Changes In Vascular Endothelial Function Research Articles

Acute effects of electronic cigarettes on vascular endothelial function: a systematic review and meta-analysis of randomized controlled trials.

The effects of e-cigarettes on endothelial function remained controversial. The study aimed to investigate the effects of e-cigarettes on vascular endothelial function. PubMed, Web of Science, Embase, and Cochrane Library were searched up to December 2021. We only included the studies in which the control group included vaping without nicotine and tobacco. Pairwise and network meta-analyses were conducted for flow-mediated dilation (FMD), pulse wave velocity (PWV), and heart rate corrected augmentation index (AIx75). Eight studies involving 372 participants were eligible for this review. Compared with vaping without nicotine, e-cigarettes significantly increase in PWV (mean difference = 3.09; 95% confidential interval: 1.51-4.68, P < 0.001) and AIx75 (mean difference = 2.11; 95% confidential interval: 1.02-3.21, P < 0.001) indicators, but not affect FMD (mean difference = 0.78; 95% confidential interval: -0.08 to 1.64, P = 0.075). But compared with traditional tobacco, e-cigarettes did not affect FMD (mean difference = 0.28, 95% confidential interval: -0.45 to 0.59, P = 0.084). According to surface under the cumulative ranking curve (SUCRA), the e-cigarette ranked first for FMD (SUCRA = 97%), tobacco ranked first for PWV (SUCRA = 75%), and AIx75 (SUCRA = 99%). In summary, evidence from our pooled analyses indicated that acute inhalation of e-cigarettes leads to negative changes in vascular endothelial function. E-cigarettes cannot be used as an alternative to public health strategies for tobacco control and should not be considered cardiovascular safety products. More future research should be conducted to verify our findings.

Time-Restricted Feeding Improved Vascular Endothelial Function in a High-Fat Diet-Induced Obesity Rat Model.

Obesity, where there is enhancement of stored body fat in adipose tissues, is associated with cardiovascular complications that are mainly related to atherosclerosis. Time-restricted feeding (TRF) is a form of restricted eating aimed at reducing weight in obese subjects. The present study aims to investigate changes in vascular endothelial function, endothelial nitric oxide synthase (eNOS), and protein kinase B (Akt) protein expressions with TRF in obese and normal rats. Male Sprague Dawley rats were divided into two normal and three obese groups; obesity was induced in the obese groups by feeding with a high-fat diet (HFD) for six weeks. After six weeks, rats were equally divided into five groups (n = 7 per group): Normal group (NR) which continued on a standard diet for six more weeks, normal group switched to TRF with a standard diet for six weeks (NR + TRFSD), obese group (OR) which continued on HFD for six more weeks, obese group switched to TRF of HFD (OR + TRFHFD), and obese group switched to TRF of a standard diet (OR + TRFSD). TRF was practiced for six weeks, after which the rats were sacrificed. Aortic endothelium-dependent and endothelium-independent relaxations and contractions were assessed using the organ bath. Aortic eNOS and Akt protein expressions were determined using immunoblotting. Fasting blood glucose, body weight, body mass index (BMI), serum lipid profile, Lee’s index, serum insulin levels, and sensitivity (HOMA-IR) were also measured. Endothelium-dependent relaxation was significantly impaired, while endothelium-dependent contraction increased in obese rats compared to that in normal rats. Both obese groups which underwent TRF with a HFD and standard diet improved their impairments in endothelium-dependent relaxation and reduced endothelium-dependent contraction; these were associated with increased expressions of aortic eNOS and Akt protein. Both obese groups with TRF reduced body weight, BMI, Lee’s index, total cholesterol, triglycerides, low-density lipoprotein cholesterol, and improved insulin sensitivity. TRF improved endothelium-dependent relaxation and reduced endothelium-dependent contraction, thus attenuating endothelial dysfunction in obese rats. These were associated with increased aortic eNOS and Akt protein expressions.

Protective Effect of Coriander (Coriandrum sativum L.) on High-Fructose and High-Salt Diet-Induced Hypertension: Relevant to Improvement of Renal and Intestinal Function.

Hypertension has become a leading cardiovascular risk factor worldwide. In this study, we explored the salutary effects and relevant mechanisms of coriander (Coriandrum sativum L.), an herbal plant with culinary and medicinal values, on high-fructose and high-salt diet (HFSD)-induced hypertension in SD rats. Our results showed that oral administration of coriander (1.0 or 2.0 g/kg·bw) effectively attenuated HFSD-induced elevation of systolic blood pressure, diastolic blood pressure, and mean arterial pressure. Coriander also increased the serum levels of vasodilator factors (PGI2, NO, and eNOS), decreased Na+ retention and serum uric acid (UA) level, and ameliorated glucolipid profiles. qPCR results revealed that coriander downregulated the mRNA expression of NHE3, a Na+/H+ exchanger responsible for Na+ absorption, in kidney and small intestine. 16S rDNA sequencing showed that coriander altered the gut microbiota composition with the beneficial bacteria Bifidobacterium and Oscillibacter significantly enriched. Correlation analysis indicated that the abundance of Bifidobacterium was evidently correlated with levels of NHE3, NO, eNOS, and UA. LC-MS/MS analysis revealed that coriander contained a variety of flavonoids including rutin and quercetin. Conclusively, long-term consumption of coriander may ameliorate HFSD-induced hypertension by mitigating HFSD-caused abnormal changes in vascular endothelial function, renal and intestinal sodium absorption, glucolipid homeostasis, and gut microbiota in rats.

Some features of the influence of nitrogen oxide on humans at rest, physical activity and pathology

The literature data on the general characteristics and mechanisms of action of nitric oxide, its role in the regulation of the functioning of the cardiovascular system and the body as a whole are used in the work. The existing NO-dependent mechanism of regulation of vascular reactivity in the conditions of endothelial dysfunction is stated; cGMP-independent mechanism of NO action on calcium homeostasis and sensitivity of smooth muscle myofibrils to calcium ions. Interesting are the results of studies that reflect the importance of nitric oxide in health. Age-related changes in vascular endothelial function due to increasing age and their importance in the development of age-related pathology are shown. Materials that reflect the importance of the use of nitric oxide donors for the treatment of diseases of various body systems, as well as factors of pharmacological correction of disorders of NO metabolism and associated with these changes endothelial dysfunction. Much attention is paid to the work, which reflects the role of nitric oxide in improving physical performance and the importance of this effect in the lives of athletes. The effect of nitric oxide on microorganisms, the use of nitric oxide in the treatment of infectious diseases, in particular during viral infection, is proved. The contribution of Ukrainian scientists in studying the effects of nitric oxide on the body of healthy and sick people, the elderly and senile, as well as the role in the creation of pharmacological drugs, nitric oxide donors for the prevention and treatment of diseases.

Effect of Tirofiban Injection on vascular endothelial function, cardiac function and inflammatory cytokines in patients with acute myocardial infarction after emergency Percutaneous Coronary Intervention.

ABSTRACTObjectives:To evaluate the effect of tirofiban injection on vascular endothelial function, cardiac function, inflammatory cytokines and other indicators in patients with acute myocardial infarction after emergency PCI and its clinical significance.Methods:Eighty patients with acute myocardial infarction admitted to Affiliated Hospital of Hebei University from March 18, 2020 to October 18, 2020 were enrolled and randomly divided into two groups: the experimental group and the control group, with 40 cases in each group. Patients in both groups underwent PCI. Patients in the control group were given oxygen inhalation, monitoring, and basic medications for myocardial infarction, such as nutritional myocardial drugs, statins, aspirin, nitrates, clopidogrel, and β-blockers. In contrast, patients in the experimental group received tirofiban 10 ug/kg intravenously over 5min immediately before PCI in addition to basic treatment, and then tirofiban 0.1 ug/(kg/min) was pumped via intravenous pump postoperatively for 48 hour. The changes of vascular endothelial function, cardiac function and adverse drug reactions (ADRs) in the two groups before treatment, one week and one month after treatment, as well as changes of inflammatory cytokines such as CRP and IL-6 in the two groups before and after treatment were compared and analyzed.Results:Compared with the control group, FMD, NO, ET-1 and other indexes in the experimental group were significantly improved one week and one month after treatment, with statistically significant differences (p<0.05). BNP, LVEDD, LVEF and additional indexes in the experimental group were significantly lower than those in the control group at one week and one month after treatment, with statistically significant differences (p=0.00). Moreover, the incidence of ST-segment fallback > 70% in the experimental group was 72.5% after treatment, which was significantly better than that of 47.5% in the control group, with a statistically significant difference (p=0.03). CRP and IL-6 in the experimental group were significantly lower than those in the control group after treatment, with a statistically significant difference (p=0.00). There was no statistical significance in the incidence of ADRs between the two groups after treatment (p=0.42).Conclusion:Tirofiban injection after emergency PCI is a beneficial treatment regime for patients with STEMI. With such a treatment regime, cardiac function and vascular endothelial function of patients can be dramatically improved, coronary blood supply will be ameliorated, inflammatory cytokines can be reduced, and no significant increase can be seen in the incidence of adverse reactions.

Стан судинного ендотелію у пацієнтів з хронічними запальними захворюваннями кишечника i різним нутритивним статусом

Актуальність. Визначення ендотеліальної функції за допомогою неінвазивних методів відіграє основну роль у прогнозуваннi перебігу різних захворювань, ризику розвитку ускладнень та оцінцi лікування. Мета: оцінка ендотеліальної функції в пацієнтів iз хронічними запальними захворюваннями кишечника (ХЗЗК) залежно від їхнього нутритивного статусу шляхом визначення стану судинного ендотелію в пробі з реактивною гіперемією та вмісту метаболітів оксиду азоту (МОА) в сироватці крові. Матеріали та методи. Сто двадцять пацієнтів iз ХЗЗК (81 — iз неспецифічним виразковим колітом (НВК) та 39 пацієнтів із хворобою Крона (ХК)) були розподілені на групи залежно від антропометричних характеристик: І — зі зниженим нутритивним статусом (n = 70); ІІ — iз нормальним (n = 20); ІІІ — iз підвищеним нутритивним статусом (n = 30). У сироватці крові пацієнтів вимірювали рівень МОА за В.А. Метельською. Для оцінки ендотеліальної функції визначали ендотелійзалежну вазодилатацію плечової артерії в пробі з реактивною гіперемією. Результати. На основі проведених досліджень встановлено вірогідне зниження вмісту МОА в сироватці крові: у пацієнтів iз НВК — у 1,7 раза (р &lt; 0,01) та з ХК — в 1,9 раза (р &lt; 0,001). Зниження вмісту МОА в сироватці крові не залежало від нутритивного статусу пацієнтів iз ХЗЗК. Порушення функції судинного ендотелію виявлено в 76,7 % випадків: зниження функції ендотелію — у 49,2 %, дисфункція — у 27,5 %. Зміни функції судинного ендотелію зареєстровано в 75,7 % пацієнтів І групи, 75 % — ІІ та у 83,4 % пацієнтів ІІІ групи, переважно внаслiдок зниження функції ендотелію. Висновки. Показано, що в 71 % пацієнтів iз ХЗЗК відбувається вірогідне зниження вмісту МОА в сироватці крові, що не залежить від їхнього нутритивного статусу. У хворих iз НВК спостерігалися більш виражені зміни у частотi виявлених порушень та більш значне зростання діаметра плечової артерії порівняно iз пацієнтами з ХК. Зниження нутритивного статусу супроводжувалося змінами функції судинного ендотелію в 75,4 % випадків.

STUDY OF VASCULAR ENDOTHELIAL DYSFUNCTION IN PATIENTS WITH INFLAMMATORY BOWEL DISEASE

Abstract. Currently, inflammatory bowel disease (IBD) is the most complex and not fully resolved problem in modern gastroenterology. IBD, with its two main subtypes, Crohn's disease (CD) and ulcerative colitis (UC), is a complex multifactorial pathology caused by external and internal factors, including host genetics, the immune system, environmental factors, and the gut microbiome. The possible involvement of endothelial dysfunction is also discussed. There is evidence that in diseases characterized by chronic systemic inflammation, it affects the properties of the arteries and causes both endothelial dysfunction and changes in arterial stiffness. The aim is to study the functional state of the vascular endothelium in patients with inflammatory bowel diseases. Material and methods. A total of 69 patients with IBD aged 18 to 70 years (44.0 ± 1.4 years) were examined. All patients were divided into 2 groups depending on the nosology. 1st group consisted of 45 patients with UC, among them 23 women (51.1 %) and 22 men (48.9 %), 2nd group – 24 patients with HC, of which 14 women (58.3 %) and 10 men (41.7 %). To assess endothelial function, the method for determining endothelium-dependent vasodilation of the brachial artery (BA) in a test with reactive hyperemia was used to assess the change in BA diameter (dPA), a ATL PHILIPS HDI 5000 SONOS CT ultrasound machine with a 7.5 MHz linear transducer was used. The endothelial function index was calculated as the difference between dPA after decompression and the initial value, expressed as a percentage. The content of a soluble vascular cell adhesion molecule 1 (VCAM-1) was determined in blood serum by an enzyme immunoassay using a test system («Bender MedSystems GmbH», Austria) using an enzyme immunoassay analyzer «Stat Fax 303 Plus» («Awareness Technology Inc.», USA). The number of desquamated endothelial cells in the peripheral blood was determined by the method of J. Hladovec. Results. In the study of endothelium-dependent vasodilation (EDVD) PA in a test with reactive hyperemia, dysfunctions of the vascular endothelium were found in 75.4 % of the examined patients. Changes in vascular endothelial function were found in 82.3 % of patients with UC and 62.5 % with CC, mainly due to endothelial dysfunction (ED). Significant differences were found between the indicators of the average increase in dPA in the test with reactive hyperemia with decreased endothelial function (DEF) and normal endothelial function (NEF), as well as with DEF and ED in patients with severe UC. ED was observed 5.2 times more often than NEF (c2 = 56.8; p &lt; 0.001) and 2.6 times more often than PFE (c2 = 31.5; p &lt; 0.001). With moderate severity of the disease, DEF and ED occurred with the same frequency and 2.2 times higher than the number of patients with NEF (c2 = 11.3; p = 0.0008), changes in endothelium-dependent vasodilation were accompanied by a significant increase in the VCAM-1 level in serum of all IBD patients, but the highest expression of VCAM-1 was observed in UC. At the same time, the concentration of VCAM-1 was inversely correlated with endothelium-dependent vasodilation of BA (r = - 0.54, p &lt; 0.01), which is confirmed by the quantitative characteristics of the level of VCAM-1 in various states of the endothelium. The study of the content of circulating desquamated endothelial cells in the peripheral blood made it possible to establish an increase in their number by 5 times with ED – up to (15.5 ± 4.8) × 104/L (p &lt; 0.05), 2 times with DEF – up to (5.7 ± 0.3) × 104/L (p &lt; 0.001) versus (3.1 ± 0.4) × 104/L in the control group. An inverse correlation was found between the number of desquamated endothelial cells and endothelium-dependent BA vasodilation (r = - 0.59, p &lt; 0.01). Conclusions. The results of a comprehensive study of the functional state of the vascular endothelium indicate that the course of IBD is accompanied by a syndrome of endothelial dysfunction (with a predominance of DE), which is characterized by a decrease in endothelium-dependent vasodilation of BA, an increase in the level of VCAM-1 and the content of circulating desquamated endothelial cells in the blood. Keywords: inflammatory bowel disease, Crohn's disease, ulcerative colitis, endothelial dysfunction.

Improvement of Vascular Endothelial Function Reflects Nonrecurrence After Catheter Ablation for Atrial Fibrillation.

BackgroundThe clinical implication of vascular endothelial dysfunction in patients with atrial fibrillation (AF) remains unclear. This study aimed to elucidate the correlation between changes in vascular endothelial function assessed by reactive hyperemia‐peripheral arterial tonometry and the effect of sinus rhythm restoration after catheter ablation (CA) for AF.Methods and ResultsConsecutive 214 patients who underwent CA for AF were included in this single center, retrospective study. The natural logarithmic transformed reactive hyperemia‐peripheral arterial tonometry index (LnRHI) of all patients was measured before CA as well as 3 and 6 months after CA. LnRHI in sinus rhythm was significantly higher than that in AF before CA. Multivariate logistic regression analysis revealed that the presence of AF was an independent risk factor for lowering of LnRHI (odds ratio, 4.092; P=0.002) before CA. The LnRHI was significantly improved 3 and 6 months after CA in patients without AF recurrence. Multivariate Cox hazard analysis revealed that changes in LnRHI from before to 3 months after CA independently correlated with recurrence of AF (hazard ratio, 0.106; P=0.001). Receiver operating characteristic analysis showed the decrease in LnRHI levels from before to 3 months after CA as a significant marker that suspects AF recurrence (area under the curve, 0.792; log‐rank test, P<0.001).ConclusionsThe presence of AF was independently correlated with the impaired vascular endothelial function assessed by the reactive hyperemia‐peripheral arterial tonometry. Long‐term sinus rhythm restoration after CA for AF might contribute to the improvement of vascular endothelial function, which may reflect the nonrecurrence of AF.

Vascular Endothelial Function as a Valid Predictor of Variations in Pulmonary Function in T2DM Patients Without Related Complications.

To assess the variations in pulmonary function and vascular endothelial function in their early stages (without related complications). A total of 162 type 2 diabetes mellitus (T2DM) patients without diabetes complications and 55 healthy people were selected, comprising the T2DM group and the control group, respectively, to evaluate changes in vascular endothelial function and lung function and determine the correlation between them. In this study, the T2DM group exhibited significantly lower pulmonary function than that of the control group (P < 0.05). The T2DM group also showed significantly lower flow-mediated dilation (FMD) and nitric oxide (NO) (P < 0.05) than those of the control group. Pulmonary functional indexes correlated positively with FMD and NO (P < 0.05) and correlated negatively with endothelin-1 (ET-1) (P < 0.05). FMD and NO correlated negatively with diabetes duration/HbA1c (P < 0.05), whereas ET-1 correlated positively with glycosylated hemoglobinA1c (HbA1c)/diabetes duration (P < 0.05). Pulmonary functional indexes negatively correlated with HbA1c/diabetes duration (P < 0.05). Multiple linear regression was used to analyze the relationship between vascular endothelial function indexes (FMD, ET-1, and NO) and pulmonary functional indexes. The results indicated that each vascular endothelial function index (FMD, ET-1, and NO) was significantly correlated with the pulmonary functional index (P < 0.05). The patients with T2DM presented changes in the subclinical vascular endothelial and pulmonary function. They also had impaired vascular endothelial functions, which were characterized by reduced vascular endothelial function relative to those of healthy people. Regulating glycemia may improve vascular endothelial and pulmonary functions. Moreover, microvascular lesions in preclinical stages, vascular endothelial function indexes (FMD, ET-1, and NO) were valid predictors of alterations in pulmonary function in T2DM patients without related complications.Clinical Trial Registration ClinicalTrials.gov, identifier NCT03575988.

Changes in endothelial function during educational hospitalization and the contributor to improvement of endothelial function in type 2 diabetes mellitus

Only a few reports have examined vascular endothelial function before and after educational hospitalization and the factors that affect it in patients with type 2 diabetes mellitus (T2DM). The aim of this study was to assess vascular endothelial function before and after educational hospitalization and identify factors that affect it. In 65 patients with T2DM who underwent peripheral arterial tonometry (EndoPAT) before and after hospitalization, vascular endothelial function (reactive hyperemia index [RHI]), glucose metabolism, lipid metabolism, and blood pressure were assessed before and after hospitalization. The primary endpoint was hospitalization-induced changes in vascular endothelial function. Educational hospitalization significantly improved the natural logarithmically scaled RHI (L_RHI) from 0.555 ± 0.212 to 0.625 ± 0.245 (p = 0.012). Multivariable logistic regression analysis identified hypoglycemia during hospitalization as the single factor that significantly altered vascular endothelial function (p = 0.019). The odds of achieving normal vascular endothelial function were 0.08 times lower (95% confidence interval, 0.01–0.67) for each episode of hypoglycemia. Furthermore, multivariable analysis identified hypoglycemia during hospitalization as the single factor that worsened L_RHI. Our study showed that educational hospitalization of patients with T2DM improved vascular endothelial function, and that the development of hypoglycemic episodes had a significant negative impact on normalization of vascular endothelial function.

Effects of diet-induced weight loss on postprandial vascular function after consumption of a mixed meal: Results of a randomized controlled trial with abdominally obese men.

Effects of weight loss on postprandial vascular function have not been studied so far. We therefore examined (i) effects of diet-induced weight loss on postprandial changes in various vascular function markers after consumption of a mixed meal and (ii) differences between normal-weight and abdominally obese men of comparable age at baseline and after weight loss. Fifty-four apparently healthy abdominally obese (waist circumference: 102-110cm) and 25 normal-weight men (waist circumference: <94cm) participated. The abdominally obese men were randomly allocated to a diet-induced weight-loss program or a no-weight loss control group. Men assigned to the weight-loss program followed a calorie-restricted diet for six weeks targeting a waist circumference of less than 102cm, followed by a weight-maintenance period for two weeks. The control group maintained their habitual diet and physical activity levels. Measurements were performed before and two hours after consumption of the test meal consisting of two muffins (containing 56.6g fat) and 300mL low-fat milk. The mean weight loss was 10.3kg in the weight-loss compared with the control group. The postprandial change in flow-mediated vasodilation of the brachial artery (FMD) was significantly higher at baseline in normal-weight as compared with the postprandial change in abdominally obese men (1.89±2.52 versus 0.48±2.50 percentage points; P=0.027). However, no differences in postprandial changes were observed in the abdominally obese men after weight loss compared with the control treatment. Also, weight reduction did not affect postprandial changes in carotid-to-femoral pulse wave velocity, retinal microvascular caliber properties, or plasma markers of microvascular endothelial function. Even though postprandial increases in triacylglycerol (P=0.028), insulin (P=0.029) and C-peptide concentrations (P<0.001) were reduced in the abdominally obese men following weight loss, postprandial changes in FMD at the end of the weight-loss treatment were still more unfavorable as compared with those observed in normal-weight individuals. In this trial with abdominally obese men, we did not find effects of diet-induced weight loss on postprandial changes in vascular endothelial function, arterial stiffness and markers of microvascular function. This trial was registered on ClinicalTrials.gov under study number NCT01675401.

Hypoglycemia Abrogates the Vascular Endothelial Protective Effect of Exenatide in Type 2 Diabetes Mellitus.

Glucagon-like peptide-1 (GLP-1) receptor agonists improve postprandial glucose, lipid metabolism, and vascular endothelial function. However, little is known about the effect of hypoglycemia on vascular endothelial function in patients on GLP-1 receptor agonist therapy. The aim of the present study was to determine the effect of hypoglycemia on vascular endothelial function in patients with type 2 diabetes mellitus (T2DM) treated with exenatide. Seventeen patients with T2DM underwent a meal tolerance test to examine the changes in vascular endothelial function and in glucose metabolism, both without exenatide and after a single subcutaneous injection of 10 μg exenatide. Vascular endothelial function was evaluated using reactive hyperemia index (RHI) measured by peripheral arterial tonometry before and 120 min after the meal loading test. The primary endpoint was the difference in changes in postprandial vascular endothelial function between the baseline and exenatide test. The results were analyzed in relation to the presence of absence of hypoglycemia. The natural logarithmically scaled RHI (L_RHI) was significantly lower after the baseline meal test but not in the exenatide test. Administration of exenatide caused symptomatic hypoglycemia in two patients during the meal tolerance test. The difference in the change in L_RHI was 0.125 ± 0.085 in the non-hypoglycemic group, whereas it was lower, − 0.487 ± 0.061, in the hypoglycemic group. The results of this study also suggest that the presence of hypoglycemia induces vascular endothelial dysfunction even during GLP-1 receptor agonist therapy.Trial registration: UMIN000015699.Electronic supplementary materialThe online version of this article (10.1007/s13300-019-0596-4) contains supplementary material, which is available to authorized users.

Effects of permanent cardiac pacemaker implantation on vascular endothelial function, blood coagulation and cardiac function in patients with bradycardia.

Changes in vascular endothelial function, blood coagulation and cardiac function indexes after the implantation of a permanent cardiac pacemaker in patients with bradycardia were investigated. A total of 53 healthy people and 117 patients with bradycardia in Jining First People's Hospital from January 2015 to August 2017 were selected. Factor VIII: coagulation (FVIII:C), von Willebr and factor (vWF), antithrombin activity (AT:A), D-dimmer (D-D), thrombomodulin (TM), tissue factor (TF), left ventricular ejection fraction (LVEF) and left ventricular end-systolic volume (LVESV) in the non-pacemaker group and the pacemaker group were significantly different from those in the control group (P<0.05), in which FVIII:C, vWF, D-D, TM, TF and LVESV were significantly higher than those in the control group, while LVEFs were significantly lower than that in the control group. After the implantation of a pacemaker, the FVIII:C, vWF, fibrinogen (FIB), D-D, TF and LVESV in patients were significantly higher than those before implantation (P<0.05), while the LVEF was significantly lower than that before implantation (P<0.05). In addition, in different pacemaker groups, there were no significant differences in blood coagulation and vascular endothelial indexes, but differences in cardiac function levels were obvious, in which LVEF in dual-chamber (DDD) pacemaker group was significantly higher than that in ventricular inhibited (VVI) pacemaker group, and LVESV in the former was significantly lower than that in the latter (P<0.05). Finally, here was no significant difference in the quality of life of patients implanted with different pacemakers (P>0.05), but the quality of life of patients in the DDD pacemaker group was better than that of patients in the VVI group. Therefore, implanting pacemakers in patients with bradycardia affects vascular endothelial function, blood coagulation, and cardiac function indexes in patients, and complications become less after the implantation of DDD pacemakers.

The level of proteinuria and the state of endothelial function in patients with chronic kidney disease combined with subclinical hypothyroidism under the influence of combined antihypertensive therapy.

Our aim was to assess the level of proteinuria and changes in vascular endothelial function in patients with chronic kidney disease (CKD) in combination with subclinical hypothyroidism (SHT) under the influence of antihypertensive combination therapy (valsartan 160 mg and amlodipine 5 mg). We examined 48 patients with CKD I-II stages and AH 1 and 2 degrees. Depending on the functional state of the thyroid gland, patients were divided into 2 groups. Within 12 weeks patients took a fixed combination of amlodipine 5 mg and valsartan 160 mg. Target BP levels were achieved in 19 (86.3%) patients of the main group and 22 (84.6%) of the comparison group. More often violation of brachial artery flow-mediated dilation and higher level of daily proteinuria were found in the main group patients. At the end of the study, the level of daily proteinuria in the main group decreased by 46.03% (p&lt;0.01), and in the comparison group – by 55.3% (p&lt;0.01). SHT can be considered as an additional factor that affects the course of CKD and AH by worsening the state of endothelial function and increasing the level of daily proteinuria. Combination of valsartan 160 mg and amlodipine 5 mg has lead to achieving of target blood pressure levels, improving of endothelial function and decreasing of daily proteinuria in both groups.

Effects of combined use of atorvastatin and losartan in treating patients with diabetic nephropathy

This study is to investigate the effect of atorvastatin combined with losartan on inflammatory factors, vascular endothelial function, and cardiovascular events in patients with diabetic nephropathy. A total of 128 patients with diabetic nephropathy treated in our hospital from January 2014 to December 2015 were selected as the study subjects, and 64 cases were randomly divided into observation group and 64 cases in the control group. The control group was treated with losartan on the basis of routine treatment, and the observation group was treated with atorvastatin on the basis of the control group. The blood lipid, inflammatory factors, changes in vascular endothelial function and cardiovascular events were compared between the two groups. The levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were not significantly different between the two groups before treatment ( P &gt; 0.05); after treatment, the levels of TC, TG, and LDL-C in the observation group were significantly lower than those of the control group, and the level of HDL-C was significantly higher than that of the control group ( P &lt; 0.05). The levels of high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6) were not statistically different between the two groups before treatment ( P &gt; 0.05); after treatment, the levels of hs-CRP, TNF-α, and IL-6 in the observation group were significantly lower than those of the control group ( P &lt; 0.05), the level of HDL-C was significantly higher than that of the control group ( P &lt; 0.05). There were no significant differences in the levels of endothelin-1 (ET-1) and nitric oxide (NO) between the two groups before treatment ( P &gt; 0.05). After treatment, the level of ET-1 in the observation group was significantly lower than that of the control group ( P &lt; 0.05), and the level of NO was significantly higher than that of the control group ( P &lt; 0.05). After treatment, all patients were followed up for 2 years, and the incidence of secondary cardiovascular events in the observation group was 12.50% (8/64), which was significantly lower than 29.69% (19/64) of the control group ( P &lt; 0.05). Combination of atorvastatin and losartan can significantly improve the levels of blood lipid, inflammatory factors, and vascular endothelial function in patients with diabetic nephropathy and can effectively reduce the incidence of cardiovascular events.

The Role of Endothelial Dysfunction Markers in Pregnant Women with Chorion Detachment, Included in the Program of Auxiliary Reproductive Technologies

An urgent medical and social problem is the restoration of reproductive function of womenwho suffer from infertility, which became possible due to auxiliary reproductive technologies. Women with induced pregnancy make thegroup of a high-risk on miscarriage, due to interrelated processes –immunological disorders and endothelial dysfunction that occur in the body of pregnant women after the use of extracorporal fertilization programs, and can lead to the chorion detachment and the formation of subchorionic hematomas.The purpose of the study is to determine the role of endothelial dysfunction as one of the leading factors that determine the development of a local non-progressive chorion detachment in infertile patients included in the program of auxiliary reproductive technologies.Materials and methods. We have examined 130 pregnant women, who were divided into groups: the control group included 30 women, whose pregnancy occurred in the natural cycle and with uncomplicated gestational course; the main group – 50 patients with induced pregnancy and risk factors of the occurrence of chorion detachment, who wereperformed the proposed pre-gravidapreparation; the comparative group – 50 pregnant women who received a standard scheme of pregnancy management before and after in-vitro fertilization. A general clinical examination, ultrasound examination, homocysteine level determination, endothelin-1 and nitrogen oxide metabolites were performed.Results. In women included into the program of auxiliary reproductive technologies with local chorion detachment were recorded changes of vascular endothelial function with a possible increase in endothelin-1 production and a decrease of the nitric oxidesynthesis. During the induced pregnancy with the presence of subchorionic hematoma, an increase of the level of endothelium-damaging factor of homocysteine was noted.Conclusions.This study identifies the parameters that reflect the main links of endothelial dysfunction and can be used as markers of local chorion detachment.

High density lipoprotein from coronary artery disease patients caused abnormal expression of long non-coding RNAs in vascular endothelial cells

Increased evidence has showed that normal high density lipoprotein (HDL) could convert to dysfunctional HDL in diseases states including coronary artery disease (CAD), which regulated vascular endothelial cell function differently. Long non-coding RNAs (lncRNAs) play an extensive role in various important biological processes including endothelial cell function. However, whether lncRNAs are involved in the regulation of HDL metabolism and HDL-induced changes of vascular endothelial function remains unclear. Cultured human umbilical vein endothelial cells (HUVECs) were treated with HDL from healthy subjects and patients with CAD and hypercholesterolemia for 24 h, then the cells were collected for lncRNA-Seq and the expressions of lncRNAs, genes and mRNAs were identified. The bioinformatic analysis was used to evaluate the relationship among lncRNAs, encoding genes and miRNAs. HDL from healthy subjects and patients with CAD and hypercholesterolemia leaded to different expressions of lncRNAs, genes and mRNAs, and further analysis suggested that the differentially expressed lncRNAs played an important role in the regulation of vascular endothelial function. Thus, HDL from patients with CAD and hypercholesterolemia could cause abnormal expression of lncRNAs in vascular endothelial cells to affect vascular function.

The effect of antihypertensive therapy and CPAP therapy on inflammatory and endothelial dysfunction markers levels in patients with severe obstructive sleep apnea syndrome in association with arterial hypertension

Objective. To evaluate the effect of antihypertensive therapy (AHT) and CPAP therapy on inflammatory and endothelial dysfunction markers levels in patients with severe obstructive sleep apnea (OSA) syndrome in association with arterial hypertension (AH). Materials and methods. The study included 43 male patients with severe OSA syndrome (Apnea-Hypopnea Index 52.4 [46.1; 58.6]) and AH (systolic blood pressure 144.0 [142.0; 156.0] mm Hg, diastolic blood pressure 90.9 [88.3; 93.5] mm Hg). Treatment with angiotensin-converting enzyme inhibitors, calcium antagonists, and thiazide-like diuretics was performed till target BP level measured with Korotkoff method was achieved. The patients who had reached target BP level (BP≤140/90 mm Hg) were randomized into two groups: group 1 included 23 patients who continued taking the AHT, group 2 included 22 patients who continued taking the AHT to which CPAP therapy was added. Peripheral blood lymphocyte immunophenotyping, cytokine panel test (IL-1β, IL-6, tumor necrosis factor a, IL-2Ra, sCD40L), adhesion molecule analysis (ICAM-1, VCAM-1), thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1a), and endothelin-1 levels in blood serum were evaluated at admission, after target BP level achievement (2nd visit) and after 3 months of AHT or AHT+CPAP therapy (3rd visit). Flow-mediated dilation of brachial artery was assessed using reactive hyperemia test by D.Celermajer. Results. Against the background of combined AHT the target BP level was achieved by 95% of patients. After target BP level achievement a significant decrease of IL-1β -0.16 [-0.5; 0], p=0.000 level and number of CD50+ cells (lymphocytes with inter-cellular adhesion molecule ICAM-3) from 2158.5 [1884.7; 2432.3] to 1949.6 [1740.9; 2158.3], p=0.050 were observed in patients with severe OSA associated with AH. There were no significant changes in vascular endothelial function observed in patients taking only AHT. Significant decrease of fibrinogen (-0.3 [-0.4; -0.1], p=0.002) and homocystein (-2.03 [-3.8; -0.2], p=0.03) levels was observed in patients taking both AHT and CPAP therapy. Conclusion. The combination of AHT and CPAP therapy in patients with severe OSA and AH not only allows reaching the target BP level but also leads to inflammatory and endothelial dysfunction markers levels decrease.

Impact of DPP-4 inhibition on acute and chronic endothelial function in humans with type 2 diabetes on background metformin therapy.

NCT01859793.

Влияние антигипертензивной и СИПАП-терапии на маркеры воспалительного ответа и эндотелиальной функции у пациентов с синдромом обструктивного апноэ сна тяжелой степени в сочетании с артериальной гипертонией

Objective. To evaluate the effect of antihypertensive therapy (AHT) and CPAP therapy on inflammatory and endothelial dysfunction markers levels in patients with severe obstructive sleep apnea (OSA) syndrome in association with arterial hypertension (AH). Materials and methods. The study included 43 male patients with severe OSA syndrome (Apnea-Hypopnea Index 52.4 [46.1; 58.6]) and AH (systolic blood pressure 144.0 [142.0; 156.0] mm Hg, diastolic blood pressure 90.9 [88.3; 93.5] mm Hg). Treatment with angiotensin-converting enzyme inhibitors, calcium antagonists, and thiazide-like diuretics was performed till target BP level measured with Korotkoff method was achieved. The patients who had reached target BP level (BP≤140/90 mm Hg) were randomized into two groups: group 1 included 23 patients who continued taking the AHT, group 2 included 22 patients who continued taking the AHT to which CPAP therapy was added. Peripheral blood lymphocyte immunophenotyping, cytokine panel test (IL-1β, IL-6, tumor necrosis factor a, IL-2Ra, sCD40L), adhesion molecule analysis (ICAM-1, VCAM-1), thromboxane B2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1a), and endothelin-1 levels in blood serum were evaluated at admission, after target BP level achievement (2nd visit) and after 3 months of AHT or AHT+CPAP therapy (3rd visit). Flow-mediated dilation of brachial artery was assessed using reactive hyperemia test by D.Celermajer. Results. Against the background of combined AHT the target BP level was achieved by 95% of patients. After target BP level achievement a significant decrease of IL-1β -0.16 [-0.5; 0], p=0.000 level and number of CD50+ cells (lymphocytes with inter-cellular adhesion molecule ICAM-3) from 2158.5 [1884.7; 2432.3] to 1949.6 [1740.9; 2158.3], p=0.050 were observed in patients with severe OSA associated with AH. There were no significant changes in vascular endothelial function observed in patients taking only AHT. Significant decrease of fibrinogen (-0.3 [-0.4; -0.1], p=0.002) and homocystein (-2.03 [-3.8; -0.2], p=0.03) levels was observed in patients taking both AHT and CPAP therapy. Conclusion. The combination of AHT and CPAP therapy in patients with severe OSA and AH not only allows reaching the target BP level but also leads to inflammatory and endothelial dysfunction markers levels decrease.