Atherosclerotic Markers Research Articles

Factors associated with carotid artery calcification in the general working-age population

Aim. To study factors associated with carotid artery calcification as an atherosclerotic marker in the general working-age population.Material and methods. The data of a representative ESSE-RF sample aged 25-64 years (n=1412) were studied. They underwent standard cardiology screening and assessment of carotid plaque (CP) characteristics using ultrasound. All respondents signed an informed consent to participate in the study. The association analysis included socio-demographic, anamnestic, laboratory, and ultrasound characteristics. Univariate and multivariate statistics were used.Results. The prevalence of detection of calcified CP (cCP) was 5,4% — 7,8% in men and 3,7% in women (odds ratio (OR)=2,2; p=0,001). The probability of cCP detection was associated with following factors: male sex (OR=3,9; p<0,001), age (OR=1,2; p<0,001), total cholesterol (women, OR=1,7; p=0,001), history of thyrotoxicosis (OR=2,1; p=0,034), osteoporosis (OR=2,6; p=0,009), and smoking (OR=1,8; p=0,046). The odds that the detected plaque would be calcified were higher in individuals in the 4th quartile of mean plaque size distribution (OR=3,8; p<0,001) and in the presence of the following factors: male sex (OR=1,9; p=0,031), age ≥55 years (OR=4,3; p<0,001), osteoporosis (OR=3,2; p=0,007), high-density lipoprotein cholesterol level ≥1,3 mmol/l (OR=2,0; p=0,025).Conclusion. The obtained data indicate an association of carotid calcification with both traditional cardiovascular risk factors and systemic diseases associated with impaired calcium and phosphorus metabolism (thyrotoxicosis, osteoporosis). The study results can be useful in practical healthcare, research, and developing preventive technologies.

Gingival inflammation and leukocyte-endothelium cell interactions in women with polycystic ovary syndrome.

Given the link between chronic inflammation and periodontal pathologies and increased cardiovascular risk, this study aims to investigate if gingivitis exacerbates the inflammatory response and subclinical atherosclerotic markers in women with polycystic ovary syndrome (PCOS). For this case-control study, women were assigned to three groups: two PCOS groups (with and without gingivitis) and a control group. Anthropometric and biochemical variables were determined, along with periodontal parameters (probing pocket depth [PPD], clinical attachment level [CAL], bleeding on probing [BOP], plaque index, calculus index, and tooth loss), systemic and neutrophil inflammatory markers (tumor necrosis factor alpha [TNFα], C-reactive protein [CRP], and c-Jun N-terminal kinase [JNK]), systemic oxidative stress mediators (myeloperoxidase [MPO] and glutathione), soluble cellular adhesion molecules, and neutrophil-endothelium cell interactions (rolling flux, velocity, and adhesion). Of 104 women recruited, 68 had PCOS, 24 of whom presented gingivitis, and 36 were controls. PCOS patients presented altered sexual hormone, lipid, and carbohydrate profiles. Levels of systemic inflammatory markers, MPO, and soluble platelet selectin (sP-selectin) were higher, and glutathione levels were lower in PCOS patients. BOP, plaque, and calculus index values were higher in PCOS patients with gingivitis. Neutrophils from PCOS patients showed increased JNK and decreased adhesion under flow conditions, with reduced rolling velocity and increased rolling flux and cellular adhesion, all of which were more pronounced in those with gingivitis. BOP was independently associated with rolling velocity, rolling flux, and cellular adhesion. Neutrophils of PCOS patients with gingivitis exhibit hyperactivity, promoting interaction with the endothelium and potentially contributing to atherosclerotic disease. Currently, there is a high prevalence of diseases that affect tooth-supporting tissues (periodontal diseases) and negatively influence the oral health and quality of life of the adult population. These pathologies lead to movement of the teeth and impairment of chewing function, eventually resulting in the loss of teeth. In recent years, the concept of periodontal medicine has arisen and consists of studying how periodontal diseases can influence our general inflammatory system and how systemic inflammatory pathologies can affect our oral health. In the present study, we evaluate a group of women with polycystic ovary syndrome (PCOS), a condition characterized by alterations of sex hormones and lipid profile and weight gain (body mass index). Our results show a high prevalence of gum inflammation among women with PCOS, which affects the interaction of their leukocytes and endothelial cells. The leukocytes of these women are hyper-responsive, presenting greater endothelial adhesion, lower flow velocity and enhanced rolling compared to those in a PCOS group without gum inflammation or controls. This study has generated a new line of research to analyze how neutrophils from patients with gingivitis exhibit hyperactivity, which promotes their interaction with the endothelium, thus contributing to the development of atherosclerotic disease.

Benzo[b]fluoranthene damages coronary artery and affects atherosclerosis markers in mice and umbilical vein endothelial cells

Polycyclic aromatic hydrocarbons (PAHs) exposure is associated with cardiovascular diseases. Toxic effects of PAHs are diverse, while cardiovascular consequences of benzo[b]fluoranthene (B[b]F) are unclear. Here, we reported the impacts of B[b]F on coronary artery and atherosclerosis markers both in mice and umbilical vein endothelial EAhy.926 cells. In mice, we found that B[b]F decreases heart-to-body weight ratio, affects aortic physiology, elevates serum low-density lipoprotein and total cholesterol, increases aortic levels of collagen fiber and atherosclerotic marker vascular cell adhesion molecule-1 (VCAM-1), and downregulates oxidative stress related nuclear factor erythroid 2-related factor 2 (Nrf2). In EAhy.926 cells, we showed that B[b]F inhibits cell proliferation and migration in a dose-dependent manner, induces cell cycle arrest and apoptosis, increases reactive oxygen species, upregulates VCAM-1 level, and suppresses expression of Nrf2. Taken together, our findings reveal that B[b]F exposure may contribute to coronary artery damage and potentially induce atherosclerosis, possibly via the Nrf2-related signaling pathways.

Adhesion molecules and atherosclerosis in ankylosing spondylitis: implications for cardiovascular risk.

Ankylosing Spondylitis (AS) stands as a chronic inflammatory arthritis within the spondyloarthritis spectrum, notably increasing cardiovascular (CV) risk and mortality through accelerated atherosclerosis compared to the non-affected population. While evidence in some studies supports a higher cardiovascular morbidity in AS patients, results from other studies reveal no significant disparities in atherosclerotic markers between AS individuals and healthy controls. This discrepancy may arise from the complex interaction between traditional CV risk factors and AS inflammatory burden. Endothelial dysfunction, a recognized antecedent of atherosclerosis prevalent among most individuals with AS, demonstrates the synergistic impact of inflammation and conventional risk factors on endothelial injury, consequently hastening the progression of atherosclerosis. Remarkably, endothelial dysfunction can precede vascular pathology in AS, suggesting a unique relationship between inflammation, atherosclerosis, and vascular damage. The role of adhesion molecules in the development of atherosclerosis, facilitating leukocyte adherence and migration into vascular walls, underscores the predictive value of soluble intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) levels for cardiovascular events. Despite significant progress in comprehending the pathogenesis of AS and its associated cardiovascular implications, the interplay among inflammation, endothelial dysfunction, and atherosclerosis remains partially elucidated. Investigations into the efficacy of therapeutic approaches involving angiotensin receptor blockers and statins have demonstrated reduced cardiovascular risk in AS patients, underscoring the imperative for additional research in this domain.

Coexistence of high visceral fat area and sarcopenia is associated with atherosclerotic markers in old-old patients with diabetes: A cross-sectional study.

To investigate whether sarcopenic obesity is associated with the progression of atherosclerotic lesions in older patients with diabetes and to identify the obesity components of sarcopenic obesity that best reflect atherosclerosis. In 118 inpatients aged ≥75 years with diabetes mellitus, sarcopenia defined as a low skeletal muscle mass and low grip strength was assessed, and sarcopenia coexisting with a high body-fat percentage or visceral fat area was defined as sarcopenic obesity. Correlations between the obesity components and atherosclerotic markers, including the carotid intima-media thickness, were analyzed; the intima-media thickness was analyzed in four groups with and without obesity and sarcopenia, and a multiple linear regression analysis adjusted for covariates was conducted to investigate whether sarcopenic obesity was independently associated with the intima-media thickness. The visceral fat area and intima-media thickness showed positive correlations in the overall patients (P = 0.032) and the sarcopenia (P = 0.016) group but showed no associations in participants without sarcopenia. The intima-media thickness in the group showing sarcopenia with a high visceral fat area was significantly higher than that in the control group (P = 0.012). Sarcopenic obesity defined by a high body-fat percentage and high visceral fat area was independently associated with the intima-media thickness even after adjusting for age, sex, and atherogenic risk factors. However, sarcopenic obesity defined by a high visceral fat area was more strongly associated with the intima-media thickness (β = 0.384, P = 0.002) than that defined by the high body-fat percentage (β = 0.237, P = 0.068). Sarcopenic obesity, especially that defined by visceral fat accumulation, reflected the risk of atherosclerotic lesion progression in older patients with diabetes.

Local vascular Klotho mediates diabetes-induced atherosclerosis via ERK1/2 and PI3-kinase-dependent signaling pathways

Background and aimsDiabetes is one of the major causes of cardiovascular disease (CVD). As high as 29 % of patients with diabetes develop atherosclerosis. Vascular Smooth Muscle Cells (VSMCs) are a key mediator in the pathogenesis of atherosclerosis, generating pro-inflammatory and proliferative characteristics in atherosclerotic lesions. MethodsWe used human atherosclerotic samples, developed diabetes-induced atherosclerotic mice, and generated loss of function and gain of function in Klotho human aortic smooth muscle cells to investigate the function of Klotho in atherosclerosis. ResultsWe found that Klotho expression is decreased in smooth muscle actin-positive cells in patients with diabetes and atherosclerosis. Consistent with human data, we found that Apoe knockout mice with streptozotocin-induced diabetes fed on a high-fat diet showed decreased expression of Klotho in SMCs. Additionally, these mice showed increased expression of TGF-β, MMP9, phosphorylation of ERK and Akt. Further, we utilized primary Human Aortic Smooth Muscle Cells (HASMCs) with d-glucose under dose-response and in time-dependent conditions to study the role of Klotho in these cells. Klotho gain of function and loss of function studies showed that Klotho inversely regulated the expression of atherosclerotic markers TGF-β, MMP2, MMP9, and Fractalkine.Further, High Glucose (HG) induced Akt, and ERK1/2 phosphorylation were enhanced or mitigated by endogenous Klotho deficiency or its overexpression respectively. PI3K/Akt and MAPK/ERK inhibition partially abolished the HG-induced upregulation of TGF-β, MMP2, MMP9, and Fractalkine. Additionally, Klotho knockdown increased the proliferation of HASMCs and enhanced α-SMA and TGF-β expression. ConclusionsTaken together, these results indicate that local vascular Klotho is involved in diabetes-induced atherosclerosis, which is via PI3K/Akt and ERK1/2-dependent signaling pathways.

Serum Paraoxonase 1 and Gene Polymorphism (PON- Q192R) as an Atherosclerotic Marker in Chronic Kidney Disease Patients in Menoufia University Hospitals- Egypt

Serum Paraoxonase 1 and Gene Polymorphism (PON- Q192R) as an Atherosclerotic Marker in Chronic Kidney Disease Patients in Menoufia University Hospitals- Egypt

Upstroke time is a more useful marker of atherosclerosis than percentage of mean arterial pressure for detecting coronary artery disease in subjects with a normal ankle-brachial index

Upstroke time (UT) and percentage of mean arterial pressure (%MAP) at the ankle have been shown to serve as atherosclerotic markers. The purpose of this study was to directly compare the diagnostic accuracy of UT with that of %MAP for clinical coronary artery disease (CAD) in subjects with a normal ankle-brachial index (ABI) in both legs. We measured UT and %MAP in 1953 subjects with a normal ABI. The optimal cutoff values of UT and %MAP derived from a receiver operating characteristic (ROC) curve to diagnose CAD were 148 ms and 40.4%, respectively. Multivariable analyses revealed that both UT ≥ 148 ms (odds ratio [OR], 2.72; p < 0.001) and %MAP ≥ 40.4% (OR, 1.28; p = 0.003) were significantly associated with CAD. When the subjects were divided into four groups according to the cutoff values of UT and %MAP, there was no significant difference in the risk of CAD between subjects with UT ≥ 148 ms and %MAP < 40.4% and those with UT ≥ 148 ms and %MAP ≥ 40.4% (OR, 1.45; p = 0.09). ROC curve analyses revealed that the area under the curve value of UT was significantly higher than that of %MAP (0.69 vs. 0.53, p < 0.001). The addition of UT to traditional risk factors significantly improved the diagnostic accuracy for CAD (0.82 to 0.84, p = 0.004), whereas the addition of %MAP to traditional risk factors did not improve the diagnostic accuracy for CAD (0.82 to 0.82, p = 0.84). UT is more useful than %MAP for identifying individuals with CAD among those with a normal ABI.

Lipoprotein(a): Levels and Reference Intervals Among People in Saudi Arabia.

Blood Lp(a) concentration is recognized as an independent risk factor for cardiovascular disease (CVD). Population-based lipoprotein(a) (Lp[a]) research in Saudi Arabia is rare. Thus, the primary goal of this pilot study was to identify age- and sex-specific reference ranges for Lp(a) levels, in addition to the associations between Lp(a) levels and other atherosclerotic markers in Saudi individuals. A five-year retrospective study of Lp(a) and lipid markers in Saudi patients was conducted using the Al-Borg diagnostics database (2015-2020). The population sample consisted of 361 Saudi individuals aged 18-93 years (162 males, 199 females). An immunoturbidimetric technique was used to determine Lp(a) concentration. The mean and median Lp(a) levels in the study population were 35 nmol/L and 50 nmol/L, respectively. Sex and age did not influence Lp(a) values. Lp(a) values showed a minor correlation with other atherosclerotic markers when the Pearson correlation coefficient was used. In Saudi Arabia, the distribution of Lp(a) concentrations is skewed to the left, favoring lower values. Lp(a) levels in individuals residing in Saudi Arabia were comparable to those observed in other ethnic groups. Additionally, standardizing Lp(a) measurements according to sex and age may enhance broader applicability and facilitate comparisons across different populations. However, larger studies are required to provide more comprehensive data for comparison.

Vascular Function and Intima-Media Thickness in Children and Adolescents with Growth Hormone Deficiency: Results from a Prospective Case-Control Study

Introduction: Growth hormone deficiency (GHD) may be associated with subtle cardiovascular abnormalities, reversible upon starting GH treatment. Data on vascular morphology and function in GHD children are scanty and inconclusive. The aim of our study was to evaluate the effects of GHD and GH treatment on endothelial function and intima-media thickness (IMT) in children and adolescents. Methods: We enrolled 24 children with GHD (10.85 ± 2.71 years) and 24 age-, sex-, and BMI-matched controls. We evaluated anthropometry, lipid profile, asymmetric dimethylarginine (ADMA), brachial flow-mediated dilatation (FMD), and IMT of common (cIMT) and internal (iIMT) carotid artery at study entry in all subjects and after 12 months of treatment in GHD children. Results: At baseline GHD, children had higher total cholesterol (163.17 ± 18.66 vs. 149.83 ± 20.68 mg/dL, p = 0.03), LDL cholesterol (91.18 ± 20.41 vs. 77.08 ± 19.73 mg/dL, p = 0.019), atherogenic index (AI) (2.94 ± 0.71 vs. 2.56 ± 0.4, p = 0.028), and ADMA (215.87 ± 109.15 vs. 164.10 ± 49.15 ng/mL, p < 0.001), compared to controls. GHD patients also exhibited increased higher waist-to-height ratio (WHtR) compared to controls (0.48 ± 0.05 vs. 0.45 ± 0.02 cm, p = 0.03). GH therapy resulted in a decrease in WHtR (0.44 ± 0.03 cm, p = 0.001), total (151.60 ± 15.23 mg/dL, p = 0.001) and LDL cholesterol (69.94 ± 14.40 mg/dL, p < 0.0001), AI (2.28 ± 0.35, p = 0.001), and ADMA (148.47 ± 102.43 ng/mL, p < 0.0001). GHD showed lower baseline FMD than controls (8.75 ± 2.44 vs. 11.85 ± 5.98%, p = 0.001), which improved after 1-year GH treatment (10.60 ± 1.69%, p = 0.001). Baseline cIMT and iIMT were comparable between the two groups, but slightly reduced in GHD patients after treatment. Conclusion: GHD children may exhibit endothelial dysfunction in addition to other early atherosclerotic markers like visceral adiposity, and altered lipids, which can be restored by GH treatment.

Association of Serum Cystatin C Level With Carotid Arterial Wall Elastic Resistance as a Potential Marker for Detection of Early Stage Atherosclerosis.

Early diagnosis of atherosclerosis is exigent in patients with known cardiovascular disease (CVD) risk factors. During the initial phases of atherosclerosis, appearance of plaques can be detected by the ultrasonic phased tracking method which measures the arterial wall elasticity. However, reliable and easily available biochemical markers are not evaluated in the diagnosis of early-stage atherosclerosis. So the current study was carried out to assess the serum cystatin C level as an atherosclerotic marker, by evaluating its association with carotid arterial elastic modulus using the phased tracking method. A cross-sectional study was conducted on 115 patients havingrisk factors for atherosclerosis but not meeting carotid intima-media thickness (IMT) criteria. The early-stage atherosclerosis was detected by using the ultrasonic phased tracking method and the patients were divided based onlow and high carotid elastic modulus. Serum levels of cystatin-C were measured in association with IMT, and elastic modulus was calculated using a novel method. This study also put forth the evaluation ofthe sensitivity and specificity of cystatin C for early diagnosis of atherosclerosis. Cystatin C was strongly related to carotid elasticity (r=0.650). Based on multi-linear regression analysis, cystatin C showed significant association with carotid elasticity (β=0.509; p<0.001). It also displayed significant positive association with high carotid elastic modulus (β=0.511; p=0.02). Cystatin C showed a sensitivity of 85% in the prediction ofhigh carotid elastic modulus. For patients who are at risk to evolve atherosclerosis but are not evident with arterial plaques, cystatin C exhibits a significant association with carotid wall elastic modulus, which eases the detection of atherosclerosis. Thus, cystatin C is a potential biochemical marker for early diagnosis of atherosclerosis.

Association between triglyceride‑glucose index and carotid atherosclerosis in patients with psoriatic arthritis.

To investigate the association of triglyceride-glucose (TyG) index with atherosclerotic risk among patients with psoriatic arthritis (PsA). This cross-sectional study included 165 consecutive PsA patients receiving carotid ultrasonography with integrated TyG index, calculated as ln [fasting triglycerides (mg/dl)×fasting glucose (mg/dl)/2]. Logistic regression models were applied to analyze the association of TyG index as continuous variables and tertiles with carotid atherosclerosis and carotid artery plaque. Fully adjusted model included sex, age, smoking, body mass index, comorbidities, and psoriatic related variables. Overall, PsA patients with carotid atherosclerosis had substantially higher TyG index than those without (8.82 ± 0.50 vs 8.54 ± 0.55, p= 0.002). The frequency of carotid atherosclerosis was increased with increases in TyG index tertiles, showing 14.8%, 34.5%, 44.6% for tertile 1, 2 and 3, respectively (p= 0.003). Multivariate logistic analyses showed that each 1-unit increase in TyG index was significantly associated with prevalent carotid atherosclerosis (unadjusted OR 2.65 [1.39-5.05]; fully-adjusted OR 2.69 [1.02-7.11]). Compared with patients with tertile 1 of TyG index, the unadjusted and fully-adjusted OR for occurrence of carotid atherosclerosis were 4.64 (1.85-11.60) and 5.10 (1.54-16.93) in patients with tertile 3. Similarly, higher prevalent carotid artery plaque was observed with increasing TyG index (unadjusted OR 3.11 [1.54-6.26]; fully-adjusted OR 3.61 [1.15-11.38]) or with tertile 3 vs. tertile 1 (unadjusted OR 10.20 [2.83-36.82]; fully-adjusted OR 17.89 [2.88-111.11]). Additionally, TyG index provided incremental predictive capacity beyond established risk factors, shown by an increase in discrimination ability (all P < 0.001). TyG index was positively correlated with the burden of atherosclerosis in PsA patients, independent of traditional cardiovascular risk factors and psoriatic-related factors. These findings suggest that TyG index may be a promising atherosclerotic marker for PsA population.

The Effects of Percutaneous Coronary Intervention on Biomarkers and Quality of Life in Patients With Chronic Total Coronary Artery Obstruction.

Chronic total occlusion (CTO) is an angiographic picture of total occlusion without blood flow which is estimated to have lasted at least 3 months. This study attempted to provide an overview of the levels of matrix metalloproteinase-9 (MMP-9), soluble suppression tumorigenicity 2 (sST2), and N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) as remodeling, inflammatory, and atherosclerotic markers, as well as changes in the angina severity in patients with CTO who underwent percutaneous coronary intervention (PCI) compared to those without PCI. This study is a preliminary report with quasi-experimental design study with a pre-test and post-test approach to compare PCI's effect in CTO patients towards changes in MMP-9, sST2, NT-pro-BNP levels, and changes in the angina severity. Twenty subjects underwent PCI and 20 subjects with optimal medical therapy, who were then assessed at baseline and 8 weeks after intervention. The results of this preliminary report showed that decreased MMP-9 (pre-test: 12.07 ± 1.27 ng/mL vs. post-test: 9.91 ± 5.19 ng/mL, P = 0.049), sST2 (pre-test: 37.65 ± 20.00 ng/mL vs. post-test: 29.74 ± 15.17 ng/mL, P = 0.026) and NT-pro-BNP (pre-test: 0.63 ± 0.23 ng/mL vs. post-test: 0.24 ± 0.10 ng/mL, P < 0.001) levels were found after 8 weeks of PCI compared to those without such intervention. The levels of NT-pro-BNP were lower in the PCI group (0.24 ± 0.10 ng/mL) than in the non-PCI group (0.56 ± 0.23 ng/mL; P < 0.001). Moreover, there was an improvement of angina severity in PCI group than without PCI (P < 0.039). Although this preliminary report found a significant decrease in MMP-9, NT-pro-BNP, and sST2 levels in CTO patients who had undergone PCI compared to those without PCI, as well as improved angina severity in these patients, this study still has limitations. The number of samples was so small that similar studies with larger sample sizes or multicenter investigations are required to deliver more trustworthy and useful results. Nevertheless, we encourage this study as a preliminary baseline for further studies in the future.

Psychiatric sequelae of thromboangiitis obliterans: a case report and review of the literature

BackgroundPeripheral manifestations secondary to progressive vascular occlusions are characteristic of the rare condition termed thromboangiitis obliternas (TAO) or Buerger’s disease. The central manifestations of this disease are however poorly characterized, particularly those of psychiatric nature, and their prevalence is largely unknown. Speculations have been made around the polymorphic nature and triggers of observed psychopathology in TAO; much however remains to be unraveled in this area.Case presentationWe present the case of a 33-year-old Caucasian male who developed first episode of psychosis at the age of 29 years. There was no history of previous mental illness either in the patient, or in any of his family members. He had been a long- term heavy smoker and was experiencing progressive lower limb claudication since the age of 22 years; however, all inflammatory, autoimmune and atherosclerotic markers were negative. His psychosis was characterized by retention of a warm affect, and despite some amelioration, was generally resistant to a fair trial of several anti-psychotic medications including Clozapine.ConclusionThe pathophysiology of psychosis secondary to Buerger’s is not yet well characterized which adds to the complexity of managing these cases. Recognizing that cerebral manifestations of this disease may evolve several years after the onset of peripheral thromboangiitic features is important for following the natural history and considering measures that may reduce the burden of illness.

Çölyak hastalığı olan çocuklar ile sağlıklı yaşıtlarının erken ateroskleroz belirteçlerinin karşılaştırılması

Purpose: We aimed to evaluate carotid intima-media thickness (cIMT) and epicardial adipose tissue thickness (EATT) concurrently as early atherosclerotic markers in pediatric patients with Celiac disease.&#x0D; Materials and Methods: Patients with Celiac disease (n=54) and healthy peers (n=54) aged 5-18 years were enrolled in this cross-sectional study. Patients who followed gluten free diet at least the past 12 months were included. Anthropometric and biochemical measurements were performed. cIMT and EATT were measured by echocardiography and compared between the patient and control groups. &#x0D; Results: Body mass index (17.4±3.0 vs. 18.4±3.1 kg/m2), blood pressure (systolic: 100 (85-120) vs. 100 (80-100) mmHg; diastolic: 60 (40-90) vs. 70 (40-90) mmHg), and lipid profile (total cholesterol: 144.6±30.2 vs. 150.8±22.6 mg/dL; triglycerides: 71.5 (27-178) vs. 92.5 (34-203) mg/dL) were not different between the patient and control groups, while there were significant differences in cIMT and EATT. The patient group had higher cIMT (0.50±0.07 vs. 0.45±0.04 mm) and EATT (5.68±0.90 vs. 4.22±0.76 mm) than the control group. The risk of vitamin D insufficiency was 2.68 times higher in the patient group (95% CI=1.19-6.03). &#x0D; Conclusions: Children with Celiac disease had higher cIMT and EATT than healthy peers. cIMT and/or EATT measurements by echocardiography may present as a reliable and easy method to investigate subclinical atherosclerosis in children with Celiac disease.

Serum levels of Activin A: Marker of insulin resistance and cardiovascular risk in prediabetics.

A substantial proportion of health burden in diabetic individuals can be attributed to cardiovascular complications. The increasing risk of cardiovascular complications along the spectrum of dysglycemia warrants the need to devise novel markers for early assessment and management. Activin A is a multifunctional cytokine with an important role in glucose homeostasis and vascular diseases. It can thus serve as a guide for early identification of cardiovascular disease (CVD) risk in prediabetes. The aim of the study was to measure serum levels of activin A in prediabetics, compare them with normoglycemic controls and find the correlation of activin A with markers of insulin resistance such as the homeostatic model assessment of insulin resistance (HOMA-IR). Sixty prediabetic patients and similar age-, sex-, blood pressure-, and BMI-matched controls were recruited in the study. In both groups, serum levels of fasting blood glucose and post prandial glucose, glycated hemoglobin (HbA1c) and fasting insulin were measured. HOMA-IR values were calculated. Serum activin A levels were measured in both groups using ELISA. The obtained values were compared between the two groups. The median (IQR) of s. fasting insulin (mIU/L) in the case group was 15.3 (12.2-18.62) which was significantly higher than that in the control group, which was 6 (4.2-7.3). The median (IQR) of s. activin A (ng/mL) in the case group was 263.55 (227.18-279.56) which was significantly higher than that in the control group, which was 159.9 (150.73-178.75) (P < 0.001). There was a very strong positive correlation of s. activin A (ng/mL) with s. fasting insulin (mIU/L) and HOMA-IR (rho = 0.67 and 0.75, respectively, P < 0.001). Activin A, if combined with other atherosclerotic markers, might improve the assessment of insulin resistance and cardiovascular risk in prediabetics and lead to focus on lifestyle modifications and preventive medical therapy, thereby contributing to the prevention of CVD-related mortality and morbidity in these patients.

Anti-Phosphatidylethanolamine and Anti-Phosphatidylserine Antibodies-Association with Renal Involvement, Atherosclerosis, Cardiovascular Manifestations, Raynaud Phenomenon and Disease Activity in Polish Patients with Systemic Lupus Erythematosus.

Objective. To evaluate the association between anti-phosphatidylethanolamine (aPE) and anti-phosphatidylserine (aPS) antibodies and cardiovascular risk, organ involvement and disease activity in systemic lupus erythematosus (SLE) patients. Methods. We studied 93 SLE patients and 30 controls. We analyzed levels of anti-phospholipid antibodies, including aPS and aPE, the profiles of antinuclear, anti-neutrophil cytoplasmic (ANCA) and anti-endothelial antibodies, carotid intima-media thickness (cITM) and atherosclerotic plaque presence, ankle-brachial and high resistance indices, atherosclerotic risk factors, organ manifestations and treatment. Results. Levels of aPS and aPE were significantly higher in SLE patients in comparison with the controls (p = 0.038 and p = 0.044, respectively). aPS was associated with the risk of Raynaud’s phenomenon (p = 0.021) development. aPE increased the risk of renal involvement (p = 0.049), cerebral stroke (p = 0.050), high vlues of cIMT (p = 0.041) development as well as occurrence of selected serological markers associated with activity of the disease such as anti-double stranded DNA (p = 0.021). The long duration of regular smoking (p = 0.021) and the high number of cigarettes/day (p = 0.015) were significantly associated with the risk of aPE occurrence. Conclusions. Patients with aPS and aPE are at risk of vascular involvement. Especially the presence of aPE may significantly increase the risk of thrombotic complications development in SLE patients without classical serological markers of APS. Finally, aPE might be used as a marker of disease activity and risk of renal injury development in this patient group. The classical atherosclerotic markers including lipid indices play an important role in complex analysis of cardiovascular risk in lupus patients and enable to identify patients at the highest risk and implement effective preventive, diagnostic and therapeutic procedures.

Effect of Roux-en-Y gastric bypass surgery on subclinical atherosclerosis, oxidative stress, and mitochondrial dynamics in leukocytes of obese patients: A one-year follow-up study

Background and Aims : Little is known about the mechanisms underlying the cardiovascular protective effect of Roux en-Y gastric bypass (RYGB) surgery. The present study aimed to investigate how RYGB influences the oxidative and mitochondrial status of leukocytes and subclinical atherosclerotic markers.Methods: This interventional study was carried out in 57 obese subjects who underwent RYGB surgery. Leukocytes were isolated at baseline and 12 months after the intervention. We evaluated oxidative stress markers by static cytometry and mitochondrial markers by western blot. Leukocyte-endothelial cell interactions - rolling flux, velocity, and adhesion - were evaluated in vitro in a parallel-plate flow chamber.Results: RYGB induced weight loss and an improvement of anthropometric clinical indicators. At the molecular level, a significant reduction of superoxide production (p<0.01) and mitochondrial membrane potential (p<0.05) was observed, while GPX1 content increased (p<0.05). In terms of mitochondria, RYGB induced upregulation of complexes (I-V) (p<0.05 and p<0.001), MIEAP (p<0.05), and Pink1 (p<0.05), and regulated the fusion-fission machinery through an increase in MFN1 (p<0.05). Likewise, a significant reduction of sICAM (p< 0.05) and sP-Selectin (p < 0.001) and of rolling flux (p< 0.05) and adhesion of leukocytes (p< 0.01) were reported at follow-up.Conclusions: Our results suggest that patients undergoing RYGB benefit from an amelioration of their prooxidant status and enhanced mitochondrial dynamics in leukocytes, which could be responsible for the reduction of subclinical markers of atherosclerosis after surgery Acknowledgements: PI19/00838, PI19/00437, FI17/00144, CD19/00180, CP19/00077 from ISCIII-ERDF (“A way to build Europe”), PROMETEO/2019/027; APOSTD/2020/145, ACIF/2020/371 from the Valencian Regional Government. Background and Aims : Little is known about the mechanisms underlying the cardiovascular protective effect of Roux en-Y gastric bypass (RYGB) surgery. The present study aimed to investigate how RYGB influences the oxidative and mitochondrial status of leukocytes and subclinical atherosclerotic markers. Methods: This interventional study was carried out in 57 obese subjects who underwent RYGB surgery. Leukocytes were isolated at baseline and 12 months after the intervention. We evaluated oxidative stress markers by static cytometry and mitochondrial markers by western blot. Leukocyte-endothelial cell interactions - rolling flux, velocity, and adhesion - were evaluated in vitro in a parallel-plate flow chamber. Results: RYGB induced weight loss and an improvement of anthropometric clinical indicators. At the molecular level, a significant reduction of superoxide production (p<0.01) and mitochondrial membrane potential (p<0.05) was observed, while GPX1 content increased (p<0.05). In terms of mitochondria, RYGB induced upregulation of complexes (I-V) (p<0.05 and p<0.001), MIEAP (p<0.05), and Pink1 (p<0.05), and regulated the fusion-fission machinery through an increase in MFN1 (p<0.05). Likewise, a significant reduction of sICAM (p< 0.05) and sP-Selectin (p < 0.001) and of rolling flux (p< 0.05) and adhesion of leukocytes (p< 0.01) were reported at follow-up. Conclusions: Our results suggest that patients undergoing RYGB benefit from an amelioration of their prooxidant status and enhanced mitochondrial dynamics in leukocytes, which could be responsible for the reduction of subclinical markers of atherosclerosis after surgery Acknowledgements: PI19/00838, PI19/00437, FI17/00144, CD19/00180, CP19/00077 from ISCIII-ERDF (“A way to build Europe”), PROMETEO/2019/027; APOSTD/2020/145, ACIF/2020/371 from the Valencian Regional Government.

Clinical Utility of Small, Dense LDL as an Atherogenic Risk Marker

Low-density lipoprotein (LDL) has a major role in the origination and development of atherosclerosis and Cardio Vascular Diseases (CVD). Over the past few years, many studies have been concerned with different subclasses of LDLs and their atherogenicity. Low-density lipoproteins (LDLs) include many subclasses. The most common are large buoyant (LB), intermediate and small dense (sd) low-density lipoprotein particles. Small dense low-density lipoproteins attracted a lot of attention. Small dense LDL (sdLDL) has recently been proven to be more atherogenic than other lipoproteins containing apolipoprotein B, which have the potential to trigger atherosclerotic reactions. Many researchers have reported that small dense low-density lipoproteins are the superior biomarker for the prediction of atherosclerosis and CVDs regarding all other markers, including total low-density lipoprotein cholesterol(LDL-C), and total serum cholesterol, non-high-density lipoprotein (non-HDL-C), high-density lipoprotein cholesterol (HDL-C), and triglyceride content. Circulating small dense, low-density lipoproteins go through several modifications in the blood, rendering them more atherogenic. These modifications may include glycation, oxidation, and desialylation. Modified particles are strong inducers of inflammation resulting in many cardiovascular diseases, making them the primary target during the treatment of coronary artery disease. This article will elaborate on the clinical utility of sdLDL as an early marker to predict atherosclerosis and CVDs, and why it is considered superior to other atherosclerotic markers.

Triglyceride-glucose index and common carotid artery intima-media thickness in patients with ischemic stroke

BackgroundTriglyceride glucose (TyG) index was recently reported to be associated with an increased risk of the development and recurrence of cardiovascular events, and atherosclerosis is a main speculative mechanism. However, data on the relationship between TyG index and atherosclerosis, especially in the setting of ischemic stroke, is rare. We aimed to explore the association between TyG index and carotid atherosclerosis in patients with ischemic stroke.MethodsA total of 1523 ischemic stroke patients with TyG index and carotid artery imaging data were enrolled in this analysis. The TyG index was calculated as ln [fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2]. Carotid atherosclerosis was measured by common carotid artery intima-media thickness (cIMT), and abnormal cIMT was defined as a mean cIMT and maximum cIMT value ≥ 1 mm. Multivariable logistic regression models and restricted cubic spline models were used to assess the relationships between TyG index and abnormal cIMT. Risk reclassification and calibration of models with TyG index were analyzed.ResultsThe multivariable-adjusted odds ratios (95% CIs) in quartile 4 versus quartile 1 of TyG index were 1.56 (1.06–2.28) for abnormal mean cIMT and 1.46 (1.02–2.08) for abnormal maximum cIMT, respectively. There were linear relationships between TyG index and abnormal mean cIMT (P for linearity = 0.005) and abnormal maximum cIMT (P for linearity = 0.027). In addition, the TyG index provided incremental predictive capacity beyond established risk factors, shown by an increase in net reclassification improvement and integrated discrimination improvement (all P < 0.05).ConclusionsA higher TyG index was associated with carotid atherosclerosis measured by cIMT in patients with ischemic stroke, suggesting that TyG could be a promising atherosclerotic marker.