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This study aimed to investigate the effects of grape seed proanthocyanidin extract (GSPE) on blood pressure and vascular endothelial function in middle-aged Japanese adults with prehypertension. We conducted a randomized, double-blind, placebo-controlled study on 6 men and 24 women aged 40–64 years old. The participants were randomized to receive tablets containing either low-dose (200 mg/day) or high-dose (400 mg/day) GSPE, or placebo, for 12 weeks. Systolic and diastolic blood pressures (SBP and DBP, respectively), brachial flow-mediated dilation (FMD), and other cardiovascular parameters were measured before and after 4, 8, and 12 weeks of treatment. The mean SBP in the high-dose group significantly decreased by 13 mmHg after 12 weeks (P = 0.028), although FMD did not change. In an ad hoc analysis of non-smoking participants (n = 21), the mean SBP, DBP, stiffness parameter β, distensibility, incremental elastic modulus (Einc), and pulse wave velocity (PWV) also significantly improved in the high-dose group after 12 weeks. Changes in Einc and PWV from baseline to 12 weeks were significantly greater in the high-dose group than in the placebo group (Einc, P = 0.023; PWV, P = 0.03). GSPE consumption could help maintain vascular elasticity and normal blood pressure in this population.

The post-exercise hypotension response is controversial among patients with coronary artery disease (CAD). Factors behind this disparity may include post-exercise differential effects on central and brachial blood pressure (BP), exercise intensity and inter-individual variability. Thus, we investigate group and individual central and brachial BP responses 5, 15 and 30-min after combined exercise of different intensities in participants with and without CAD. Seventeen participants with stable CAD and eighteen aged-matched controls (52–81 years) completed an acute bout of high and moderate-intensity combined exercise. Brachial and central systolic (cSBP) pressures were assessed via oscillometry and carotid tonometry, respectively. Central pulse wave velocity was also measured. Group mean changes were examined with linear mixed models, and bSBP and cSBP post-exercise individual responsiveness quantified via the region of practical equivalence and highest density interval, a Bayesian decision rule. Regardless of exercise intensity, cSBP was persistently increased during recovery in participants with CAD (difference 30 –baseline (d 30-bas ) = 10, 95% CI: 4 to 17 mmHg, p = 0.001) but reduced in controls (d 30-bas = -13, 95% CI: -19 to -7 mmHg, p = 0.003). bSBP was unchanged in both groups (CAD: d 30-bas = 1, 95% CI: -3 to 6 mmHg, p = 0.995, control: d 30-bas = -4, 95% CI: -2 to 8 mmHg, p = 0.999). Most participants with CAD exhibited sustained elevations in cSBP (n = 10), while most controls were post-exercise hypertensive responders (n = 11) with changes >|5| mmHg. We found differential post-exercise effects on central and brachial BP independent from combined exercise intensity but not clinical population. Clinical trials.gov registration ID : NCT06617117

Aims Epidemiological studies suggest the existence of a relationship between aircraft noise exposure and increased risk for myocardial infarction and stroke. Patients with established coronary artery disease and endothelial dysfunction are known to have more future cardiovascular events. We therefore tested the effects of nocturnal aircraft noise on endothelial function in patients with or at high risk for coronary artery disease. Methods 60 Patients (50p 1–3 vessels disease; 10p with a high Framingham Score of 23 %) were exposed in random and blinded order to aircraft noise and no noise conditions. Noise was simulated in the patients’ bedroom and consisted of 60 events during one night. Polygraphy was recorded during study nights, endothelial function (flow-mediated dilation of the brachial artery), questionnaires and blood sampling were performed on the morning after each study night. Results The mean sound pressure levels L eq(3) measured were 46.9 ± 2.0 dB(A) in the Noise 60 nights and 39.2 ± 3.1 dB(A) in the control nights. Subjective sleep quality was markedly reduced by noise from 5.8 ± 2.0 to 3.7 ± 2.2 ( p  < 0.001). FMD was significantly reduced (from 9.6 ± 4.3 to 7.9 ± 3.7 %; p  < 0.001) and systolic blood pressure was increased (from 129.5 ± 16.5 to 133.6 ± 17.9 mmHg; p  = 0.030) by noise. The adverse vascular effects of noise were independent from sleep quality and self-reported noise sensitivity. Conclusions Nighttime aircraft noise markedly impairs endothelial function in patients with or at risk for cardiovascular disease. These vascular effects appear to be independent from annoyance and attitude towards noise and may explain in part the cardiovascular side effects of nighttime aircraft noise.

Anthocyanins have been shown to improve endothelial function in animal models. However, whether these compounds have similar beneficial effects in humans is largely unknown. In a short-term crossover study, 12 hypercholesterolemic individuals were given oral anthocyanins (320 mg) isolated from berries or placebo. Brachial artery flow-mediated dilation (FMD) was assessed before and after the intervention. In a long-term intervention trial (12 weeks), 150 hypercholesterolemic individuals were given anthocyanins (320 mg/day, n = 75) or placebo (n = 75), after which we measured FMD, plasma cGMP, and other serum biomarkers. Another short-term intervention was conducted in the presence of NO-cGMP inhibitors in 6 people and in a rat aortic ring model (n = 8). Significant increases of FMD from 8.3% (0.6%) at baseline to 11.0% (0.8%) at 1 h and 10.1% (0.9%) at 2 h were observed after short-term anthocyanin consumption, concomitantly with increases of plasma anthocyanin concentrations (P < 0.05). In the study participants who received long-term anthocyanin intervention, compared with the control group, we observed significant increases in the FMD (28.4% vs 2.2%), cGMP (12.6% vs -1.2%), and HDL-cholesterol concentrations, but decreases in the serum soluble vascular adhesion molecule-1 and LDL cholesterol concentrations (P < 0.05). The changes in the cGMP and HDL cholesterol concentrations positively correlated with FMD in the anthocyanin group (P < 0.05). In the presence of NO-cGMP inhibitors, the effects of anthocyanin on endothelial function were abolished in human participants and in a rat aortic ring model. Anthocyanin supplementation improves endothelium-dependent vasodilation in hypercholesterolemic individuals. This effect involves activation of the NO-cGMP signaling pathway, improvements in the serum lipid profile, and decreased inflammation.

In this study, we aimed to assess the effects of enhanced external counterpulsation (EECP) and individual shear rate therapy (ISRT) on peripheral artery function in patients with lower extremity atherosclerotic disease (LEAD). We randomly assigned 45 LEAD patients to receive 35 sessions of 45 min of EECP ( n  = 15), ISRT ( n  = 15), or sham-control ( n  = 15). Flow-mediated dilation in the brachial artery (brachial-FMD); 6-min walk distance; blood flow in the popliteal, posterior tibial, anterior tibial, and dorsalis pedis arteries; and plasma levels were measured before and after the 7 weeks treatment. 36-item Short Form Health Survey [SF-36] was analyzed before, after 7 weeks, and 3-month follow-ups. EECP treatment significantly improved brachial-FMD and quality of life, increased walking distance, and increased blood flow and the diameters of the popliteal artery and posterior tibial artery (all P  < 0.01). Conversely, ISRT markedly increased blood flow in the anterior tibial artery ( P  < 0.05). EECP and ISRT decreased the endothelin-1 and asymmetrical dimethylarginine levels in patients with LEAD (both P  < 0.01). Additionally, sVCAM-1 was significantly reduced after EECP intervention ( P  = 0.004). Our findings demonstrate that EECP and ISRT have beneficial effects on walking distance, quality of life, flow-mediated dilation, endothelial-derived vasoactive agents, and inflammatory and oxidative stress in LEAD patients. Date of registration: 2021-06-21. Trial registration: ChiCTR2100048086.

Background: Determinants of coronary artery disease, such as endothelial dysfunction and oxidative stress, could be attenuated by high-intensity aerobic interval exercise training (HIIT). However, the volume of this type of training is not well established. Objective: To assess the impact of two volumes of HIIT, low (LV-HIIT, <10 min at high intensity) and high (HV-HIIT, >10 min at high intensity), on vascular-endothelial function in individuals after an acute myocardial infarction (AMI). Materials and methods: Clinical trial in 80 AMI patients (58.4 ± 8.3 years, 82.5% men) with three study groups: LV-HIIT (n = 28) and HV-HIIT (n = 28) with two sessions per week for 16 weeks and control group (CG, n = 24) with unsupervised physical activity recommendations. Endothelial function (brachial flow-mediated dilation, FMD), atherosclerosis (carotid intima-media thickness ultrasound, cIMT), and levels of oxidized low-density lipoprotein (ox-LDL) as a marker of oxidative stress were determined before and after the intervention period. Results: After the intervention, in the exercise groups, there was an increase in FMD (LV-HIIT, ↑58.8%; HV-HIIT, ↑94.1%; p < 0.001) concurrently with a decrease in cIMT (LV-HIIT, ↓3.0%; HV-HIIT, ↓3.2%; p = 0.019) and LDLox (LV-HIIT, ↓5.2%; HV-HIIT, ↓8.9%; p < 0.001), with no significant changes in the CG. Furthermore, a significant inverse correlation was observed between ox-LDL and endothelial function related to the volume of HIIT training performed (LV-HIIT: r = −0.376, p = 0.031; HV-HIIT: r = −0.490, p < 0.004), with no significance in the CG (r = 0.021, p = 0.924). Conclusion: In post-AMI patients, HIIT may lead to a volume-dependent enhancement in endothelial function, attributed to a decrease in oxidative stress, with added beneficial effects in reducing vascular wall thickness. An LV-HIIT program, with less than 10 min at high intensity per session, has proven enough efficiency to initiate favorable vascular-endothelial adaptations, potentially reducing cardiovascular risk among patients with coronary artery disease. Trial registration: INTERFARCT, ClinicalTrials.gov: NCT02876952. Graphical abstract Main adaptations to supervised high-intensity interval training (HIIT) programs for 16 weeks on vascular-endothelial function in patients with symptomatic atherosclerosis manifested by acute myocardial infarction compared to traditional training recommendations.

Background: Traffic-related air pollution is consistently associated with cardiovascular morbidity and mortality. Recent human and animal studies suggest that exposure to air pollutants affects vascular function. Diesel exhaust (DE) is a major source of traffic-related air pollution. Objectives: Our goal was to study the effects of short-term exposure to DE on vascular reactivity and on mediators of vascular tone. Methods: In a double-blind, crossover, controlled exposure study, 27 adult volunteers (10 healthy and 17 with metabolic syndrome) were exposed in randomized order to filtered air (FA) and each of two levels of diluted DE (100 or 200$\\mu {\\rm g}/{\\rm m}^{3}$of fine particulate matter) in 2-hr sessions. Before and after each exposure, we assessed the brachial artery diameter (BAd) by B-mode ultrasound and collected blood samples for endothelin-1 (ET-1) and catecholamines. Postexposure we also assessed endothelium-dependent flow-mediated dilation (FMD). Results: Compared with FA, DE at$200\\ \\mu {\\rm g}/{\\rm m}^{3}$elicited a decrease in BAd (0.11 mm; 95% confidence interval, 0.02-0.18), and the effect appeared linearly dose related with a smaller effect at$100\\ \\mu {\\rm g}/{\\rm m}^{3}$. Plasma levels of ET-1 increased after$200\\ \\mu {\\rm g}/{\\rm m}^{3}$DE but not after FA (p = 0.01). There was no consistent impact of DE on plasma catecholamines or FMD. Conclusions: These results demonstrate that short-term exposure to DE is associated with acute endothelial response and vasoconstriction of a conductance artery. Elucidation of the signaling pathways controlling vascular tone that underlie this observation requires further study.

Abstract Rationale Diesel exhaust inhalation, which is the model traffic-related air pollutant exposure, is associated with vascular dysfunction. Objectives To determine whether healthy subjects exposed to diesel exhaust exhibit acute vasoconstriction and whether this effect could be modified by the use of antioxidants or by common variants in the angiotensin II type 1 receptor (AGTR1) and other candidate genes. Methods In a genotype-stratified, double-blind, four-way crossover study, 21 healthy adult subjects were exposed at rest in a randomized, balanced order to diesel exhaust (200 μg/m3 particulate matter with an aerodynamic diameter ≤ 2.5 μm [PM2.5]) and filtered air, and to pretreatment with antioxidants (N-acetylcysteine and ascorbate) and placebo. Before and after each exposure, brachial artery diameter (BAd) was assessed using ultrasound. Changes in BAd were compared across pretreatment and exposure sessions. Gene–exposure interactions were evaluated in the AGTR1 A1166C polymorphism, on which recruitment was stratified, and other candidate genes, including TRPV1 and GSTM1. Measurements and Main Results Compared with filtered air, exposure to diesel exhaust resulted in a significant reduction in BAd (mean, −0.09 mm, 95% confidence interval [CI], −0.01 to −0.17; P = 0.03). Pretreatment with antioxidants augmented diesel exhaust–related vasoconstriction with a mean change in BAd of −0.18 mm (95% CI, −0.28 to −0.07 mm; P = 0.001). Diesel exhaust–related vasoconstriction was primarily observed in the variant alleles of AGTR1 and TRPV1. No association was found between diesel exhaust inhalation and flow-mediated dilation. Conclusions We confirmed that short-term exposure to diesel exhaust in healthy subjects is associated with acute vasoconstriction in a conductance artery and found suggestive evidence of involvement of nociception and renin–angiotensin systems in this effect. Pretreatment with an antioxidant regimen increased vasoconstriction.

In this randomized, double-blind, single-center trial (ANZCTR number ACTRN12619000436178) we aimed to investigate changes in endothelium-dependent vasodilation induced by ubiquinol, the reduced form of coenzyme Q10 (CoQ10), in healthy subjects with moderate dyslipidemia. Fifty-one subjects with low-density lipoprotein (LDL) cholesterol levels of 130–200 mg/dL, not taking statins or other lipid lowering treatments, moderate (2.5%–6.0%) endothelial dysfunction as measured by flow-mediated dilation (FMD) of the brachial artery, and no clinical signs of cardiovascular disease were randomized to receive either ubiquinol (200 or 100 mg/day) or placebo for 8 weeks. The primary outcome measure was the effect of ubiquinol supplementation on FMD at the end of the study. Secondary outcomes included changes in FMD on week 4, changes in total and oxidized plasma CoQ10 on week 4 and week 8, and changes in serum nitrate and nitrite levels (NOx), and plasma LDL susceptibility to oxidation in vitro on week 8. Analysis of the data of the 48 participants who completed the study demonstrated a significantly increased FMD in both treated groups compared with the placebo group (200 mg/day, +1.28% ± 0.90%; 100 mg/day, +1.34% ± 1.44%; p < 0.001) and a marked increase in plasma CoQ10, either total (p < 0.001) and reduced (p < 0.001). Serum NOx increased significantly and dose-dependently in all treated subjects (p = 0.016), while LDL oxidation lag time improved significantly in those receiving 200 mg/day (p = 0.017). Ubiquinol significantly ameliorated dyslipidemia-related endothelial dysfunction. This effect was strongly related to increased nitric oxide bioavailability and was partly mediated by enhanced LDL antioxidant protection.

The anti-inflammatory agent, mesalamine (5-aminosalicylic acid) has been shown to decrease mucosal inflammation in ulcerative colitis. The effect of mesalamine in HIV-infected individuals, who exhibit abnormal mucosal immune activation and microbial translocation (MT), has not been established in a placebo-controlled trial. We randomized 33 HIV-infected subjects with CD4 counts <350 cells/mm3 and plasma HIV RNA levels <40 copies/ml on antiretroviral therapy (ART) to add mesalamine vs. placebo to their existing regimen for 12 weeks followed by a 12 week crossover to the other arm. Compared to placebo-treated subjects, mesalamine-treated subjects did not experience any significant change in the percent CD38+HLA-DR+ peripheral blood CD4+ and CD8+ T cells at week 12 (P = 0.38 and P = 0.63, respectively), or in the CD4+ T cell count at week 12 (P = 0.83). The percent CD38+HLA-DR+ CD4+ and CD8+ T cells also did not change significantly in rectal tissue (P = 0.86, P = 0.84, respectively). During the period of mesalamine administration, plasma sCD14, IL-6, D-dimer, and kynurenine to tryptophan ratio were not changed significantly at week 12 and were similarly unchanged at week 24. This study suggests that, at least under the conditions studied, the persistent immune activation associated with HIV infection is not impacted by the anti-inflammatory effects of mesalamine. ClinicalTrials.gov NCT01090102.