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Abstract Background Obstructive sleep apnea (OSA) is associated with high blood pressure that responds poorly to usual antihypertensive therapy. Methods and results Forty-one subjects with OSA had 25% higher plasma norepinephrine and 42% higher epinephrine measured every 2 h over 24 h than 20 control subjects. They also excreted more sodium during sleep. This suggested that that a sympatholytic would be a more successful antihypertensive than a diuretic. To test this hypothesis we treated a second group of 23 hypertensive apneics with placebo, 6 weeks of the sympatholytic guanfacine and 6 weeks of hydrochlorothiazide in a crossover study. Guanfacine lowered 24-hour blood pressure by 9.6/6.7 mmHg, more than the 5.4/2.9 mmHg effect of hydrochlorothiazide (P

Introduction: Cardiovascular disease (CVD) accounts for a significant percentage of global deaths and emphasizes the importance of early detection for prevention. Endothelial dysfunction serves as a reversible precursor of atherosclerosis and plays a crucial role in the development of complications such as heart attacks and strokes. Assessment of endothelial function using flow-mediated dilation (FMD) in the brachial artery utilizing noninvasive ultrasound imaging provides promising opportunities for early detection and intervention strategies in cardiovascular health. Material and Method: The study employs meticulous data collection procedures through ultrasonographic scanning of the brachial artery to ensure precise measurements of parameters such as mean velocity, diameter, flow, shear stress, and percentage flow-mediated dilation. Result: Significantly, the study results revealed variations in blood sugar levels and % FMD between the control and case groups, highlighting potential differences in endothelial function and vascular health. Additionally, the study conducted a comparative analysis of data from different studies, providing valuable insights into the impact of shear stress on endothelial homeostasis and cardiovascular health. Conclusion: The comprehensive assessment of endothelial function and its correlation with cardiovascular disease risk, through advanced methodologies and meticulous data analysis, empowers researchers and healthcare practitioners with crucial insights into refining risk assessments and personalized treatment strategies in cardiovascular health. [ABSTRACT FROM AUTHOR]

Poor cardiorespiratory fitness may mediate vascular impairments at rest and following an acute bout of exercise in young healthy individuals. This study aimed to compare flow mediated dilation (FMD) and vascular augmentation index (AIx75) between young adults with low, moderate, and high levels of cardiorespiratory fitness before and after an acute bout of aerobic exercise. Forty-three participants (22 men; 21 women) between 18 and 29 years of age completed the study. Participants were classified into low, moderate, and high health-related cardiorespiratory fitness groups according to age- and sex-based relative maximal oxygen consumption (V˙O2 max) percentile rankings. FMD was performed using Doppler ultrasound and AIx75 was performed using pulse wave analysis at baseline and 60-min after a 30-min bout of treadmill running at 70% V˙O2 max. A significant interaction (p ​= ​0.047; ηp2 ​= ​0.142) was observed, with the moderate fitness group exhibiting a higher FMD post-exercise compared with baseline ([6.7% ​± ​3.1%] vs. [8.5% ​± ​2.8%], p ​= ​0.028; d ​= ​0.598). We found a significant main effect of group for AIx75 (p ​= ​0.023; ηp2 ​= ​0.168), with the high fitness group exhibiting lower AIx75 compared to low fitness group ([−10% ​± ​10%] vs. [2% ​± ​10%], respectively, p ​= ​0.019; g ​= ​1.07). This was eliminated after covarying for body fat percentage (p ​= ​0.489). Our findings suggest that resting FMD and AIx75 responses are not significantly influenced by cardiorespiratory fitness, but FMD recovery responses to exercise may be enhanced in individuals with moderate cardiorespiratory fitness levels.

Atrial fibrillation (AF), the most common cardiac arrhythmia, is associated with adverse CV outcomes. Vascular aging (VA), which is defined as the progressive deterioration of arterial function and structure over a lifetime, is an independent predictor of both AF development and CV events. A timing identification and treatment of early VA has therefore the potential to reduce the risk of AF incidence and related CV events. A network of scientists and clinicians from the COST Action VascAgeNet identified five clinically and methodologically relevant questions regarding the relationship between AF and VA and conducted a narrative review of the literature to find potential answers. These are: (1) Are VA biomarkers associated with AF? (2) Does early VA predict AF occurrence better than chronological aging? (3) Is early VA a risk enhancer for the occurrence of CV events in AF patients? (4) Are devices measuring VA suitable to perform subclinical AF detection? (5) Does atrial-fibrillation-related rhythm irregularity have a negative impact on the measurement of vascular age? Results showed that VA is a powerful and independent predictor of AF incidence, however, its role as risk modifier for the occurrence of CV events in patients with AF is debatable. Limited and inconclusive data exist regarding the reliability of VA measurement in the presence of rhythm irregularities associated with AF. To date, no device is equipped with tools capable of detecting AF during VA measurements. This represents a missed opportunity to effectively perform CV prevention in people at high risk. Further advances are needed to fill knowledge gaps in this field. [ABSTRACT FROM AUTHOR]

Poor cardiorespiratory fitness may mediate vascular impairments at rest and following an acute bout of exercise in young healthy individuals. This study aimed to compare flow mediated dilation (FMD) and vascular augmentation index (AIx75) between young adults with low, moderate, and high levels of cardiorespiratory fitness before and after an acute bout of aerobic exercise. Forty-three participants (22 men; 21 women) between 18 and 29 years of age completed the study. Participants were classified into low, moderate, and high health-related cardiorespiratory fitness groups according to age- and sex-based relative maximal oxygen consumption (V̇O2 max) percentile rankings. FMD was performed using Doppler ultrasound and AIx75 was performed using pulse wave analysis at baseline and 60-min after a 30-min bout of treadmill running at 70% V̇O2 max. A significant interaction (p = 0.047; ηp ² = 0.142) was observed, with the moderate fitness group exhibiting a higher FMD post-exercise compared with baseline ([6.7% ± 3.1%] vs. [8.5% ± 2.8%], p = 0.028; d = 0.598). We found a significant main effect of group for AIx75 (p = 0.023; ηp ² = 0.168), with the high fitness group exhibiting lower AIx75 compared to low fitness group ([10% ± 10%] vs. [2% ± 10%], respectively, p = 0.019; g = 1.07). This was eliminated after covarying for body fat percentage (p = 0.489). Our findings suggest that resting FMD and AIx75 responses are not significantly influenced by cardiorespiratory fitness, but FMD recovery responses to exercise may be enhanced in individuals with moderate cardiorespiratory fitness levels. [ABSTRACT FROM AUTHOR]

Background: Female sexual dysfunction (FSD) has been suggested to be correlated with the burden of cardiovascular risk factors. Aim: We aimed to evaluate the possible association between functional indices of vascular function and FSD scores in apparently healthy postmenopausal women. Methods: This cross-sectional study included 116 postmenopausal women who underwent assessment of endothelial function with measurement of flow-mediated dilation (FMD) of the branchial artery and arterial stiffness estimation with measurement of the carotid-femoral pulse wave velocity (PWV). We used the Greene Climacteric Scale to evaluate vasomotor symptomatology, the Female Sexual Function Index (FSFI) to evaluate FSD and the Beck Depression Inventory to evaluate mood disorder. Low sexual function was defined as an FSFI score <26.55. Outcomes: These included FSFI and low sexual function scores as well as measures of PWV and FMD. Results: Sexual function scores were associated with measures of blood pressure (normal vs low sexual function; systolic blood pressure: 120.2 ± 15.0 mm Hg vs 113.4 ± 14.6 mm Hg; analysis of covariance P =.026; diastolic blood pressure: 75.9 ± 10.5 mm Hg vs 70.3 ± 9.9 mm Hg; analysis of covariance P =.012; both adjusted for age, body mass index, current smoking, and PWV). Systolic blood pressure, but not diastolic blood pressure, was associated with FSFI (B = 0.249, P =.041) and PWV (B = 0.392, P <.001). PWV measures were associated with FSFI (B = −0.291, P =.047) and pulse pressure (B = 0.355, P =.017). FMD measures were also associated with FSFI (B = 0.427, P =.033). All models were adjusted for age, body mass index, current smoking, insulin resistance, vasomotor symptomatology, and Beck Depression Inventory. Clinical implications: Our findings demonstrate that lower scores of sexual function are associated with deteriorated vascular function mainly manifested as arterial stiffening, further contributing to systolic blood pressure changes. Strengths and limitations: The strength of this study is the carefully selected healthy sample of postmenopausal women, with simultaneous assessment of climacteric symptomatology and mood disorders. The limitations include the small sample size, the cross-sectional design, and the recruitment of consecutive outpatients of a university menopause clinic. Conclusion: Longitudinal studies and interventions to improve FSD should further assess the clinical relevance of these findings. [ABSTRACT FROM AUTHOR]

Folic acid might improve endothelial function, but the results are inconclusive. This systematic review evaluated the effect of folic acid supplementation on endothelial parameters and arterial stiffness in adults. The study protocol was registered with the PROSPERO database (CRD42021290195). The PubMed, Web of Sciences, Cochrane and Scopus databases were searched to identify English-language randomised controlled trials of the effect of folate supplementation on arterial stiffness and endothelial function markers in adults. There were significant differences between the effect of folic acid and placebo on flow-mediated dilation (random-effects model, standardized mean differences (SMD): 0.888, 95% confidence interval (CI): 0.447, 1.329, p < 0.001) and monocyte chemotactic protein 1 (random-effects model, SMD: −1.364, 95% CI: −2.164, −0.563, p < 0.001), but there was no significant difference in the central pulse wave velocity (fixed-effects model, SMD: −0.069, 95% CI: −0.264, 0.125, p = 0.485) and peripheral pulse wave velocity (fixed-effects model, SMD: −0.093, 95% CI: −0.263, 0.077, p = 0.284). In conclusion, folic acid might have a favourable effect on endothelial function but may not affect arterial stiffness. Further studies are needed to confirm these results. [ABSTRACT FROM AUTHOR]

Objective: There has been increasing awareness that micro-vascular alteration or vascular inflammation has been associated with levodopa-induced dyskinesia in PD. Vascular endothelial function assessed by flow mediated dilation (FMD) is known to reflect early microvascular change. We compare the impact of levodopa or dopamine agonist treatment on the change of FMD in de novo PD patients. Methods: This retrospective study used a selected sample from registry. We identified de-novo PD patients who underwent FMD at baseline, and follow-up FMD after 1 year (± 2 month) of levodopa (n = 18) or dopamine agonist (n = 18) treatment. Results: FMD decreased after levodopa (8.60 ± 0.46 to 7.21 ± 0.4, p = 0.002) but there were no significant changes after DA treatment (8.33 ± 0.38 to 8.22 ± 0.33, p = 0.26). Homocysteine rose (11.52 ± 0.45 to 14.33 ± 0.68, p < 0.05) during levodopa treatment, but dopamine agonist had no effect (10.59 ± 0.38 to 11.38 ± 0.67, p = 0.184). Correlation analysis revealed that the changes in homocysteine level had non-significant correlation with FMD change (r = − 0.30, p = 0.06). FMD change was not associated with age (p = 0.47), disease duration (p = 0.81), baseline motor UPDRS (p = 0.43), motor UPDRS change (p = 0.64), levodopa equivalent dose change (p = 0.65). Conclusions: We found that 1-year levodopa treatment may adversely affect vascular endothelial function in de novo PD. Further studies are needed to clarify the exact pathogenesis and clinical implication of levodopa-induced endothelial dysfunction in PD. [ABSTRACT FROM AUTHOR]

Tobacco cigarette (TC) smoking has never been lower in the United States, but electronic cigarette (EC) vaping has reached epidemic proportions among our youth. Endothelial dysfunction, as measured by flow-mediated vasodilation (FMD) is a predictor of future atherosclerosis and adverse cardiovascular events and is impaired in young TC smokers, but whether FMD is also reduced in young EC vapers is uncertain. The aim of this study in otherwise healthy young people was to compare the effects of acute and chronic tobacco cigarette (TC) smoking and electronic cigarette (EC) vaping on FMD. FMD was compared in 47 nonsmokers (NS), 49 chronic EC vapers, and 40 chronic TC smokers at baseline and then after EC vapers (n = 31) and nonsmokers (n = 47) acutely used an EC with nicotine (ECN), EC without nicotine (EC0), and nicotine inhaler (NI) at ~4-wk intervals and after TC smokers (n = 33) acutely smoked a TC, compared with sham control. Mean age (NS, 26.3 ± 5.2 vs. EC, 27.4 ± 5.45 vs. TC, 27.1 ± 5.51 yr, P = 0.53) was similar among the groups, but there were more female nonsmokers. Baseline FMD was not different among the groups (NS, 7.7 ± 4.5 vs. EC:6.6 ± 3.6 vs. TC, 7.9 ± 3.7%∆, P = 0.35), even when compared by group and sex. Acute TC smoking versus control impaired FMD (FMD pre-/postsmoking, -2.52 ± 0.92 vs. 0.65 ± 0.93%∆, P = 0.02). Although the increase in plasma nicotine was similar after EC vapers used the ECN versus TC smokers smoked the TC (5.75 ± 0.74 vs. 5.88 ± 0.69 ng/mL, P = 0.47), acute EC vaping did not impair FMD. In otherwise healthy young people who regularly smoke TCs or ECs, impaired FMD compared with that in nonsmokers was not present at baseline. However, FMD was significantly impaired after smoking one TC, but not after vaping an equivalent "dose" (estimated by change in plasma nicotine) of an EC, consistent with the notion that non-nicotine constituents in TC smoke mediate the impairment. Although it is reassuring that acute EC vaping did not acutely impair FMD, it would be dangerous and premature to conclude that ECs do not lead to atherosclerosis.NEW & NOTEWORTHY In our study of otherwise healthy young people, baseline flow-mediated dilation (FMD), a predictor of atherosclerosis and increased cardiovascular risk, was not different among tobacco cigarette (TC) smokers or electronic cigarette (EC) vapers who had refrained from smoking, compared with nonsmokers. However, acutely smoking one TC impaired FMD in smokers, whereas vaping a similar EC "dose" (as estimated by change in plasma nicotine levels) did not. Finally, although it is reassuring that acute EC vaping did not acutely impair FMD, it would be premature and dangerous to conclude that ECs do not lead to atherosclerosis or increase cardiovascular risk.

Abstract Background Endothelial dysfunction serves as an early marker for the risk of cardiovascular disease (CVD); therefore, it is an attractive site of therapeutic interventions to reduce the risk of CVD. This study was conducted to investigate the effect of folic acid supplementation on endothelial function markers in randomized controlled trials (RCTs). Methods PubMed, ISI web of science, and Scopus databases were searched up to July 2022 for detecting eligible studies. A random-effects model was used for meta-analysis, and linear Meta-regression and non-linear dose-response analysis were performed to assess whether the effect of folic acid supplementation was affected by the dose and duration of intervention. Cochrane tools were also used to assess the risk of bias in the included studies. Results Twenty-one studies, including 2025 participants (1010 cases and 1015 controls), were included in the present meta-analysis. Folic acid supplementation significantly affected the percentage of flow-mediated dilation (FMD%) (WMD: 2.59%; 95% CI: 1.51, 3.67; P

Background: Rosacea may contribute to the development of cardiovascular (CV) diseases by causing endothelial dysfunction (ED), which is known to be the initial step of atherosclerosis, due to its inflammatory features. Objective: This study aimed to assess ED in rosacea patients using the flow‐mediated dilatation (=dilation) (FMD) method. Methods: Seventy‐three rosacea patients and 73 age, gender‐matched healthy volunteers were enrolled. Individuals with cardiac risk factors, pregnant, and lactating women were excluded. Demographic, clinical data and anthropometric measurements were recorded. FMD measurement was performed ultrasonographically by a cardiologist. Systolic and diastolic blood pressures (BP) were measured and hemogram, erythrocyte sedimentation rate (ESR), C‐Reactive Protein (CRP), total cholesterol, triglyceride, low‐density lipoprotein (LDL), high‐density lipoprotein (HDL), neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), mean platelet volume (MPV), and fasting blood glucose values were assessed. Results: The FMD value was statistically lower in rosacea patients compared with healthy controls (p = 0.000). Metabolic syndrome, systolic and diastolic BPs, and plasma NLR were higher in the rosacea group (p = 0.009, p = 0.000, p = 0.000, p = 0.000, respectively). According to the multivariate linear regression analysis, rosacea type significantly predicted FMD. Conclusions: Rosacea is not only a disease limited to the skin, but it may also have systemic involvement. A significant difference was found between FMD values measured in between the case and control groups, suggesting rosacea may have an atherogenic effect. Possible cardiac risks should be considered in rosacea patients, and further evaluation could be warranted. [ABSTRACT FROM AUTHOR]

This article explores the cardiovascular consequences of ultramarathons, which are running events longer than a marathon. The study examines the acute effects of extreme endurance exercise on peripheral micro- and macrovascular function and central hemodynamics before, during, and after a 50 km ultramarathon. The findings suggest that 50 km ultramarathon training does not impair macrovascular function and challenge the hypothesis of a "J-shaped" relationship between exercise volume and cardiovascular health. However, more studies are needed to gain further insight into this relationship and determine the potential threshold at which exercise training might start to confer cardiovascular harm. [Extracted from the article]

Background: Endothelial dysfunction serves as an early marker for the risk of cardiovascular disease (CVD); therefore, it is an attractive site of therapeutic interventions to reduce the risk of CVD. This study was conducted to investigate the effect of folic acid supplementation on endothelial function markers in randomized controlled trials (RCTs). Methods: PubMed, ISI web of science, and Scopus databases were searched up to July 2022 for detecting eligible studies. A random-effects model was used for meta-analysis, and linear Meta-regression and non-linear dose-response analysis were performed to assess whether the effect of folic acid supplementation was affected by the dose and duration of intervention. Cochrane tools were also used to assess the risk of bias in the included studies. Results: Twenty-one studies, including 2025 participants (1010 cases and 1015 controls), were included in the present meta-analysis. Folic acid supplementation significantly affected the percentage of flow-mediated dilation (FMD%) (WMD: 2.59%; 95% CI: 1.51, 3.67; P < 0.001) and flow-mediated dilation (FMD) (WMD: 24.38 μm; 95% CI: 3.08, 45.68; P = 0.025), but not end-diastolic diameter (EDD) (WMD: 0.21 mm; 95% CI: − 0.09, 0.52; P = 0.176), and intercellular adhesion molecule (ICAM) (WMD: 0.18 ng/ml; 95% CI: − 10.02, 13.81; P = 0.755). Conclusions: These findings suggest that folic acid supplementation may improve endothelial function by increasing FMD and FMD% levels. Trial registration: PROSPERO registration cod: CRD42021289744. [ABSTRACT FROM AUTHOR]

Aims: Gestational diabetes mellitus (GDM) is a common medical complication during pregnancy. Endothelial dysfunction is considered an early step in the progression of atherosclerosis that may contribute to subclinical target organ damage. This meta‐analysis aimed to systemically review the existing data regarding endothelial dysfunction between women with and without GDM during pregnancy and post‐partum using flow‐mediated dilation (FMD). Materials and Methods: Eligible studies (cohort and observational) published until October 2021 were identified in the MEDLINE, Scopus, Cochrane Library database and grey literature sources were searched. Results: The search yielded 2272 studies, of which 17 were fully reviewed and 12 studies (N = 740 pregnant women) were finally included. Pregnant women with GDM exhibited a significantly lower FMD compared to pregnant women without GDM (pooled mean difference −3.12; 95% CI −5.36 to −0.88). Moreover, in the immediate (1–6 months) post‐partum period, women with previous GDM showed lower FMD compared to healthy women without GDM history (pooled mean difference −7.52; 95% CI −9.44 to −5.59), whereas FMD did not differ in the late post‐partum period (more than 4 years). Conclusions: Flow‐mediated dilation is decreased in women with GDM during pregnancy and in the immediate post‐partum period, compared to women without GDM, indicating that the endothelial dysfunction noted during the pregnancy in those women persists in the immediate post‐partum period too. Clinical trial registration: PROSPERO CRD42021283113 (www.ClinicalTrials.gov). [ABSTRACT FROM AUTHOR]

Folic acid might improve endothelial function, but the results are inconclusive. This systematic review evaluated the effect of folic acid supplementation on endothelial parameters and arterial stiffness in adults. The study protocol was registered with the PROSPERO database (CRD42021290195). The PubMed, Web of Sciences, Cochrane and Scopus databases were searched to identify English-language randomised controlled trials of the effect of folate supplementation on arterial stiffness and endothelial function markers in adults. There were significant differences between the effect of folic acid and placebo on flow-mediated dilation (random-effects model, standardized mean differences (SMD): 0.888, 95% confidence interval (CI): 0.447, 1.329, p < 0.001) and monocyte chemotactic protein 1 (random-effects model, SMD: −1.364, 95% CI: −2.164, −0.563, p < 0.001), but there was no significant difference in the central pulse wave velocity (fixed-effects model, SMD: −0.069, 95% CI: −0.264, 0.125, p = 0.485) and peripheral pulse wave velocity (fixed-effects model, SMD: −0.093, 95% CI: −0.263, 0.077, p = 0.284). In conclusion, folic acid might have a favourable effect on endothelial function but may not affect arterial stiffness. Further studies are needed to confirm these results.

In this study, a physics-based model is developed to describe the entire flow mediated dilation (FMD) response. A parameter quantifying the arterial wall's tendency to recover arises from the model, thereby providing a more elaborate description of the artery's physical state, in concert with other parameters characterizing mechanotransduction and structural aspects of the arterial wall. The arterial diameter's behavior throughout the full response is successfully reproduced by the model. Experimental FMD response data were obtained from healthy volunteers. The model's parameters are then adjusted to yield the closest match to the observed experimental response, hence delivering the parameter values pertaining to each subject. This study establishes a foundation based on which future potential clinical applications can be introduced, where endothelial function and general cardiovascular health are inexpensively and noninvasively quantified., Competing Interests: Declaration of competing interest The authors have no conflicts of interest to declare., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Copyright of Koomesh: Journal of Semnan University of Medical Sciences is the property of Koomesh: Journal of Semnan University of Medical Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Saudi Medical Journal is the property of Saudi Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Our aim was to assess whether systemic endothelial dysfunction, evaluated non-invasively by flow mediated dilation (FMD), is associated with diabetic macular edema (DME) and to determine if it is further impaired in patients with diffuse-DME. Consecutive patients (n = 84) with type-2 diabetes mellitus (T2DM) and diabetic retinopathy were enrolled. DME was not present in 38 (non-DME) and present in 46 patients; 25 with focal and 21 with diffuse-DME. No differences were detected between DME and non-DME groups regarding the clinical and demographic characteristics, except for the age of T2DM initiation (lower in non-DME). FMD values were significantly impaired in DME compared with non-DME patients, even after adjustment for multiple covariates (3.56 ± 1.03 vs 4.57 ± 1.25%, P = .003). Among DME patients, no differences were found concerning the clinical and demographic data, while FMD levels were significantly lower in diffuse-DME patients, compared with the focal-DME ones, regardless of the impact several confounders (2.88 ± 0.65 vs 4.08 ± 0.95%, P = .002). It is noteworthy that FMD values of non-DME and focal-DME patients did not differ significantly (4.52 ± 1.24 vs 4.21 ± 1.06%, P = .307). Moreover, among DME patients, impaired FMD was an independent predictor of diffuse-DME (odds ratio: 0.06, 95% CI 0.01-0.47, P = .007). [ABSTRACT FROM AUTHOR]

Endothelial dysfunction represents a key feature of the pathological process underlying micro and macro-vascular damage in Systemic Sclerosis (SSc). This study aims to improve knowledge of the physiopathology of vascular damage in SSc through the assessment of the endothelial dysfunction by Flow Mediated Dilation (FMD) and serum levels of circulating endothelial dysfunction markers and the correlation of macrovascular damage with clinical findings and microvascular capillaroscopic patterns. 57 SSc patients and 37 healthy subjects were recruited. All included subjects underwent radial artery FMD test and Nailfold Video-Capillaroscopy; serum levels of Vascular Endothelial Growth Factor (VEGF), Vascular Cell Adhesion Molecule-1 (VCAM-1) and angiopoietin-2 were evaluated. Compared to healthy subjects, in SSc patients lower FMD and higher time needed to obtain the maximal FMD responsewere observed, whereas serum levels of VEGF, VCAM-1, and angiopoietin-2 were significantly higher. The impairment of FMD values was associated with disease duration, pulmonary arterial hypertension, and digital ulcers and correlates with greater microvascular damage evaluated by Nailfold Video-Capillaroscopy... An inverse relationship between VEGF, angiopoietin-2, VCAM-1 levels and FMD was observed, but only VEGF and angiopoietin-2 were significantly higher in patients with digital ulcers and pulmonary arterial hypertension. FMD ultrasound test and circulating levels of endothelial dysfuncion markers could be useful as biomarkers of vasculopathy and could be a helpful tool in the overall assessment of vascular injury in Systemic Sclerosis patients. [Display omitted] [ABSTRACT FROM AUTHOR]

Potential future directions of ACEs and cardiovascular health research include examining whether sleep, an important health behavior that influences vascular function, may mediate the effects of ACEs on vascular function. However, the interaction between ACEs, social determinants of health, and health behaviors remain important areas for future research to further clarify the association between ACEs and CVDs. Despite the pervasiveness of ACEs and robust evidence supporting the association between ACEs and CVD, our current understanding of how ACEs promote CVD is limited. [Extracted from the article]

Abstract A high sodium (Na+) meal impairs peripheral vascular function. In rodents, chronic high dietary Na+ impairs cerebral vascular function, and in humans, habitual high dietary Na+ is associated with increased stroke risk. However, the effects of acute high dietary Na+ on the cerebral vasculature in humans are unknown. The purpose of this study was to determine if acute high dietary Na+ impairs cerebrovascular reactivity in healthy adults. Thirty‐seven participants (20F/17M; 25 ± 5 years; blood pressure [BP]: 107 ± 9/61 ± 6 mm Hg) participated in this randomized, cross‐over study. Participants were given a low Na+ meal (LSM; 138 mg Na+) and a high Na+ meal (HSM; 1,495 mg Na+) separated by ≥ one week. Serum Na+, beat‐to‐beat BP, middle cerebral artery velocity (transcranial Doppler), and end‐tidal carbon dioxide (PETCO2) were measured pre‐ (baseline) and 60 min post‐prandial. Cerebrovascular reactivity was assessed by determining the percent change in middle cerebral artery velocity to hypercapnia (via 8% CO2, 21% oxygen, balance nitrogen) and hypocapnia (via mild hyperventilation). Peripheral vascular function was measured using brachial artery flow‐mediated dilation (FMD). Changes in serum Na+ were greater following the HSM (HSM: Δ1.6 ± 1.2 mmol/L vs. LSM: Δ0.7 ± 1.2 mmol/L, p

Background The role of the glycocalyx as the endothelial sensor of an increase in blood flow was assessed in the iliac artery in vivo. Methods Acetylcholine-induced flow mediated dilation was evaluated before and after vascular glycocalyx disruption. This was accomplished by exposing the iliac lumen to the chemotactic agent fMLP (1 μM; n = 6 pigs), concomitant heparinase III (100 mU ml−1) and hyaluronidase (14 mg ml−1) (n = 4), and neuraminidase (140 mU ml−1; n = 5), for 20 min in separate iliac artery preparations. Only one lumen intervention per iliac was conducted. Results For the heparinase III + hyaluronidase experiment, the iliac diameter increased by an average of 0.54 ± 0.11 mm before and 0.45 ± 0.03 mm after the enzymes (P = 0.42; paired Student’s t test). The iliac diameter increased by 0.31 ± 0.02 mm before and 0.29 ± 0.07 mm after fMLP exposure (P = 0.7) and the diameter increased by 0.54 ± 0.11 mm before and 0.54 ± 0.09 mm after neuraminidase exposure (P = 0.98). In all cases, the shear stress changes before and after lumen exposure were not significantly different to each other. Conclusion There was no significant reduction in flow mediated dilation of the iliac in response to any of the interventions conducted. Therefore, the vascular endothelial glycocalyx as whole is not required for flow mediated dilation in conduit arteries in the intact animal.

Background Athletes are increasingly exploring ways to enhance their physical performance. Increasing blood flow to the working tissues through endothelium-dependent vasodilation is one factor athletes use to realize these results. Sports supplements such as pre-workouts tout this benefit; however, many have not been tested under laboratory conditions to examine the effects of commonly used supplements on vasodilation. Two popular supplements are Nitrosigine® and citrulline malate (CM). Thus, the purpose of this experiment was to determine the effects of Nitrosigine and CM on vasodilation using ultrasound and flow mediated dilation (FMD). Methods Healthy, normotensive, and physically active male (n = 16) and female (n = 8) young adults participated in the present investigation. We utilized a randomized, double-blind, within-subjects design where participants reported for three trials, each preceded by a 7-day washout period. Baseline FMD measurement was obtained for each visit, followed by consumption of one clinical dose CM (8 g), Nitrosigine (1.5 g), or dextrose placebo (8 g). Following a 60-min digestion period, FMD was repeated. Supplementation order was randomized controlling for potential order effects. Results Repeated measures ANOVA yielded a significant supplement (3) x time (2) effect (p

Abstract Background Currently, many methodological approaches have been developed to assess peripheral endothelial function. However, a development of the noninvasive and automated technique for routinely assessing endothelial function is still required. We evaluated the potential value of a new method to measure peripheral endothelial function with reactive hyperemia peripheral arterial volume (RH-PAV) in patients with chest pain. Methods We used a novel oximeter-like probe to detect the peripheral arterial volume (PAV) of the finger and compared it with brachial flow-mediated dilation (FMD) performed in 93 consecutive patients with chest pain. The RH-PAV index was defined as the ratio of the digital pulse volume during reactive hyperemia relative to the baseline. Results Ninety-three patients (53 men, 58 ± 5 years) completed the study, and 53 patients demonstrated coronary artery disease (CAD) following scheduled coronary angiography. There was a moderate linear relationship between PAV and FMD (r = 0.69, p

Abstract Background Vascular endothelial dysfunction induced by hyperglycemia and elevated insulin resistance is a potent risk factor for cardiovascular disease and likely contributes to multiple chronic disease complications associated with aging. The aim of this study was to systematically review and quantify the effects of exercise on endothelial function (EF) in type 2 diabetes (T2D). Methods Five electronic databases were searched (until June 2017) for studies that met the following criteria: (i) randomized controlled trials; (ii) T2D aged ≥ 18 years; (iii) measured EF by brachial artery flow-mediated dilation (FMD); (iv) structured and supervised exercise intervention for ≥ 8 weeks. Results Thirteen cohorts, selected from eight studies (306 patients, average age 59 years), met the inclusion criteria. Exercise training significantly increased FMD (mean ES = 0.41, 95% CI 0.21–0.62, P

Assessment of endothelial dysfunction in cancer survivors may have a role in the early identification of non-communicable diseases and cardiovascular late effects. Oncological therapies may impair endothelial function. Therefore, in patients such as childhood cancer survivors who could benefit from early cardioprotective pharmacological interventions, it is essential to monitor endothelial function, even if the optimal methodology for investigating the multifaceted aspects of endothelial dysfunction is still under debate. Biochemical markers, as well as invasive and non-invasive tools with and without pharmacological stimuli have been studied. Human clinical studies that have examined lifestyle or cancer treatment protocols have yielded evidence showing the involvement of lipid and lipoprotein levels, glycemic control, blood pressure, adiposity, inflammation, and oxidative stress markers on the state of endothelial health and its role as an early indicator of cardiometabolic risk. However, with regards to pharmacological interventions, cautious interpretation of the result attained whilst monitoring the endothelial function is warranted due to methodological limitations and substantial heterogeneity of the results reported in the published studies. In this narrative review, an overview of evidence from human clinical trials examining the effects of cancer therapies on endothelial disease is provided together with a discussion of endothelial function assessment using the different non-invasive techniques available for researchers and clinicians, in recent years.

Background and Aims: Data from animals suggest that immunoglobulins G (IgG) play a mechanistic role in atherosclerosis and diabetes through endothelial dysfunction and insulin resistance. Patients with common variable immunodeficiency (CVID), who have low circulating levels of IgG and are treated with intravenous polyclonal IgG (IVIgG), may provide an ideal model to clarify whether circulating IgG modulate endothelial function and affect insulin sensitivity in humans.Methods and Results: We studied 24 patients with CVID and 17 matched healthy controls (HC). Endothelial function was evaluated as flow mediated dilation (FMD) of the brachial artery at baseline and 1, 7, 14, and 21 days after IVIgG infusion in the CVID patients. We measured also plasma glucose, insulin, and calculated the HOMA-IR index. We also investigated the role of human IgG on the production of Nitric Oxide (NO) in vitro in Human Coronary Artery Endothelial Cells (HCAEC). Compared to HC, FMD of CVID patients was significantly impaired at baseline (9.4 ± 0.9 and 7.6 ± 0.6% respectively, p < 0.05) but rose above normal levels 1 and 7 days after IVIgG infusion to return at baseline at 14 and 21 days. Serum insulin concentration and HOMA-IR index dropped by 50% in CVID patients after IVIgG (p < 0.002 vs. baseline). In vitro IgG stimulated NO production in HCAEC.Conclusions: Reduced IgG levels are associated with endothelial dysfunction and IVIgG stimulates endothelial function directly while improving insulin sensitivity. The current findings may suggest an anti-atherogenic role of human IgG. [ABSTRACT FROM AUTHOR]

A high sodium (Na+) meal impairs peripheral vascular function. In rodents, chronic high dietary Na+ impairs cerebral vascular function, and in humans, habitual high dietary Na+ is associated with increased stroke risk. However, the effects of acute high dietary Na+ on the cerebral vasculature in humans are unknown. The purpose of this study was to determine if acute high dietary Na+ impairs cerebrovascular reactivity in healthy adults. Thirty‐seven participants (20F/17M; 25 ± 5 years; blood pressure [BP]: 107 ± 9/61 ± 6 mm Hg) participated in this randomized, cross‐over study. Participants were given a low Na+ meal (LSM; 138 mg Na+) and a high Na+ meal (HSM; 1,495 mg Na+) separated by ≥ one week. Serum Na+, beat‐to‐beat BP, middle cerebral artery velocity (transcranial Doppler), and end‐tidal carbon dioxide (PETCO2) were measured pre‐ (baseline) and 60 min post‐prandial. Cerebrovascular reactivity was assessed by determining the percent change in middle cerebral artery velocity to hypercapnia (via 8% CO2, 21% oxygen, balance nitrogen) and hypocapnia (via mild hyperventilation). Peripheral vascular function was measured using brachial artery flow‐mediated dilation (FMD). Changes in serum Na+ were greater following the HSM (HSM: Δ1.6 ± 1.2 mmol/L vs. LSM: Δ0.7 ± 1.2 mmol/L, p <.01). Cerebrovascular reactivity to hypercapnia (meal effect: p =.41) and to hypocapnia (meal effect: p =.65) were not affected by the HSM. Contrary with previous findings, FMD was not reduced following the HSM (meal effect: p =.74). These data suggest that a single high Na+ meal does not acutely impair cerebrovascular reactivity, and suggests that despite prior findings, a single high Na+ meal does not impair peripheral vascular function in healthy adults. [ABSTRACT FROM AUTHOR]

Retinal vein occlusion (RVO) is a common retinal vascular lesion, and a leading cause of visual impairment. Patients with RVO have an increased risk for cardiovascular disease and share multiple common risk factors. In this study, we investigated the endothelial function and arterial stiffness of patients with RVO compared to healthy-control (CL) subjects. We enrolled 40 consecutive patients with RVO and 40 CL subjects. RVO was diagnosed by an ophthalmologist, endothelial function was evaluated by flow mediated dilation (FMD) in the brachial artery, and carotid-femoral pulse wave velocity (PWV) and augmentation index (AIx) of the radial artery were measured to evaluate arterial stiffness and reflected waves, respectively. No significant differences were detected between the studied groups in sex, age, presence of hypertension or dyslipidemia, body mass index, systolic and diastolic blood pressure levels, total cholesterol levels, and smoking habits (p > 0.05 for all). However, patients with RVO had impaired FMD (p = 0.002) and increased PWV (p = 0.004), even after adjustment for several confounders. Both FMD and PWV were also significantly and independently associated with the development of RVO. Furthermore, a significant and positive correlation between PWV and systolic blood pressure existed only in the CL group. Therefore, we have shown that RVO is associated with significant endothelial dysfunction and increased arterial stiffness. Our results strengthen the vascular theory, according to which, systemic endothelial dysfunction and arteriosclerosis play a significant role in the pathogenesis of RVO. [ABSTRACT FROM AUTHOR]

Endothelial dysfunction and atherosclerosis are linked by multiple mechanisms. Brachial artery flow-mediated dilation (FMD) rate is used to evaluate endothelial function and has been independently associated with adverse cardiac outcomes. The relationship between brachial artery FMD rate and severity of subclinical atherosclerosis by coronary computed tomography angiography (CCTA) is not understood. We hypothesized that brachial FMD is inversely associated with burden of subclinical atherosclerosis measured by CCTA. This is a retrospective study of 100 participants with intermediate cardiac risk and atypical symptoms to examine association between brachial artery FMD rate and surrogate markers of severity of subclinical atherosclerosis on CCTA. Multivariate linear regression analysis was used to understand the relationship between brachial artery FMD rate and markers of plaque burden on CCTA including coronary artery calcium (CAC) score, segment involvement score (SIS; total number of segments with any plaque), segment stenosis score (SSS, sum of maximal stenosis score per segment), and total plaque score (TPS, the sum of all segments plaque burden). 52 participants (42%) were female. Mean age of the cohort was 59.3 ± 10.4 years. After adjusting for traditional risk factors, brachial artery FMD rate was inversely associated with higher CAC, TPS, SIS and SSS (p < 0.05 for all). FMD <4.5 predicted the presence of CAC >0 and ≤ 100 most effectively, with a sensitivity of 62.2% and a specificity of 66.7%, respectively (area under the curve (AUC) of 0.5729, p = 0.0302). FMD <2.7 predicted the presence of CAC >100 most effectively, with a sensitivity of 34% and a specificity of 83% respectively (AUC of 0.6226, p = 0.0095). Brachial FMD is independently associated with the presence and extent of subclinical atherosclerosis on CCTA. Our findings provide more detailed evidence that mechanistically, FMD, a surrogate marker of systemic endothelial dysfunction is a correlate of atherosclerotic burden, assessed by CCTA and CAC. Image 1 • Impaired flow-mediated dilation (FMD) can serve as a non-invasive indicator of the presence and severity of subclinical atherosclerosis on coronary computed tomography angiography (CTA). • This can help in risk stratification of cardiovascular outcomes in patients. [ABSTRACT FROM AUTHOR]

Background: The role of the glycocalyx as the endothelial sensor of an increase in blood flow was assessed in the iliac artery in vivo. Methods: Acetylcholine-induced flow mediated dilation was evaluated before and after vascular glycocalyx disruption. This was accomplished by exposing the iliac lumen to the chemotactic agent fMLP (1 μM; n = 6 pigs), concomitant heparinase III (100 mU ml--1 ) and hyaluronidase (14 mg ml--1 ) (n = 4), and neuraminidase (140 mU ml--1 ; n = 5), for 20 min in separate iliac artery preparations. Only one lumen intervention per iliac was conducted. Results: For the heparinase III + hyaluronidase experiment, the iliac diameter increased by an average of 0.54 ± 0.11 mm before and 0.45 ± 0.03 mm after the enzymes (P = 0.42; paired Student's t test). The iliac diameter increased by 0.31 ± 0.02 mm before and 0.29 ± 0.07 mm after fMLP exposure (P = 0.7) and the diameter increased by 0.54 ± 0.11 mm before and 0.54 ± 0.09 mm after neuraminidase exposure (P = 0.98). In all cases, the shear stress changes before and after lumen exposure were not significantly different to each other. Conclusion: There was no significant reduction in flow mediated dilation of the iliac in response to any of the interventions conducted. Therefore, the vascular endothelial glycocalyx as whole is not required for flow mediated dilation in conduit arteries in the intact animal. [ABSTRACT FROM AUTHOR]

Background: Athletes are increasingly exploring ways to enhance their physical performance. Increasing blood flow to the working tissues through endothelium-dependent vasodilation is one factor athletes use to realize these results. Sports supplements such as pre-workouts tout this benefit; however, many have not been tested under laboratory conditions to examine the effects of commonly used supplements on vasodilation. Two popular supplements are Nitrosigine® and citrulline malate (CM). Thus, the purpose of this experiment was to determine the effective of Nitrosigine and CM on vasodilation using ultrasound and flow mediated dilation (FMD). Methods: Healthy, normotensive, and physically active male (n = 16) and female (n = 8) young adults participated in the present investigation. We utilized a randomized, double-blind, within-subjects design where participants reported for three trials, each preceded by a 7-day washout period. Baseline FMD measurement was obtained for each visit, followed by consumption of one clinical dose CM (8 g), Nitrosigine (1.5 g), or dextrose placebo (8 g). Following a 60-min digestion period, FMD was repeated. Supplementation order was randomized controlling for potential order effects. Results: Repeated measures ANOVA yielded a significant supplement (3) x time (2) effect (p <.001), such that Nitrosigine and CM yielded a greater improvement in FMD response than placebo. After supplementation, Nitrosigine and CM increased FMD by 31 and 34%, respectively, compared to a decrease of 2% during the placebo trial. After allometric scaling of the FMD values, supplement x time effect remained significant (p =.001) and changes were similar to non-scaled results. Nitrosigine (23%) and CM (25%) generated significantly greater allometric scaled FMD values when compared to the placebo trail (0.60%). Discussion: Both Nitrisigine and CM increased endothelial-dependent vasodilation as measured by a change in FMD. Increased vasodilation leads to an increase in skeletal muscle blood flow resulting in potential improvements in exercise performance. [ABSTRACT FROM AUTHOR]

Regular resistance exercise is associated with metabolic, neuromuscular and cardiovascular adaptations which improve quality of life and health. However, sedentary subjects have shown acute impairments in endothelial function after high-intensity resistance exercise. The aim of this study was to evaluate endothelial function in sedentary middle-aged men after a single session of resistance exercise at different intensities. Eleven sedentary middle-aged men (40.1 ± 3.9 years; 27.3 ± 1.4 kg/m2) underwent three different conditions of assessment: (1) single knee extension exercise at moderate intensity (MI) [4 sets of 12 repetitions at 50% of one repetition maximum (1RM) for each leg], (2) single knee extension exercise at high intensity (HI) (4 sets of 8 repetitions at 80% of 1RM for each leg), (3) resting for the control condition (CON). Flow-mediated dilation (FMD) was assessed before, 30 and 60 min after exercise. Plasma concentrations of endothelin-1 (ET-1), nitrites and nitrates (NOx) and thiobarbituric acid reactive substances (TBARS) were measured before, immediately after and 60 min after exercise. Blood pressure (BP) was measured prior to the experimental protocols, and in the following times: immediately following, and 2, 5, 10, 15, 30, and 60 min after exertion. There was a significant improvement in FMD 30 min after MI condition (12.5 ± 4.10 vs. 17.2 ± 3.9%; p = 0.016). NOx levels were significantly higher immediately after MI (6.8 ± 3.3 vs. 12.6 ± 4.2 μM; p = 0.007) and there was a significant increase in the concentration of ET-1 immediately after HI (20.02 ± 2.2 vs. 25.4 ± 2.1 pg/mL; p = 0.004). However, there was no significant difference for BP (MI vs. HI) and TBARS among the experimental conditions. Resistance exercise performed at moderate intensity improved vasodilatation via increases on NOx levels and FMD in sedentary middle-aged men.

Vascular endothelial function is a strong marker of cardiovascular health and it refers to the ability of the body to maintain the homeostasis of vascular tone. The endothelial cells react to mechanical and chemical stimuli modulating the smooth muscle cells relaxation. The extent of the induced vasodilation depends on the magnitude of the stimulus. During exercise, the peripheral circulation is mostly controlled by the endothelial cells response that increases the peripheral blood flow in body districts involved but also not involved with exercise. However, whether vascular adaptations occur also in the brachial artery as a result of isolated leg extension muscles (KE) training is still an open question. Repetitive changes in blood flow occurring during exercise may act as vascular training for vessels supplying the active muscle bed as well as for the vessels of body districts not directly involved with exercise. This study sought to evaluate whether small muscle mass (KE) training would induce improvements in endothelial function not only in the vasculature of the lower limb (measured at the femoral artery level in the limb directly involved with training), but also in the upper limb (measured at the brachial artery level in the limb not directly involved with training) as an effect of repetitive increments in the peripheral blood flow during training sessions. Ten young healthy participants (five females, and five males; age: 23 ± 3 years; stature: 1.70 ± 0.11 m; body mass: 66 ± 11 kg; BMI: 23 ± 1 kg ⋅ m-2) underwent an 8-week KE training study. Maximum work rate (MWR), vascular function and peripheral blood flow were assessed pre- and post-KE training by KE ergometer, flow mediated dilatation (FMD) in the brachial artery (non-trained limb), and by passive limb movement (PLM) in femoral artery (trained limb), respectively. After 8 weeks of KE training, MWR and PLM increased by 44% (p = 0.015) and 153% (p = 0.003), respectively. Despite acute increase in brachial artery blood flow during exercise occurred (+25%; p < 0.001), endothelial function did not change after training. Eight weeks of KE training improved endothelial cells response only in the lower limb (measured at the femoral artery level) directly involved with training, likely without affecting the endothelial response of the upper limb (measured at the brachial artery level) not involved with training.

There is an emerging body of literature relating to the effectiveness of frequent aerobic exercise as a prophylactic for age-associated dysfunction of large arteries, yet systematic evaluation and precise estimate of this effect is unknown. We conducted a systematic review and meta-analysis of controlled studies examining flow mediated dilatation (FMD) of athletic older persons and otherwise healthy sedentary counterparts to (i) compare FMD as a determinant of endothelial function between athletes and sedentary individuals and, (ii) summarize the effect of exercise training on FMD in studies of sedentary aging persons. Studies were identified from systematic search of major electronic databases from inception to January 2018. Study quality was assessed before conducting a random effects meta-analysis to calculate a pooled ES (mean difference) with 95% CI's. Thirteen studies [4 interventional (n = 125); 10 cross-sectional [including one study from the interventional analysis; (n = 485)] with age ranges from 62 to 75 years underwent quantitative pooling of data. The majority of study participants were male. Older athletes had more favorable FMD compared with sedentary controls (2.1%; CI: 1.4, 2.8%; P < 0.001). There was no significant improvement in the vascular function of sedentary cohorts following a period of exercise training (0.7%; CI: −0.675, 2.09%; P = 0.316). However, there was a significant increase in baseline diameter from pre to post intervention (0.1 mm; CI: 0.07, 0.13 mm; P < 0.001). In addition, there was no significant difference in endothelial independent vasodilation between the trained and sedentary older adults (1.57%; CI: −0.13, 3.27%; P = 0.07), or from pre to post exercise intervention (1.48%; CI: −1.34, 4.3%; P = 0.3). In conclusion, long-term aerobic exercise appears to attenuate the decline in endothelial vascular function, a benefit which is maintained during chronological aging. However, currently there is not enough evidence to suggest that exercise interventions improve vascular function in previously sedentary healthy older adults.

OBJECTIVE: Resistant hypertension (RH) may be associated with Obstructive Sleep Apnea (OSA), determining a remarkable increase in cardiovascular risk. The aim of the study was to assess the effect of six months with continuous positive airway pressure (CPAP) treatment on blood pressure (BP) values, cardiovascular risk markers, and exercise tolerance in patients with RH and OSA. PATIENTS AND METHODS: Twenty-four patients with RH and OSA were recruited and 24-hour ambulatory BP, intima-media thickness (IMT), flow mediated dilation (FMD), renal resistive index (RRI), and endurance cardiopulmonary exercise testing (CPET) were obtained at enrollment and after 6-month treatment. RESULTS: Significant reduction in clinic systolic and diastolic BP, IMT, and RRI (p = 0.003, p = 0.009, p = 0.020, p = 0.04, respectively) and increase in the left ventricular ejection fraction (p = 0.035) were observed after a 6-month therapy with CPAP. Moreover, improvement in all polysomnographic parameters (number of apneas/hypopneas per hour (p < 0.001), number of episodes of night-time hemoglobin desaturation (ODI) (p = 0.010)), an improvement in Epworth Sleepiness Scale (p < 0.001), as well as in endurance time during constant workload CPET (p = 0.017) were observed too. CONCLUSIONS: CPAP treatment for six months reduces BP and improves cardiovascular risk and exercise tolerance in patients with RH and OSA. An extended cardiovascular assessment, including exercise testing, might be helpful in this population, given the possible reversibility of some endothelial dysfunction and atherosclerotic markers with CPAP treatment, as reported in our study. [ABSTRACT FROM AUTHOR]

Objectives: In the article we describe the new, high frequency, 20 MHz scanning/Doppler probe designed to measure the flow mediated dilation (FMD) and shear rate (SR) close to the radial artery wall. Methods: We compare two US scanning systems, standard vascular modality working below 12 MHz and high frequency 20 MHz system designed for FMD and SR measurements. Axial resolutions of both systems were compared by imaging of two closely spaced food plastic foils immersed in water and by measuring systolic/diastolic diameter changes in the radial artery. The sensitivities of Doppler modalities were also determined. The diagnostic potential of a high frequency system in measurements of FMD and SR was studied in vivo, in two groups of subjects, 12 healthy volunteers and 14 patients with stable coronary artery disease (CAD). Results: Over three times better axial resolution was demonstrated for a high frequency system. Also, the sensitivity of the external single transducer 20 MHz pulse Doppler proved to be over 20 dB better (in terms of a signal-to-noise ratio) than the pulse Doppler incorporated into the linear array. Statistically significant differences in FMD and FMD/SR values for healthy volunteers and CAD patients were confirmed, p-values < 0:05. The areas under Receiver Operating Characteristic (ROC) curves for FMD and FMD/SR for the prediction CAD had the values of 0.99 and 0.97, respectively. Conclusions: These results justify the usefulness of the designed high-frequency scanning system to determine the FMD and SR in the radial artery as predictors of coronary arterial disease. [ABSTRACT FROM AUTHOR]

Aim: Minimal paravalvular leaks (PVL) through microdefects around the annulus have been demonstrated immediately after valvular replacement surgery and usually disappear after regional tissue healing. It has been recognized that endothelium takes place in physiological processes during wound healing including mitogenesis, fibrosis, and inflammation. In this study, we aimed to investigate the role of endothelial functions in patients with persistent PVLs detected in the early postoperative period. Material and Method: This study enrolled a total of 33 patients (14 female, mean age: 47.9±10.4 years) who had PVL detected by means of transesophageal echocardiograpy within 3 months after prosthetic valve replacements, and 40 control subjects (19 female, mean age: 49.9±13.0 years) without PVL in the early postoperative period. Endothelial functions were evaluated by measurement of endothelium dependent flow mediated dilation (FMD) secondary to reactive hyperemia. Results: The demographic, echocardiographic and laboratory parameters did not differ between the groups except for hemoglobin and lactate dehydrogenase (LDH) levels. Hemoglobin was significantly lower and LDH was significantly higher in PVL group. Calculated FMD values were found to be significantly lower in PVL group than the control group (12.9±1.8 vs 13.8±1.6%; p=0.022). In multivariate analysis, low FMD and high LDH levels were independent predictors of PVL. Furthermore, there was a weak and negative correlation between FMD values and the number of paravalvular defects (r= -0.246; p=0.036). Conclusion: Endothelial dysfunction in patients with prosthetic heart valves may play an important role in the development of PVL during the early postoperative period. [ABSTRACT FROM AUTHOR]

Regular resistance exercise is associated with metabolic, neuromuscular and cardiovascular adaptations which improve quality of life and health. However, sedentary subjects have shown acute impairments in endothelial function after high-intensity resistance exercise. The aim of this study was to evaluate endothelial function in sedentary middle-aged men after a single session of resistance exercise at different intensities. Eleven sedentary middle-aged men (40.1 ± 3.9 years; 27.3 ± 1.4 kg/m2) underwent three different conditions of assessment: (1) single knee extension exercise at moderate intensity (MI) [4 sets of 12 repetitions at 50% of one repetition maximum (1RM) for each leg], (2) single knee extension exercise at high intensity (HI) (4 sets of 8 repetitions at 80% of 1RM for each leg), (3) resting for the control condition (CON). Flow-mediated dilation (FMD) was assessed before, 30 and 60 min after exercise. Plasma concentrations of endothelin-1 (ET-1), nitrites and nitrates (NOx) and thiobarbituric acid reactive substances (TBARS) were measured before, immediately after and 60 min after exercise. Blood pressure (BP) was measured prior to the experimental protocols, and in the following times: immediately following, and 2, 5, 10, 15, 30, and 60 min after exertion. There was a significant improvement in FMD 30 min after MI condition (12.5 ± 4.10 vs. 17.2 ± 3.9%; p = 0.016). NOx levels were significantly higher immediately after MI (6.8 ± 3.3 vs. 12.6 ± 4.2 μM; p = 0.007) and there was a significant increase in the concentration of ET-1 immediately after HI (20.02 ± 2.2 vs. 25.4 ± 2.1 pg/mL; p = 0.004). However, there was no significant difference for BP (MI vs. HI) and TBARS among the experimental conditions. Resistance exercise performed at moderate intensity improved vasodilatation via increases on NOx levels and FMD in sedentary middle-aged men. [ABSTRACT FROM AUTHOR]

Vascular endothelial function is a strong marker of cardiovascular health and it refers to the ability of the body to maintain the homeostasis of vascular tone. The endothelial cells react to mechanical and chemical stimuli modulating the smooth muscle cells relaxation. The extent of the induced vasodilation depends on the magnitude of the stimulus. During exercise, the peripheral circulation is mostly controlled by the endothelial cells response that increases the peripheral blood flow in body districts involved but also not involved with exercise. However, whether vascular adaptations occur also in the brachial artery as a result of isolated leg extension muscles (KE) training is still an open question. Repetitive changes in blood flow occurring during exercise may act as vascular training for vessels supplying the active muscle bed as well as for the vessels of body districts not directly involved with exercise. This study sought to evaluate whether small muscle mass (KE) training would induce improvements in endothelial function not only in the vasculature of the lower limb (measured at the femoral artery level in the limb directly involved with training), but also in the upper limb (measured at the brachial artery level in the limb not directly involved with training) as an effect of repetitive increments in the peripheral blood flow during training sessions. Ten young healthy participants (five females, and five males; age: 23 ± 3 years; stature: 1.70 ± 0.11 m; body mass: 66 ± 11 kg; BMI: 23 ± 1 kg ⋅ m-2) underwent an 8-week KE training study. Maximum work rate (MWR), vascular function and peripheral blood flow were assessed pre- and post-KE training by KE ergometer, flow mediated dilatation (FMD) in the brachial artery (non-trained limb), and by passive limb movement (PLM) in femoral artery (trained limb), respectively. After 8 weeks of KE training, MWR and PLM increased by 44% (p = 0.015) and 153% (p = 0.003), respectively. Despite acute increase in brachial artery blood flow during exercise occurred (+25%; p < 0.001), endothelial function did not change after training. Eight weeks of KE training improved endothelial cells response only in the lower limb (measured at the femoral artery level) directly involved with training, likely without affecting the endothelial response of the upper limb (measured at the brachial artery level) not involved with training. [ABSTRACT FROM AUTHOR]

The mechanistic role of arterial shear stress in the regulation of cerebrovascular responses to physiological stimuli (exercise and hypercapnia) is poorly understood. We hypothesised that, if shear stress is a key regulator of arterial dilation, then matched increases in shear, induced by distinct physiological stimuli, would trigger similar dilation of the large extra-cranial arteries. Participants (n = 10) participated in three 30-min experimental interventions, each separated by ≥48 h: (1) mild-hypercapnia (FICO2:∼0.045); (2) submaximal cycling (EX; 60%HRreserve); or (3) resting (time-matched control, CTRL). Blood flow, diameter, and shear rate were assessed (via Duplex ultrasound) in the internal carotid and vertebral arteries (ICA, VA) at baseline, during and following the interventions. Hypercapnia and EX produced similar elevations in blood flow and shear rate through the ICA and VA (p < 0.001), which were both greater than CTRL. Vasodilation of ICA and VA diameter in response to hypercapnia (5.3 ± 0.8 and 4.4 ± 2.0%) and EX (4.7 ± 0.7 and 4.7 ± 2.2%) were similar, and greater than CTRL (p < 0.001). Our findings indicate that matched levels of shear, irrespective of their driving stimulus, induce similar extra-cranial artery dilation. We demonstrate, for the first time in humans, an important mechanistic role for the endothelium in regulating cerebrovascular response to common physiological stimuli in vivo. [ABSTRACT FROM AUTHOR]

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Background We sought to determine the effects of unilateral lower-limb external pneumatic compression (EPC) on bilateral lower-limb vascular reactivity and skin blood flow. Methods Thirty-two participants completed this two-aim study. In AIM1 (n = 18, age: 25.5 ± 4.7 years; BMI: 25.6 ± 3.5 kg/m²), bilateral femoral artery blood flow and reactivity (flow mediated dilation [FMD]) measurements were performed via ultrasonography at baseline (PRE) and immediately following 30-min of unilateral EPC treatment (POST). AIM2 (n = 14, age: 25.9 ± 4.5; BMI: 27.2 ± 2.7 kg/m²) involved 30-min unilateral EPC (n = 7) or sham (n = 7) treatment with thermographic bilateral lower-limb mean skin temperature (MST) measurements at baseline, 15-min of treatment (T15) and 0, 30 and 60-min (R0, R30, R60) following treatment. Results Comparative data herein are presented as mean ± 95% confidence interval. AIM1: No significant effects on total reactive hyperemia blood flow were observed for the treated (i.e., compressed) or untreated (i.e., non-compressed) leg. A significant effect of time, but no time*leg interaction, was observed for relative FMD indicating higher reactivity bilaterally with unilateral EPC treatment (FMD: +0.41 ± 0.09% across both legs; p < 0.05). AIM2: Unilateral EPC treatment was associated with significant increases in whole-leg MST from baseline during (T15: +0.63 ± 0.56 °C in the visible untreated/contralateral leg, p < 0.025) and immediately following treatment (i.e., R0) in both treated (+1.53 ± 0.59 °C) and untreated (+0.60 ± 0.45 °C) legs (p < 0.0125). Across both legs, MST remained elevated with EPC at 30-min post-treatment (+0.60 ± 0.45 °C; p < 0.0167) but not at 60-min post (+0.27 ± 0.46 °C; p = 0.165). Sham treatment was associated with a significant increase in the treated leg immediately post-treatment (+1.12 ± 0.31 °C; p < 0.0167), but not in the untreated leg (−0.27 ± 0.12 °C). MST in neither the treated or untreated leg were increased relative to baseline at R30 or R60 (p > 0.05). Finally, during treatment and at all post-treatment time points (i.e., R0, R30 and R60), independent of treatment group (EPC vs. sham), there was a significant effect of region. The maximum increase in MST was observed at the R0 time point and was significantly (p < 0.05) larger in the thigh region (+1.02 ± 0.31 °C) than the lower-leg (+0.47 ± 0.29 °C) region. However, similar rates of MST decline from R0 in the thigh and lower leg regions were observed at the R30 and R60 time points. Discussion Unilateral EPC may be an effective intervention for increasing skin blood flow and/or peripheral conduit vascular reactivity in the contralateral limb. While EPC was effective in increasing whole-leg MST bilaterally, there appeared to be a more robust response in the thigh compared to the lower-leg. Thus, proximity along the leg may be an important consideration in prospective treatment strategies. [ABSTRACT FROM AUTHOR]