CAVI measurement and stress echocardiography within a three-month window. Coronary angiography was utilized to evaluate anatomical stenosis (>50%). We used multivariate analysis to identify predictors of the ischemic threshold. Results In our cohort of 127 patients (average age 61.4 ± 9.1, 78% male), the prevalence of hypertension, dyslipidemia, and diabetes was 76%, 68% and 47% of patients, respectively. Prior coronary intervention and a history of myocardial infarction were showed significant prevalence at 33% and 9%, respectively. CAD distribution included absence in 15%, left main (LM) disease in 8%, proximal left anterior descending (LAD) artery disease in 38%, mid-to-distal LAD disease in 50%, left circumflex artery disease in 46%, and right coronary artery disease in 57%. A robust correlation between GLS and WMSI was observed both at rest and during peak stress (r=0.68 and r=0.57, p<0.001, respectively). High CAVI (≥8.5), resting GLS in the LAD(<-15.5%), and peak GLS during stress (<-15.3%) emerged as significant ischemic threshold predictors in multivariate analysis (AUC = 0.82, p<0.0001). Conclusion The correlation between WMSI and GLS provides valuable insights into cardiac mechanics. These findings underscore the clinical relevance of incorporating CAVI, GLS, and WMSI into routine assessments for patients with suspected CAD to enhance prognostic stratification.ROC for final predictive model

Circulating levels of amyloid-beta (1-40) peptide associate with cardiometabolic traits and risk for metabolic dysfunction-associated steatotic liver disease

Abstract Background and Aims The ageing-associated amyloid-beta 1-40 peptide (Αbeta40) has recently emerged as a blood-based biomarker of cardiovascular disease (CVD). Its levels predict future cardiovascular death and MACE in patients with established CVD. The clinical value of Abeta40 in patients with metabolic syndrome who do not concomitantly have clinically overt CVD or other end-organ damage remains poorly understood. At the present study we investigated the clinical value of plasma Αbeta40 in patients with pre- or established metabolic syndrome who are at risk for metabolic dysfunction-associated steatotic liver disease (MASLD). Methods Αbeta40 was measured in plasma by enzyme-linked immunosorbent assay and cardiometabolic traits were determined in a mixed population (n=888) of patients with established (n=243) and pre- or without metabolic syndrome (n=645) who did not have clinical signs of established cardiometabolic disease (heart failure, coronary artery disease, MASLD, chronic kidney disease). The endpoint of the study was the association of Abeta40 with cardiometabolic indices and risk (BARD score) for MASLD. Odds ratio (OR) was calculated by ordinal regression analysis for the increasing incidence of metabolic syndrome components per increasing Abeta40 (1-SD) after adjustment for age, sex, smoking status and hyperlipidemia. Results Abeta40 levels are associated with the presence of metabolic syndrome and with higher odds for increasing incidence of metabolic syndrome components after adjustment for sex, age, smoking status, hypertension and dyslipidemia. Increased Abeta40 plasma levels were associated with decreased HDL-C levels (OR: 1.004, 95% CI:1.000-1.009, P=0.049) and increased triglyceride levels (OR: 1.007, 95%CI: 1.001-1.012, P=0.033) after adjustment for traditional cardiovascular risk factors (age, sex, smoking status, hypertension and hyperlipidemia). Among the total population (n=888), we identified n=473 subjects with increased MASLD risk if any of the following was present: hepatic steatosis index≥36 or fatty liver index≥60 or Fib-4 index≥2.67 or NAFLD score≥0.675. Among patients with high-risk for MASLD, patients with increased BARD score had significantly higher Abeta40 levels (median Abeta40 concentration in patients with BARD score≥2 vs. patients with BARD score<2: 54.9 pg/ml (IQR=38.25) vs. 41.9 pg/m (IQR=30.35), P=0.012). Increased Abeta40 levels were associated with increased odds for AST/ALT≥0.8 ratio and increased odds for BARD score≥2 after adjustment for age, sex, smoking status, hypertension and hyperlipidemia. Conclusion Our findings suggest that Abeta40 peptide is associated with cardiometabolic traits and risk for MASLD. Whether Abeta40 may emerge as an early cardiometabolic prognostic biomarker, future longitudinal studies are warranted to determine the prognostic value of Abeta40 for the development of cardiometabolic diseases in patients with metabolic syndrome.

Neutrophil-to-High-Density Lipoprotein Ratio (NHR) and Neutrophil-to-Lymphocyte Ratio (NLR) as prognostic biomarkers for incident cardiovascular disease and all-cause mortality: A comparison study

Cardiovascular diseases (CVD) remain a leading cause of global mortality, with atherosclerosis and inflammation playing pivotal roles in their development. The neutrophil-to-lymphocyte ratio (NLR) and neutrophil-to-HDL cholesterol ratio (NHR) have emerged as potential biomarkers for assessing CVD risk. In this community-based cohort study conducted in Taiwan, involving 3278 participants, we investigated the associations between NHR, NLR, and the risks of CVD and all-cause mortality. Our findings revealed that both NHR and NLR were effective in identifying individuals at high risk for CVD. However, when assessing their joint effect, NHR alone demonstrated a stronger predictive value for CVD prognosis than NLR or the combination of both markers. Furthermore, NLR alone showed potential as a predictor of all-cause mortality when compared with NHR alone or in combination with NLR and NHR. These findings underscore the complex interplay between inflammation and lipid metabolism in the pathogenesis of CVD. While NHR shows promise as a cost-effective tool for CVD risk assessment, NLR emerges potential as a prognostic marker for mortality. Further research is warranted to explore the dynamic changes in these markers and their implications for clinical practice.

Non-enzymatic cholesterol biosensor: Electrochemical sensing based on peptide-polylactic acid thin film

Cholesterol is a fundamental lipid prevalent in eukaryotic cell membranes and circulating in the bloodstream bound to lipoproteins. It serves as a precursor to steroid hormones and is regarded as a biomarker for cardiovascular disease and other metabolic disorders. Numerous cholesterol detection methods predominantly rely on enzymes, which suffer from instability, leading to non-cost-effective biosensors with low sensitivity and poor reusability. Therefore, monitoring cholesterol levels with a feasible, rapid, and stable biosensor is critical for diagnosing and treating various disorders. This study aimed to develop a non-enzymatic cholesterol biosensor based on a selected cholesterol recognition peptide as the detection element. Screen-printed carbon electrodes (SPEs) modified with biocompatible poly-L-lactic acid (PLLA) porous nanomembranes (NMs) were utilized as support for the covalent immobilization of the peptide. Data obtained from electrochemical impedance spectroscopy (EIS) demonstrated the peptide's effective binding affinity towards cholesterol, paving the way for its implementation. The determination of cholesterol with the proposed biosensor exhibited a low limit of detection of 6.31 μM with linear responses ranging from 2–15 μM and 20–40 μM. These findings present an alternative method for cholesterol sensing by integrating novel peptides as biorecognition motifs with biocompatible polymeric materials, potentially useful as biocompatible and future point-of-care sensors.

Old, the new, more or less and the conundrum for biomarkers in cardiovascular diseases?

Biomarkers are critical for diagnostic, monitoring and management of cardiovascular diseases. Opportunities to improve how biomarkers are used are important. This editorial on biomarkers in coronary artery disease provides commentary on the study as well as broad benchmarks on what make ideal biomarkers. Biomarker discovery is difficult and opportunities to expand and improve their use should be encouraged.

An improved amperometric cholesterol biosensor based on cholesterol oxidase nanostructures for pre-diagnosis of myocardial infarction

Cholesterol plays a pivotal role in human health, serving as a crucial biomarker for cardiovascular diseases, including myocardial infarction. This study presents the development of an innovative amperometric cholesterol biosensor that enhances the detection and quantification of cholesterol levels in serum. The biosensor integrates cholesterol oxidase (ChOx) nanoparticles with a modified electrode, leveraging the unique properties of platinum nanoparticles (PtNPs) and graphene nanosheets (GNs) to improve sensitivity and stability. The synthesis of PtNPs was achieved using Camellia sinensis extract, while graphene oxide was reduced to form GNs. At 2.39 mg/mL or above is deemed a biomarker for cardiovascular disorders, peripheral artery disease, heart attack, diabetes mellitus, strokes, and hypertension. The monitoring of serum cholesterol level is therefore very significant. In the present study, an innovative amperometric cholesterol biosensor was constructed by immobilizing nanoparticles of cholesterol oxidase onto a pencil graphite (PG) electrode modified with graphene nanosheets (GNs), platinum nanoparticles (PtNPs), and chitosan (CHIT). At various stages of construction, the modified electrode was characterized by employing electrical impedance spectroscopy (EIS) and cyclic voltammetry (CV), scanning electron microscopy (SEM), and energy dispersive X-ray (EDX) spectroscopy. The biosensor responded best when run at 0.14Vs-1 at optimal pH and temperature of 8.0 and 35°C respectively. The biosensor has a wide linear range (0.1mg/mL-7.5 mg/mL), with great sensitivity (0.89 mA cm−1mgmL−1) and a low limit of detection (0.97 mg/mL). This research not only contributes to the field of biosensing but also offers a promising tool for the early diagnosis of cholesterol-related health issues, paving the way for enhanced cardiovascular disease management.

7669 Higher Serum Uric Acid Levels Are Associated With a Deleterious Metabolic and Inflammatory Profile in Brazilian Adolescents: An Exploratory Cross-Sectional Analysis

Abstract Disclosure: F.Q. Iorra: None. M.P. Guahnon: None. P.G. Rodrigues: None. A.T. Barcelos: None. F.V. Cureau: None. M. Drehmer: None. B.D. Schaan: None. Introduction: The association of high serum uric acid (sUA) with metabolic syndrome (MetS) and its components have been widely studied, but there are still gaps in how this breakdown product of purine metabolism might refine cardiovascular risk assessment and correlate with other cardiovascular disease biomarkers, especially in children and adolescents. Objective: To evaluate if sUA is associated with metabolic syndrome components and inflammatory markers in Brazilian adolescents. Methods: For this cross-sectional study, 786 individuals aged 12 to 17 years old, previously enrolled in the Study of Cardiovascular Risk in Adolescents (ERICA) - a Brazilian nationwide school based study, and who were from the city of Porto Alegre, had their sUA measured from blood samples that were stored in a biorepository. Anthropometric, biochemical and blood pressure data were collected. MetS diagnosis was based on the International Diabetes Federation age-specific criteria (2005), and insulin resistance was assessed by the HOMA-IR. In accordance with a non-parametric distribution, sUA was divided into quartiles (3.7 mg/dL, 4.4 mg/dL, 5.3 mg/dL for the 25th, 50th, and 75th percentiles, respectively) for the analysis. A linear regression model and a Poisson regression model with robust error variance were used, both adjusted for age, sex and skin color. Results: Participants were 14.8 ± 1.5 years-old, predominantly women (61.7%), self-identified as white skin color (72%) and eutrophic (66.9%). Through the linear regression model, significant positive associations were found between high sUA levels and body mass index Z-score, waist circumference, systolic and diastolic blood pressure, total cholesterol, triglycerides, HOMA-IR and C-reactive protein, and significant negative associations were observed for HDL cholesterol and adiponectin. No association was found between sUA and glucose or HbA1c. We also computed a metabolic risk score as the mean Z score of waist circumference, systolic blood pressure, HDL cholesterol (negative Z score), triglycerides and glucose, which was positive related to sUA (β ± SE = 0.13 ± 0.02; p < 0.001). Finally, the Poisson regression model was applied to estimate the prevalence ratios (PR) for MetS and its components, between adolescents with sUA in the 4th quartile to those in the 1st quartile. An association was observed for MetS (PR 6.37, 95% CI 1.39 - 29.21, p 0.017), high waist circumference (PR 4.61, 95% CI 2.55 - 8.36, p < 0.001) and increased triglycerides (PR 4.76, 95% CI 1.47 - 15.44, p 0.009). Conclusion: High sUA levels were associated with a worse metabolic and inflammatory profile, as well as a greater prevalence of MetS and some of its components in adolescents. Therefore, uric acid should be considered as a potential additional marker of cardiovascular risk in this population. Support: CNPq, CAPES, FIPE, FAPERGS. Presentation: 6/1/2024

9193 Higher Serum Uric Acid Levels Are Associated With a Deleterious Metabolic and Inflammatory Profile in Brazilian Adolescents: An Exploratory Cross-Sectional Analysis

Abstract Disclosure: F.Q. Iorra: None. M.P. Guahnon: None. P.G. Rodrigues: None. A.T. Barcelos: None. F.V. Cureau: None. M. Drehmer: None. B.D. Schaan: None. Introduction: The association of high serum uric acid (sUA) with metabolic syndrome (MetS) and its components have been widely studied, but there are still gaps in how this breakdown product of purine metabolism might refine cardiovascular risk assessment and correlate with other cardiovascular disease biomarkers, especially in children and adolescents. Objective: To evaluate if sUA is associated with metabolic syndrome components and inflammatory markers in Brazilian adolescents. Methods: For this cross-sectional study, 786 individuals aged 12 to 17 years old, previously enrolled in the Study of Cardiovascular Risk in Adolescents (ERICA) - a Brazilian nationwide school based study, and who were from the city of Porto Alegre, had their sUA measured from blood samples that were stored in a biorepository. Anthropometric, biochemical and blood pressure data were collected. MetS diagnosis was based on the International Diabetes Federation age-specific criteria (2005), and insulin resistance was assessed by the HOMA-IR. In accordance with a non-parametric distribution, sUA was divided into quartiles (3.7 mg/dL, 4.4 mg/dL, 5.3 mg/dL for the 25th, 50th, and 75th percentiles, respectively) for the analysis. A linear regression model and a Poisson regression model with robust error variance were used, both adjusted for age, sex and skin color. Results: Participants were 14.8 ± 1.5 years-old, predominantly women (61.7%), self-identified as white skin color (72%) and eutrophic (66.9%). Through the linear regression model, significant positive associations were found between high sUA levels and body mass index Z-score, waist circumference, systolic and diastolic blood pressure, total cholesterol, triglycerides, HOMA-IR and C-reactive protein, and significant negative associations were observed for HDL cholesterol and adiponectin. No association was found between sUA and glucose or HbA1c. We also computed a metabolic risk score as the mean Z score of waist circumference, systolic blood pressure, HDL cholesterol (negative Z score), triglycerides and glucose, which was positive related to sUA (β ± SE = 0.13 ± 0.02; p < 0.001). Finally, the Poisson regression model was applied to estimate the prevalence ratios (PR) for MetS and its components, between adolescents with sUA in the 4th quartile to those in the 1st quartile. An association was observed for MetS (PR 6.37, 95% CI 1.39 - 29.21, p 0.017), high waist circumference (PR 4.61, 95% CI 2.55 - 8.36, p < 0.001) and increased triglycerides (PR 4.76, 95% CI 1.47 - 15.44, p 0.009). Conclusion: High sUA levels were associated with a worse metabolic and inflammatory profile, as well as a greater prevalence of MetS and some of its components in adolescents. Therefore, uric acid should be considered as a potential additional marker of cardiovascular risk in this population. Support: CNPq, CAPES, FIPE, FAPERGS. Presentation: 6/1/2024

MicroRNAs as diagnostic biomarkers in cardiovascular diseases that cause sudden cardiac death: comparison between methods used in discovery and validation phases in major research studies

MicroRNAs as diagnostic biomarkers in cardiovascular diseases that cause sudden cardiac death: comparison between methods used in discovery and validation phases in major research studies

Synergy Between NK Cells and Monocytes in Potentiating Cardiovascular Disease Risk in Severe COVID-19.

Evidence suggests that COVID-19 predisposes to cardiovascular diseases (CVDs). While monocytes/macrophages play a central role in the immunopathogenesis of atherosclerosis, less is known about their immunopathogenic mechanisms that lead to CVDs during COVID-19. Natural killer (NK) cells, which play an intermediary role during pathologies like atherosclerosis, are dysregulated during COVID-19. Here, we sought to investigate altered immune cells and their associations with CVD risk during severe COVID-19. We measured plasma biomarkers of CVDs and determined phenotypes of circulating immune subsets using spectral flow cytometry. We compared these between patients with severe COVID-19 (severe, n=31), those who recovered from severe COVID-19 (recovered, n=29), and SARS-CoV-2-uninfected controls (controls, n=17). In vivo observations were supported using in vitro assays to highlight possible mechanistic links between dysregulated immune subsets and biomarkers during and after COVID-19. We performed multidimensional analyses of published single-cell transcriptome data of monocytes and NK cells during severe COVID-19 to substantiate in vivo findings. During severe COVID-19, we observed alterations in cardiometabolic biomarkers including oxidized-low-density lipoprotein, which showed decreased levels in severe and recovered groups. Severe patients exhibited dysregulated monocyte subsets, including increased frequencies of proinflammatory intermediate monocytes (also observed in the recovered) and decreased nonclassical monocytes. All identified NK-cell subsets in the severe COVID-19 group displayed increased expression of activation and tissue-resident markers, such as CD69 (cluster of differentiation 69). We observed significant correlations between altered immune subsets and plasma oxidized-low-density lipoprotein levels. In vitro assays revealed increased uptake of oxidized-low-density lipoprotein into monocyte-derived macrophages in the presence of NK cells activated by plasma of patients with severe COVID-19. Transcriptome analyses confirmed enriched proinflammatory responses and lipid dysregulation associated with epigenetic modifications in monocytes and NK cells during severe COVID-19. Our study provides new insights into the involvement of monocytes and NK cells in the increased CVD risk observed during and after COVID-19.

Is cardiovascular risk profiling from UK Biobank retinal images using explicit deep learning estimates of traditional risk factors equivalent to actual risk measurements? A prospective cohort study design

ObjectiveDespite extensive exploration of potential biomarkers of cardiovascular diseases (CVDs) derived from retinal images, it remains unclear how retinal images contribute to CVD risk profiling and how the results can...

Циркулирующие микроРНК тромбоцитарного происхождения как потенциальные биомаркеры STEMI у пациентов с гипертонической болезнью

Background: Circulating extracellular platelet-derived microRNAs have been actively studied over the last decade as promising biomarkers of cardiovascular disease (CVD), since platelet activation plays a key role in the pathogenesis of CVD. The aim of the study: To compare platelet-derived microRNA profiles in patients with uncomplicated hypertension (HT) and in patients with HT and acute myocardial infarction with ST-segment elevation (STEMI). Materials and methods: The study included 20 patients with uncomplicated HT and 15 patients with HT and STEMI. At least 90% of the participants in each group received antiplatelet therapy. A blood sample was collected from each patient in a CTAD anticoagulant tube and blood plasma was obtained by two-step centrifugation. The degree of hemolysis of the plasma samples was determined spectrophotometrically. MicroRNAs were isolated from plasma samples and used for reverse transcription and quantification of relative levels of eight main circulating extracellular platelet-derived microRNAs (miR-223-3p, miR-126-3p, miR21-5p, miR-24-3p, miR-320a-3p, miR-191-5p, miR-150-5p and miR-23a-3p) by quantitative PCR using the TaqMan Advanced technology (Thermo Fisher Scientific, USA). Normalized relative expression levels for each miRNA were calculated. Differences were considered statistically significant at p < 0.05 (Mann-Whitney test). Results: Patient groups did not differ in age, BMI, platelet count, lipid profile and degree of hemolysis of plasma samples. No differences were found between the ratio of platelet-derived and erythrocyte-derived microRNA between patient groups. No statistically significant differences were found in the relative levels of circulating microRNA between the study groups. Principal component analysis and heatmap analysis of microRNA expression in the samples showed a division of the samples into groups based more on the degree of hemolysis than on the presence/absence of STEMI. Conclusion: In the studied sample of hypertensive patients, the effect of hemolysis of plasma samples on circulating platelet-derived microRNA profiles was more significant than the presence of STEMI.

THE EFFECT OF FUNCTIONAL PRODUCTS ON BIOMARKERS DIAGNOSING CARDIOVASCULAR DISEASES

Functional foods and their biologically active compounds have been widely studied as a group of foods of great importance for preventing the development of chronic diseases. Cardiovascular disease is a global health problem that can be alleviated with functional foods. The reduction in the risk of cardiovascular disease can be measured using specific biomarkers of cardiovascular disease, such as lipid profile, endothelial function, platelet activation, hemostasis and biomarkers of inflammation. Some functional biologically active compounds may play an important role in the prevention and treatment of cardiovascular diseases, beneficially affecting the levels of these biomarkers.The purpose of this study was to study the effect of functional foods on biomarkers of cardiovascular diseases, as well as the possible improvement of indicators when taking a functional food mixture.Methods: A literature search to identify articles was conducted using PubMed, Science Direct.The results were analyzed in twenty-seven publications. In all these publications, the positive effect of functional products on biomarkers has been reported. Most often, positive results were noted from the use of soy products, dairy products, pomegranates, cranberries and vegetarian diets and the Okinawa diet.

Chemerin in the Spotlight: Revealing Its Multifaceted Role in Acute Myocardial Infarction.

Chemerin, an adipokine known for its role in adipogenesis and inflammation, has emerged as a significant biomarker in cardiovascular diseases, including acute myocardial infarction (AMI). Recent studies have highlighted chemerin's involvement in the pathophysiological processes of coronary artery disease (CAD), where it modulates inflammatory responses, endothelial function, and vascular remodelling. Elevated levels of chemerin have been associated with adverse cardiovascular outcomes, including increased myocardial injury, left ventricular dysfunction, and heightened inflammatory states post-AMI. This manuscript aims to provide a comprehensive review of the current understanding of chemerin's role in AMI, detailing its molecular mechanisms, clinical implications, and potential as a biomarker for diagnosis and prognosis. Additionally, we explore the therapeutic prospects of targeting chemerin pathways to mitigate myocardial damage and improve clinical outcomes in AMI patients. By synthesizing the latest research findings, this review seeks to elucidate the multifaceted role of chemerin in AMI and its promise as a target for innovative therapeutic strategies.

Prospects of using miRNA-378 as a biomarker for cardiovascular diseases: A literature review

Currently, there is an active search for new biomarkers and therapeutic targets to develop effective approaches to risk stratification and secondary prevention of cardiovascular diseases (CVD). Microribonucleic acids (miRNAs) are of particular interest to investigators. MiRNAs are endogenous small noncoding RNAs that regulate the transcription of factors that play a role in the proliferation, differentiation, cell growth, and tissue remodeling processes in CVD. MiRNA-378 is currently being analyzed as a biomarker for CVD. Thus, in this review, we aimed to describe the regulatory role of miRNA-378 and provide strong evidence for its feasibility as a biomarker. Further preclinical and clinical studies are required to identify the potential benefits of miRNA-378 as a biomarker in CVD.

Non-linear association of the platelet/high-density lipoprotein cholesterol ratio with bone mineral density a cross-sectional study

BackgroundNumerous studies have demonstrated shared risk factors and pathophysiologic mechanisms between osteoporosis and cardiovascular disease. High-density lipoprotein cholesterol (HDL-C) and platelets have long been recognized as crucial factors for cardiovascular health. The platelet to HDL-C ratio (PHR) combines platelet count and high-density lipoprotein cholesterol (HDL-C) level, It is a novel biomarker for metabolic syndrome and cardiovascular disease. The platelet to HDL-C ratio (PHR) possibly reflects the balance between proinflammatory and anti-inflammatory states in the body. Therefore, we hypothesized that changes in PHR ratios may predict a predisposition to pro-inflammatory and increased bone resorption. However, the relationship between the platelet to HDL-C ratio (PHR) and bone mineral density (BMD) remains insufficiently understood. This study aimed to elucidate the relationship between the platelet to HDL-C ratio (PHR) index and bone mineral density (BMD).MethodsData from the NHANES 2005–2018 were analyzed, excluding adults with missing key variables and specific conditions. Nonlinear relationships were explored by fitting smoothed curves and generalized additive models, with threshold effects employed to calculate inflection points. Additionally, subgroup analyses and interaction tests were conducted.ResultsThe study included 13,936 individuals with a mean age of 51.19 ± 16.65 years. Fitted smoothed curves and generalized additive models revealed a nonlinear, inverted U-shaped relationship between the two variables. Threshold effect analysis showed a significant negative association between PHR and total femur bone mineral density (BMD) beyond the inflection point of platelet to HDL-C ratio (PHR) 33.301. Subgroup analyses showed that a significant interaction between these two variables was observed only in the age and sex subgroups (P-interaction < 0.05).ConclusionsOur study identified a complex, nonlinear, inverted U-shaped relationship between platelet to HDL-C ratio (PHR) and total femur bone mineral density (BMD). These findings underscore the importance of maintaining optimal PHR levels to support bone health, especially in high-risk populations.

Telomere Length Is Associated with Increased Risk of Cardiovascular Events in Patients with End-Stage Kidney Disease on Hemodialysis

Introduction: Patients with chronic kidney disease, especially those with end-stage kidney disease (ESKD) on hemodialysis (HD), are at increased risk for cardiovascular disease (CVD), including myocardial infarction and ischemic stroke. A shortening in telomere length, as a parameter for accelerated vascular aging, is an established biomarker for CVD in the general population. We aimed to elucidate the role of telomere length in ESKD patient on HD and its association with cardiovascular outcomes. Methods: Telomere length was measured in a prospective population-based cohort study of prevalent HD patients. DNA was isolated from whole blood, sampled at baseline, and analyzed for telomere length via a qPCR-based approach. The risk for the occurrence of the independently adjudicated three-point major adverse cardiovascular event outcome (myocardial infarction, ischemic stroke, and cardiovascular death) was statistically analyzed considering the competing risk of non-cardiovascular death. Results: In the cohort of 308 patients with ESKD (115 [37.3%] women, median [25th–75th percentile] age: 67.0 [56.8–76.0]), the median telomere length was 1.51 kb (25th–75th percentile 0.6–3.2 kb). The 3P-MACE outcome occurred with an incidence rate of 9.4 per 100 patient-years. Patients with longer telomere length more frequently had vascular nephropathy compared to patients with shorter telomere length. Interestingly, patients in the highest quartile of telomere length had a 1.8-fold increased risk for 3P-MACE (95% CI: 1.051–3.201, p = 0.033), after multivariable adjustment for age, history of stroke, myocardial infarction, venous thromboembolism, presence of heart valve replacement, atrial fibrillation, smoking, anticoagulation, or immunosuppressive use. Conclusion: Surprisingly, in this high-risk cohort of patients with ESKD on HD, longer telomere lengths were associated with increased risk of cardiovascular events.

The impact of breast cancer radiation therapy exposure on the prevalence of breast arterial calcification.

Mammographic breast arterial calcification (BAC) is an emerging imaging biomarker of cardiovascular disease (CVD) risk in women. The purpose of this study was to assess if breast radiation therapy (RT) exposure impacts the screening utility of this imaging biomarker. This cross-sectional study included women ages 40-75 years who underwent index screening mammography between January 1, 2011 and December 31, 2012. Chart review was performed to extract data on the breast cancer RT exposure and CVD risk factors. Mammograms were reviewed for the presence of BAC. Multivariate logistic regression was used to examine breast RT exposure and BAC, with adjustment for age, body mass index, smoking status, hypertension, Type 2 diabetes, statin medication use, and antihypertensive medication use. Of the 1155 women included in this analysis, 222 (19.2%) had mammographic evidence of BAC, 122 (10.6%) had a history of RT exposure, and 39 (32%) women with RT exposure had mammographic BAC. Women with breast RT exposure had higher odds of BAC compared to women without (odds ratio: 2.18, 95% CI: 1.43, 3.28; P-value = .0008). However, this association became non-significant after multivariable adjustment, with the maximally adjusted model demonstrating an odds ratio of 1.52 (95% CI: 0.95, 2.40; P-value = .07). Our findings suggest that breast RT exposure does not impact the prevalence of mammographic BAC. Therefore, it does not affect its utility as an imaging biomarker of CVD risk. This is the first observational study addressing the knowledge gap pertaining to the influence of breast RT exposure on BAC.

Serum BAFF level is associated with the presence and severity of coronary artery disease and acute myocardial infarction

ObjectiveThe aim of this study was to investigate the relationship between circulating levels of B cell activating factor (BAFF) and the presence and severity of coronary artery disease (CAD) and acute myocardial infarction (AMI) in humans, as its biological functions in this context remain unclear.MethodsSerum BAFF levels were measured in a cohort of 723 patients undergoing angiography, including 204 patients without CAD (control group), 220 patients with stable CAD (CAD group), and 299 patients with AMI (AMI group). Logistic regression analyses were used to assess the association between BAFF and CAD or AMI.ResultsSignificantly elevated levels of BAFF were observed in patients with CAD and AMI compared to the control group. Furthermore, BAFF levels exhibited a positive correlation with the SYNTAX score (r = 0.3002, P < 0.0001) and the GRACE score (r = 0.5684, P < 0.0001). Logistic regression analysis demonstrated that increased BAFF levels were an independent risk factor for CAD (adjusted OR 1.305, 95% CI 1.078–1.580) and AMI (adjusted OR 2.874, 95% CI 1.708–4.838) after adjusting for confounding variables. Additionally, elevated BAFF levels were significantly associated with a high GRACE score (GRACE score 155 to 319, adjusted OR 4.297, 95% CI 1.841–10.030). BAFF exhibited a sensitivity of 75.0% and specificity of 71.4% in differentiating CAD patients with a high SYNTAX score, and a sensitivity of 75.5% and specificity of 72.8% in identifying AMI patients with a high GRACE score.ConclusionCirculating BAFF levels serve as a valuable diagnostic marker for CAD and AMI. Elevated BAFF levels are associated with the presence and severity of these conditions, suggesting its potential as a clinically relevant biomarker in cardiovascular disease.

Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction.

S100A8 and S100A9, which are prominent members of the calcium-binding protein S100 family and recognized as calprotectin, form a robust heterodimer known as S100A8/A9, crucial for the manifestation of their diverse biological effects. Currently, there is a consensus that S100A8/A9 holds promise as a biomarker for cardiovascular diseases (CVDs), exerting an influence on cardiomyocytes or the cardiovascular system through multifaceted mechanisms that contribute to myocardial injury or dysfunction. In particular, the dualistic nature of S100A8/A9, which functions as both an inflammatory mediator and an anti-inflammatory agent, has garnered significantly increasing attention. This comprehensive review explores the intricate mechanisms through which S100A8/A9 operates in cardiovascular diseases, encompassing its bidirectional regulatory role in inflammation, the initiation of mitochondrial dysfunction, the dual modulation of myocardial fibrosis progression, and apoptosis and autophagy. The objective is to provide new information on and strategies for the clinical diagnosis and treatment of cardiovascular diseases in the future.