Assessment Of Endothelial Dysfunction Research Articles

The Need for Separate Testing with Acetylcholine for the Assessment of Endothelial Dysfunction and Coronary Artery Spasm

Intracoronary acetylcholine (ACH) testing is clinically useful to diagnose the presence of the coronary vasomotor disorders coronary endothelial dysfunction and coronary epicardial/microvascular spasm. In Western countries, continuous intracoronary injection of ACH for 2–3 minutes without a pacemaker is the usual method, while rapid injection of ACH for 20–30 seconds with a pacemaker is the traditional procedure in Japan. Coronary microvascular spasm is often observed in Western populations, whereas coronary epicardial spasm is frequently seen in Japanese subjects. Methodological differences between Western and Japanese protocols may lead to the opposite prevalence of coronary vasomotor disorders. This article discusses the optimal method for diagnosing endothelial dysfunction and epicardial/microvascular spasm based on previous reports, and compares intracoronary ACH testing performed by Western cardiologists with that by Japanese physicians.

Anti TNF-Alpha Treatment Improves Microvascular Endothelial Dysfunction in Rheumatoid Arthritis Patients

Nailfold capillaroscopy is a non-invasive investigation, which allows for the study of the microvasculature (anatomical and functional). Rheumatoid arthritis (RA) is associated with a high risk of cardiovascular atherosclerotic diseases, with endothelial dysfunction (macrovascular and microvascular) representing the first step in atherosclerosis development. The aim of this study is represented by the assessment of microvascular endothelial dysfunction in RA patients by means of nailfold capillaroscopy and to assess its evolution after a period of 12 months of anti TNF-alpha treatment. The study included 70 consecutive patients with RA and 70 healthy subjects, matched for age and gender, as the control group. Rheumatoid factor, anti-cyclic citrullinated peptide antibodies, serum TNF-α, C reactive protein, and erythrocytes sedimentation rate were evaluated in all patients, but in controls, only rheumatoid factor, serum TNF-α, C reactive protein, and erythrocytes sedimentation rate were measured. The RA activity was measured by DAS28. Nailfold capillaroscopy was carried out in all patients and controls, determining the baseline nailfold capillary density (Db), nailfold capillary density during reactive hyperemia (Dh), and nailfold capillary density after venous congestion (Dc). Data were presented as mean ± standard deviation. Statistical analysis was performed using ANOVA and Pearson’s correlation, with p < 0.05 being statistically significant. Db, Dh, and Dc were lower in RA patients than in controls (p < 0.0001), correlating with RA activity and TNF-α (p < 0.05). After 12 months of anti TNF-α treatment, microvascular endothelial dysfunction improved (p < 0.0001). Microvascular endothelial dysfunction can be assessed by nailfold capillaroscopy, with anti TNF-α medication contributing to its improvement.

Persistent Post COVID-19 Endothelial Dysfunction and Oxidative Stress in Women

The assessment of endothelial dysfunction and free radical homeostasis parameters were performed in 92 women, aged 45 to 69 years, divided into the following groups: women without COVID-19 (unvaccinated, no antibodies, control); women with acute phase of COVID-19 infection (main group, COVID-19+); 12 months post COVID-19+; women with anti-SARS-CoV-2 IgG with no symptoms of COVID-19 in the last 12 months (asymptomatic COVID-19). Compared to the control, patients of the main group had lower glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities, decreased advanced glycation end products (AGEs) level, higher glutathione reductase (GR) activity, and higher glutathione S transferases pi (GSTpi), thiobarbituric acid reactants (TBARs), endothelin (END)-1, and END-2 concentrations (all p ≤ 0.05). The group with asymptomatic COVID-19 had lower 8-OHdG and oxidized glutathione (GSSG) levels, decreased total antioxidant status (TAS), and higher reduced glutathione (GSH) and GSH/GSSG levels (all p ≤ 0.05). In the group COVID-19+, as compared to the group without clinical symptoms, we detected lower GPx and SOD activities, decreased AGEs concentration, a higher TAS, and greater GR activity and GSTpi and TBARs concentrations (all p ≤ 0.05). The high content of lipid peroxidation products 12 months post COVID-19+, despite decrease in ENDs, indicates long-term changes in free radical homeostasis. These data indicate increased levels of lipid peroxidation production contribute, in part, to the development of free radical related pathologies including long-term post COVID syndrome.

FABP4 as potential indicator for GDM-induced fetal endothelial dysfunction

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): DFG project no. 288034826—International Research Training Group (IRTG) 2251 Background Gestational diabetes mellitus (GDM) is linked to an elevated risk of developing cardiovascular diseases (CVD) both for the mother and the baby in later life. Previous studies have identified fatty acid-binding protein 4 (FABP4) as a prime candidate involved in the pathophysiology of GDM. FABP4 is known to promote an inflammatory response and vascular permeability, induce oxidative stress in endothelial cells (ECs), and impair the nitric oxide signaling pathway, thereby promoting endothelial dysfunction. Indeed, women with GDM exhibit elevated blood levels of FABP4, suggesting its potential as a biomarker for endothelial dysfunction and cardiovascular risk assessment in GDM. However, the role that FABP4 plays in the fetal endothelial function remains poorly understood. Purpose Thus, our aim is to understand the role of FABP4 in fetal endothelial dysfunction and its regulation to mitigate the impact of GDM on the vasculature. Methods Fetoplacental vessels and primary human umbilical vein endothelial cells (HUVECs) were isolated from placentas and umbilical cords obtained from both normoglycemic (NG) and GDM pregnancies. We also obtained the clinical data from the mothers and collected the cord blood. Total mRNA from HUVECs was used for bulk RNA sequencing to compare gene expression, while gene expression analysis in the vessels was conducted using RT-qPCR. Additionally, NG HUVECs were pooled and cultured under high laminar flow conditions (30 dyn/cm²) or subjected to various treatments, including insulin (5nM), glucose (25mM), simvastatin (10nm), or VEGF-A stimulation. Subsequent RT-qPCRs were performed to analyze the gene expression of several genes of interest. Results The bulk RNA sequencing data analysis revealed FABP4 as an overexpressed gene in GDM HUVECs compared to NG. Furthermore, the analysis of data through Gene Set Enrichment Analysis provided a list of different gene sets that are enriched in GDM samples. Among these gene sets are pathways or processes implicated in endothelial dysfunction, such as angiogenesis, PI3K/AKT/mTOR signaling, reactive oxygen species pathway, or inflammatory response. In vitro experiments provided evidence for an elevated FABP4 mRNA expression after VEGF treatment of HUVECs. Conversely, both simvastatin treatment and exposure to laminar flow reduced FABP4 mRNA expression and increased eNOS expression, suggesting a potential inhibitory effect of nitric oxide on FABP4. Conclusion We provided evidence that FABP4 could be involved in fetal GDM-induced endothelial dysfunction. Shear stress and statins might protect the endothelium against the negative impact of FABP4.

Evaluating cardiovascular risk in metabolic steatosis with precision medicine non-invasive approaches: insights from a cohort study.

Metabolic associated steatotic liver disease (MASLD) is the most common liver condition. It is associated with increased liver-related morbidity and mortality, and also with high risk of cardiovascular events (CVD), representing itself an independent risk factor for it. This makes MASLD a presentation of high interest for internal medicine, also because of its association with metabolic syndrome (MetS). It is crucial to assess its risks in a noninvasive way. With the aim of finding specific risk profiles for CVD development in MASLD by performing a noninvasive assessment of: (1) preclinical signs of endothelial dysfunction (ED); (2) clinical assessment of CVD risk by Framingham Heart Risk Score (FHRs); (3) genomic characterization of MASLD associated polymorphisms; (4) specific untargeted metabolomic profiles, we enrolled 466 MASLD patients non-invasively classified in 4 group of liver fibrosis severity (group-A: low-fibrosis risk, group-B: high-fibrosis risk, group-C: MASLD-cirrhosis, group-D: MASLD-HCC) and 73 healthy controls. FHRs was similar in controls and low-fibrosis group and significantly higher in high-fibrosis patients, cirrhosis, and HCC, increasing among classes. At a multivariable regression, FHRs wasassociated with liver disease severity and diabetes. 38.2% of patients had altered EndoPAT,resembling ED.Patients with high FHRs (> 40%) and ED had different metabolomics compared to those without ED. Our study reveals that a deep, non-invasive characterization of MASLD patients through precision medicine approaches (untargeted metabolomics, SNPs, ED assessment) was able to show a peculiar pattern in MASLD patients with increased CVD risk, mostly correlated with liver disease severity.

Assessment of endothelial dysfunction in cushing's syndrome

Assessment of endothelial dysfunction in cushing's syndrome

Value of serum osteoprotegerin in the assessment of endothelial dysfunction in obesity

ObjectiveOsteoprotegerin is a member of the tumor necrosis factor receptor superfamily. The study aimed to assess serum osteoprotegerin and endothelial dysfunction relationship in obese non-diabetic subjects. Elucidating the association linking serum osteoprotegerin level to obesity and insulin resistance.Materials and methodsSixty obese non-diabetic subjects attending the outpatient endocrine clinic were compared with 20 controls. All subjects went through history taking, clinical examination, and anthropometric measuring. Laboratory tests included fasting blood glucose, HbA1c, HOMA-IR, lipid profile, and serum osteoprotegerin level—assessment of endothelial dysfunction measured by carotid intimal thickening and flow meter dilatation.ResultsObese subjects had significantly higher rates of insulin resistance and dyslipidemia compared with controls (P = 0.017 and 0.002, respectively). Serum osteoprotegerin levels were significantly lower in obese subjects compared with controls (P = 0.011). In obese subjects, there was a significant positive correlation between osteoprotegerin and HOMA-IR (r = 0.272; P = 0.035), whereas there was no significant correlation between OPG and endothelial dysfunction.ConclusionThe study showed that osteoprotegerin significantly decreased in obese non-diabetic individuals in comparison with control subjects. A significant positive correlation between osteoprotegerin and HOMA-IR has been reported in obese non-diabetic subjects. OPG can be considered a serum biomarker to predict insulin resistance in obese individuals.

Association between Nfr2, HO-1, NF-kB Expression, Plasma ADMA, and Oxidative Stress in Metabolic Syndrome.

Endothelial dysfunction is one of the major factors in the pathogenesis of metabolic syndrome (MetS), and its molecular mechanisms are not completely understood. The present study aimed to examine the connection between nuclear factor2-related factor2 (Nrf2), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), heme oxygenase 1 (HO-1), and plasma asymmetric dimethylarginine (ADMA) and malondialdehyde (MDA) in people with MetS. Participants in the study were as follows: with MetS (n = 30) and without MetS (Control) (n = 14). Expression of Nrf2, NF-kB, and HO-1 was measured in peripheral blood mononuclear cells (PBMCs). Plasma ADMA was determined using the ELISA technique and MDA via the thiobarbituric acid method. Our study showed that mRNA of NF-kB, Nrf2, and HO-1 levels in PBMCs in the MetS group were significantly higher than in the controls by 53%, 130%, and 185% (p < 0.05), respectively. Similarly, elevated levels of MDA (by 78%, p < 0.001) and ADMA (by 18.7%, p < 0.001) were established in the MetS group. Our findings show the importance of transcription factor Nrf2, playing an integral role in the protection of the endothelium, and of NF-κB, a transcription factor mediating the inflammatory response in MetS. Knowledge of complex cellular-molecular mechanisms would allow the use of biomarkers such as Nrf2, NF-kB, HO-1, and ADMA for the assessment of endothelial dysfunction in clinical practice.

Gut Microbiota and Derived Short-Chain Fatty Acids Are Linked to Evolution of Heart Failure Patients.

There is a lack of direct evidence regarding gut microbiota dysbiosis and changes in short-chain fatty acids (SCFAs) in heart failure (HF) patients. We sought to assess any association between gut microbiota composition, SCFA production, clinical parameters, and the inflammatory profile in a cohort of newly diagnosed HF patients. In this longitudinal prospective study, we enrolled eighteen newly diagnosed HF patients. At admission and after 12 months, blood samples were collected for the assessment of proinflammatory cytokines, monocyte populations, and endothelial dysfunction, and stool samples were collected for analysis of gut microbiota composition and quantification of SCFAs. Twelve months after the initial HF episode, patients demonstrated improved clinical parameters and reduced inflammatory state and endothelial dysfunction. This favorable evolution was associated with a reversal of microbiota dysbiosis, consisting of the increment of health-related bacteria, such as genus Bifidobacterium, and levels of SCFAs, mainly butyrate. Furthermore, there was a decrease in the abundance of pathogenic bacteria. In vitro, fecal samples collected after 12 months of follow-up exhibited lower inflammation than samples collected at admission. In conclusion, the favorable progression of HF patients after the initial episode was linked to the reversal of gut microbiota dysbiosis and increased SCFA production, particularly butyrate. Whether restoring butyrate levels or promoting the growth of butyrate-producing bacteria could serve as a complementary treatment for these patients deserves further studies.

Mitochondrial dysfunction in the pathogenesis of endothelial dysfunction.

Cardiovascular diseases (CVDs) are a matter of concern worldwide, and mitochondrial dysfunction is one of the major contributing factors. Vascular endothelial dysfunction has a major role in the development of atherosclerosis because of the abnormal chemokine secretion, inflammatory mediators, enhancement of LDL oxidation, cytokine elevation, and smooth muscle cell proliferation. Endothelial cells transfer oxygen from the pulmonary circulatory system to the tissue surrounding the blood vessels, and a majority of oxygen is transferred to the myocardium by endothelial cells, which utilise a small amount of oxygen to generate ATP. Free radicals of oxide are produced by mitochondria, which are responsible for cellular oxygen uptake. Increased mitochondrial ROS generation and reduction in agonist-stimulated eNOS activation and nitric oxide bioavailability were directly linked to the observed change in mitochondrial dynamics, resulting in various CVDs and endothelial dysfunction. Presently, the manuscript mainly focuses on endothelial dysfunction, providing a deep understanding of the various features of mitochondrial mechanisms that are used to modulate endothelial dysfunction. We talk about recent findings and approaches that may make it possible to detect mitochondrial dysfunction as a potential biomarker for risk assessment and diagnosis of endothelial dysfunction. In the end, we cover several targets that may reduce mitochondrial dysfunction through both direct and indirect processes and assess the impact of several different classes of drugs in the context of endothelial dysfunction.

Endothelial function predicts 5-year adverse outcome in patients hospitalized in an emergency department chest pain unit.

Although endothelial function is a marker for cardiovascular risk, endothelial dysfunction assessment is not routinely used in daily clinical practice. A growing challenge has emerged in identifying patients prone to cardiovascular events. We aim to investigate whether abnormal endothelial function may be associated with adverse 5-year outcomes in patients presenting to a chest pain unit (CPU). Following endothelial function testing using EndoPAT 2000 in 300 consecutive patients without a history of coronary artery disease, patients underwent coronary computerized tomographic angiography (CCTA) or single-photon emission computed tomography according to availability. Mean 10-year Framingham risk score (FRS) was 6.6 ± 5.9%; mean 10-year atherosclerotic cardiovascular disease (ASCVD) risk was 7.1 ± 7.2%; median reactive hyperemia index (RHI) as a measure of an endothelial function 2.0 and mean was 2.0 ± 0.4. During a 5-year follow-up, the 30 patients who developed major adverse cardiovascular events (MACE), including all-cause mortality, nonfatal myocardial infarction, hospitalization for heart failure or angina pectoris, stroke, coronary artery bypass grafting, and percutaneous coronary interventions, had higher 10-year FRS (9.6 ± 7.8 vs. 6.3 ± 5.6%; P = 0.032), higher 10-year ASCVD risk (10.4 ± 9.2 vs. 6.7 ± 6.9%; P = 0.042), lower baseline RHI (1.6 ± 0.5 vs. 2.1 ± 0.4; P < 0.001) and a greater degree of coronary atherosclerotic lesions (53 vs. 3%, P < 0.001) on CCTA compared with patients without MACE. Multivariate analysis demonstrated that RHI below the median was an independent predictor of 5-year MACE (odds ratio 5.567, 95% confidence interval 1.955-15.853; P = 0.001). Our findings suggest that noninvasive endothelial function testing may contribute to clinical efficacy in triaging patients in the CPU and in predicting 5-year MACE. NCT01618123.

Endothelial function measured by peripheral arterial tonometry in patients with chronic myeloid leukemia on tyrosine kinase inhibitor therapy: a pilot study

BackgroundArterial occlusive events are an emerging problem in patients with chronic myeloid leukemia (CML) receiving tyrosine kinase inhibitor (TKI) therapy. Endothelial cell damage is thought to play an important role in the development of vascular events. Measurement of the peripheral vasodilator response by peripheral arterial tonometry (PAT) has reportedly been useful in the non-invasive assessment of endothelial dysfunction. To date, no studies have assessed endothelial function using PAT in patients with CML receiving TKIs.MethodWe measured the reactive hyperemia index (RHI) using PAT in young patients with CML (men aged ≤ 55 years and women aged ≤ 65 years) receiving TKIs.ResultsThirty patients with CML were examined (mean age, 43.5 ± 9.8 years; men, 57%). The median RHI was 1.81. Among these patients, 16.7% and 83.3% were taking imatinib and second- or third-generation TKIs, respectively. There were no differences in the baseline characteristics between the low RHI (< 1.67, n = 10), borderline RHI (≥ 1.67 and < 2.10, n = 14), and normal RHI (≥ 2.10, n = 6) groups. Serum uric acid (UA) levels and the RHI were significantly negatively correlated (r = -0.40, p = 0.029).ConclusionOne-third of young patients with CML receiving TKI therapy were classified as having a low RHI. The RHI was negatively correlated with serum UA level. Larger prospective studies are necessary to examine whether the RHI predicts cardiovascular events in such patients.

Assessment of endothelial dysfunction and inflammation in type 2 diabetic postmenopausal women

Objective: Vascular complications in type 2 diabetes mellitus are an important cause of morbidity and mortality. Also, endothelial dysfunction arises with vascular ageing during the postmenopausal period. Our objective in this study was to evaluate inflammation and endothelial function parameters and their possible diagnostic roles in type 2 diabetic postmenopausal patients. Material and Methods: The study was conducted on four groups, including type 2 diabetic premenopausal (n:20), non-diabetic premenopausal (n:20), type 2 diabetic postmenopausal (n:20), and non-diabetic postmenopausal subjects (n:20). Serum endothelin-1 (ET-1), endothelial nitric oxide synthetase (eNOS), interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), and chitinase-3-like protein 1 (YKL-40) levels were determined as inflammatory and endothelial function markers using ELISA kits. Results: Serum ET-1, IL-6, and YKL-40 levels were higher in the type 2 diabetic postmenopausal group compared to the non-diabetic premenopausal group (p&lt;0.01, p&lt;0.05, and p&lt;0.01, respectively). ET-1, IL-6, and YKL-40 levels were higher in the type 2 diabetic postmenopausal group compared to the non-diabetic postmenopausal group (p&lt;0.001, p&lt;0.05, and p&lt;0.01 respectively). ROC analysis revealed serum ET-1 (AUC 0.933, sensitivity 87.5%, specificity 85.7%), IL-6 (AUC 0.812, sensitivity 56.3%, specificity 92.8%), and YKL-40 (AUC 0.880, sensitivity 81.2%, specificity 92.8%), as good diagnostic parameters, especially in the type 2 diabetic premenopausal vs. non-diabetic premenopausal cohorts. Conclusion: Serum ET-1, IL-6, and YKL-40 levels were at the highest levels in the 2 diabetic postmenopausal group, and the increase in these markers was remarkable in diabetes compared with menopausal periods. Also, ET-1, IL-6, and YKL-40 were good diagnostic parameters for detecting endothelial function and inflammation in type 2 diabetic postmenopausal and non-diabetic premenopausal cohorts.

Assessment of Endothelial Dysfunction in Patients with Covid-19 Based on Chronic Heart Failure and its Significance in the Effectiveness of the Treatment

This article discusses the importance of endothelial dysfunction in patients with COVID-19 due to chronic heart failure and the effectiveness of its treatment.

Blunted Microvascular Reactivity in Psoriasis Patients in the Absence of Cardiovascular Disease, as Assessed by Laser Speckle Contrast Imaging.

Psoriasis is associated with accelerated rates of cardiovascular disease (CVD). Laser Speckle Contrast Imaging (LSCI) is a novel, non-interventional technique for the dynamic assessment of microvascular endothelial dysfunction, which represents an early precursor of CVD. We investigated whether skin microvascular reactivity is impaired in psoriasis and whether an association exists with large artery stiffening. Skin microvascular reactivity was assessed with LSCI combined with post-occlusive reactive hyperaemia protocol in psoriasis patients and controls in the absence of established CVD. Arterial stiffness and central hemodynamics were assessed throughout a whole 24 h period with the Mobil-O-Graph device. Most LSCI indices of microvascular reactivity were impaired in psoriasis patients (n = 90) compared to controls (n = 45) [baseline flux; occlusion flux; peak-to-baseline magnitude; baseline cutaneous vascular conductance (CVC); percentage increase in CVC, p &lt; 0.001 for all comparisons]. In multivariate analysis, psoriatic disease predicted the above markers independently of classical CVD risk factors. Augmentation index, peripheral pulse pressure, and central systolic/diastolic blood pressure correlated with LSCI microvascular responses in the study population (n = 135). Pulse wave velocity significantly correlated with nearly all LSCI parameters, while the association with baseline flux was independent of CVD risk factors and psoriatic disease in multivariate analysis (beta = 0.096, p = 0.039). This study provides evidence of altered skin microvascular responses in psoriasis by use of LSCI, and interaction with macrovascular dysfunction, before the establishment of overt CVD. A non-interventional approach of skin microcirculation with LSCI might be used as an early indicator of vascular health in psoriasis.

Assessment of vessels endothelial dysfunction by protease-activated receptors (PARs) signaling in COVID-19 patients

PAR-1-mediated the endothelial disruption that occurs in the context of thromboinflammation. In addition, PAR1 promotes a profibrotic phenotype in fibroblasts, alveolar inflammation, and apoptosis. This is an active area of research; more data are needed to clarify similarities and differences of the PARs and their modulators in Post and Critical cases of COVID-19. Such issues are especially relevant given the potential use PAR-1 as a marker of promote thrombosis and tissue injury through a proposed mechanism between inflammation and thrombosis that was reported previously. This paper would track the theoretical role of PAR-1 as a marker of promote thrombosis in COVID-19 cases by looking for the following questions: What is the Cross Talk Between Thromboinflammation and Protease-activated receptors during Post and Critical cases of COVID-19?

Assessment of Endothelial Dysfunction in Patients with Kawasaki Disease: A Meta-Analysis.

Kawasaki disease (KD) is a well-known systemic inflammatory vasculitis. Endothelial dysfunction is one of most easily overlooked non-coronary complications of KD. Several studies have assessed endothelial dysfunction using flow-mediated dilatation (FMD), nitroglycerin-mediated dilation (NMD), and biomarkers (E-selectin, P-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular cellular adhesion molecule-1 (VCAM-1)). However, the results were inconsistent and incomplete. We searched five databases for eligible studies until March 8, 2022. The summarized weighted mean difference (WMD) with 95% confidence intervals (CIs) were estimated for FMD, NMD, and four biomarkers level between KD and healthy children. A meta-analysis with subgroup analysis was conducted. 40 studies with a total of 2670 children (1665 KD patients and 1005 healthy children) were identified. During the acute phase, KD patients had lower FMD compared to the control group (WMD = -10.39, 95% CI: -13.80- -6.98). During the subacute phase, KD patients had lower FMD compared to the control group (WMD = -15.07, 95% CI: -17.61- -12.52). During the convalescence phase, KD patients had lower FMD and similar NMD compared to the control group (WMD = -4.95, 95% CI: -6.32- -3.58; WMD = -0.92, 95% CI: -2.39-0.55, respectively). During the convalescence phase, those KD patients without coronary artery lesion (CAL), with CAL, even with coronary artery aneurysm, had progressively lower FMD compared to healthy children (WMD = -3.82, 95% CI: -7.30- -0.34; WMD = -6.32, 95% CI: -7.60- -5.04; and WMD = -6.97, 95% CI: -7.99- -5.95, respectively). Compared to KD patients without CAL, those with CAL had lower FMD (WMD = -1.65, 95% CI: -2.92- -0.37). KD patients had higher levels of E-selectin, P-selectin, and ICAM-1 compared to healthy controls during different phases. KD patients had a higher level of VCAM-1 compared to healthy controls only during the acute phase (WMD = 61.62, 95% CI: 21.38-101.86). Endothelial dysfunction is present since the onset of KD and persists for years, confirmed by the measurement of FMD and biomarkers from different phases. An assumption is advanced that FMD impairment (the severity of endothelial dysfunction) may be positively correlated with CAL severity during the convalescence phase.

Endothelial Microparticles as Potential Biomarkers in the Assessment of Endothelial Dysfunction in Hypercholesterolemia.

Background and Objectives: Endothelial microparticles (EMP) particularly CD31+/42−/AV+, CD144+/AV+ and CD62e+/AV+ have been reported as having increased in cardiovascular-related diseases, making them potential biomarkers for endothelial dysfunction. This study aimed to compare these EMPs in patients with hypercholesterolemia and healthy controls and to correlate their levels with endothelium-dependent vasodilation (EDV) assessed via pulse wave analysis (PWA); an established method of assessing endothelial function. Materials and Methods: EMPs from 88 subjects (44 hypercholesterolemia patients and 44 controls) were quantified from whole blood using flow cytometry analysis. Endothelial function was determined using PWA combined with pharmacological challenge. Results: CD31+/42−/AV+ (3.45 ± 4.74 count/µL vs. 1.33 ± 4.40 count/µL; p = 0.03), CD144+/AV+ (7.37 ± 12.66 count/µL vs. 1.42 ± 1.71 count/µL; p = 0.003) and CD62e+/AV+ (57.16 ± 56.22 count/µL vs. 20.78 ± 11.04 count/µL; p < 0.001) were significantly elevated in the hypercholesterolemic group compared with the controls, respectively. There was a significant inverse moderate correlation between all circulating EMPs and EDV: CD31+/42−/AV+ (r = −0.36, p = 0.001), CD144+/AV+ (r = −0.37, p = 0.001) and CD62e+/AV+ (r = −0.35, p = 0.002). Conclusions: All EMPs were raised in the patients with hypercholesterolemia, and these values correlated with the established method of assessing endothelial function.

Endothelial Progenitor Cells as Biomarkers of Cardiovascular Pathologies: A Narrative Review.

Endothelial progenitor cells (EPC) may influence the integrity and stability of the vascular endothelium. The association of an altered total EPC number and function with cardiovascular diseases (CVD) and risk factors (CVF) was discussed; however, their role and applicability as biomarkers for clinical purposes have not yet been defined. Endothelial dysfunction is one of the key mechanisms in CVD. The assessment of endothelial dysfunction in vivo remains a major challenge, especially for a clinical evaluation of the need for therapeutic interventions or for primary prevention of CVD. One of the main challenges is the heterogeneity of this particular cell population. Endothelial cells (EC) can become senescent, and the majority of circulating endothelial cells (CEC) show evidence of apoptosis or necrosis. There are a few viable CECs that have properties similar to those of an endothelial progenitor cell. To use EPC levels as a biomarker for vascular function and cumulative cardiovascular risk, a correct definition of their phenotype, as well as an update on the clinical application and practicability of current isolation methods, are an urgent priority.

Characterization and assessment of endothelial dysfunction in adolescents with obesity and vitamin D deficiency

Background. Obesity and vitamin D deficiency in children are widespread in economically developed countries. Among children with obesity and components of the metabolic syndrome, vitamin D deficiency is more common than in children with a normal body mass index (BMI). The growth of metabolic disorders, atherosclerosis, early onset of type 2 diabetes mellitus lead to fatal vascular accidents in young people, and therefore the search for new ways of early diagnosis of these processes is relevant.&#x0D; Aim. To study of the relationship of endothelial dysfunction with vitamin D deficiency, obesity and associated metabolic disorders among adolescents in Saint Petersburg.&#x0D; Materials and methods. 5 adolescents aged 1416 years (150.76 years) with primary obesity were examined. Anthropometric parameters were studied: waist circumference, weight, height, calculation of BMI, stage of puberty according to Tanner. Laboratory examination included the following parameters: serum glucose, cholesterol, triglycerides, high density lipoproteins, low density lipoproteins, insulin, 25(OH)D. Atherogenicity index (AI), insulin resistance index (HOMA-IR), vitamin D sufficiency were calculated. Endothelial function was assessed by the value of the reactive hyperemia index (RHI), automatically calculated by the EndoPAT 2000 device (Itamar Medical, Israel).&#x0D; Results. All examined patients had abdominal obesity (median BMI 33.5 kg/m2 [30.9; 34.2]) and reduced vitamin D supply (median 25(OH)D 17.2 ng/ml). Hypercholesterolemia and dyslipidemia due to an increase in low density lipoproteins were diagnosed in 1 (20%) case. Dyslipidemia due to a decrease in high density lipoproteins was detected in 3 (60%) patients. An increase in IA was found in 4 (80%) people. Insulin resistance was present in 60% of the examined, the median value of HOMA-IR was 5.6. The median RHI was 1.74 [1.72; 2.13]. Optimum RHI values were observed in 2 (40%) patients; in most (60%) adolescents, the RHI values corresponded to subnormal values and were close to the lower limit of this zone. A significant inverse correlation of RHI with AI was obtained (R=-0.63, p0.05).&#x0D; Conclusion. Taking into account the risk factors previously identified in the examined patients (dyslipidemia, insulin resistance, reduced vitamin D supply), endothelial dysfunction in these patients was regarded as a cardiovascular risk factor. A manageable risk factor is a reduced supply of vitamin D, which can be corrected by an additional donation of cholecalciferol.