Higher systolic blood pressure with normal vascular function measurements in preterm-born children

2014 ◽  
Vol 103 (9) ◽  
pp. 904-912 ◽  
Author(s):  
Martin O. Edwards ◽  
William John Watkins ◽  
Sarah J. Kotecha ◽  
Julian P. J. Halcox ◽  
Frank D. Dunstan ◽  
...  
2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Javier I. Ottaviani ◽  
Abigail Britten ◽  
Debora Lucarelli ◽  
Robert Luben ◽  
Angela A. Mulligan ◽  
...  

Abstract Flavan-3-ols are a group of bioactive compounds that have been shown to improve vascular function in intervention studies. They are therefore of great interest for the development of dietary recommendation for the prevention of cardio-vascular diseases. However, there are currently no reliable data from observational studies, as the high variability in the flavan-3-ol content of food makes it difficult to estimate actual intake without nutritional biomarkers. In this study, we investigated cross-sectional associations between biomarker-estimated flavan-3-ol intake and blood pressure and other CVD risk markers, as well as longitudinal associations with CVD risk in 25,618 participants of the European Prospective Investigation into Cancer (EPIC) Norfolk cohort. High flavan-3-ol intake, achievable as part of an habitual diet, was associated with a significantly lower systolic blood pressure (− 1.9 (− 2.7; − 1.1) mmHg in men and − 2.5 (− 3.3; − 1.8) mmHg in women; lowest vs highest decile of biomarker), comparable to adherence to a Mediterranean Diet or moderate salt reduction. Subgroup analyses showed that hypertensive participants had stronger inverse association between flavan-3-ol biomarker and systolic blood pressure when compared to normotensive participants. Flavanol intake could therefore have a role in the maintenance of cardiovascular health on a population scale.


Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2618
Author(s):  
Chesney K. Richter ◽  
Ann C. Skulas-Ray ◽  
Trent L. Gaugler ◽  
Stacey Meily ◽  
Kristina S. Petersen ◽  
...  

Emerging cardiovascular disease (CVD) risk factors, including central vascular function and HDL efflux, may be modifiable with food-based interventions such as cranberry juice. A randomized, placebo-controlled, crossover trial was conducted in middle-aged adults with overweight/obesity (n = 40; mean BMI: 28.7 ± 0.8 kg/m2; mean age: 47 ± 2 years) and elevated brachial blood pressure (mean systolic/diastolic BP: 124 ± 2/81 ± 1 mm Hg). Study participants consumed 500 mL/d of cranberry juice (~16 fl oz; 27% cranberry juice) or a matched placebo juice in a randomized order (8-week supplementation periods; 8-week compliance break), with blood samples and vascular measurements obtained at study entry and following each supplementation period. There was no significant treatment effect of cranberry juice supplementation on the primary endpoint of central systolic blood pressure or central or brachial diastolic pressure. Cranberry juice significantly reduced 24-h diastolic ambulatory BP by ~2 mm Hg compared to the placebo (p = 0.05) during daytime hours. Cranberry juice supplementation did not alter LDL-C but significantly changed the composition of the lipoprotein profile compared to the placebo, increasing the concentration of large LDL-C particles (+29.5 vs. −6.7 nmol/L; p = 0.02) and LDL size (+0.073 vs. −0.068 nm; p = 0.001). There was no effect of treatment on ex vivo HDL efflux in the total population, but exploratory subgroup analyses identified an interaction between BMI and global HDL efflux (p = 0.02), with greater effect of cranberry juice in participants who were overweight. Exploratory analyses indicate that baseline C-reactive protein (CRP) values may moderate treatment effects. In this population of adults with elevated blood pressure, cranberry juice supplementation had no significant effect on central systolic blood pressure but did have modest effects on 24-hr diastolic ambulatory BP and the lipoprotein profile. Future studies are needed to verify these findings and the results of our exploratory analyses related to baseline health moderators.


2008 ◽  
Vol 294 (2) ◽  
pp. E456-E462 ◽  
Author(s):  
Andreas D. Flouris ◽  
Giorgos S. Metsios ◽  
Athanasios Z. Jamurtas ◽  
Yiannis Koutedakis

Experimental evidence for the physiological effects of secondhand smoke (SHS) is limited, although it affects millions of people globally and its prevalence is increasing, despite currently adopted antismoking measures. Also, scarce evidence suggests that the effects of SHS may be more pronounced in men. We conducted a randomized single-blind crossover study to investigate the sex-specific SHS effects in a controlled simulated bar/restaurant environment on gonadal and thyroid hormones, inflammatory cytokines, and vascular function. Twenty-eight (women = 14) nonsmoking adults underwent a 1-h exposure to moderate SHS and a 1-h control trial. Serum and urine cotinine, gonadal and thyroid hormones, inflammatory cytokines, heart rate, and arterial blood pressure were assessed before exposure and immediately after in both trials. Results showed that testosterone ( P = 0.019) and progesterone ( P < 0.001) in men and 17β-estradiol ( P = 0.001) and progesterone ( P < 0.001) in women were significantly decreased after SHS. In men, SHS was accompanied by increased free thyroxine ( P < 0.001), triiodothyronine ( P = 0.020), and decreased the triiodothyronine-to-free thyroxine ratio ( P = 0.033). In women, significant SHS-induced change was observed only in free thyroxine ( P = 0.010), with considerable sex variation in free thyroxine and triiodothyronine and a decrease in luteinizing hormone ( P = 0.026) and follicle-stimulating hormone ( P < 0.001). After SHS, IL-1β ( P = 0.001) and systolic blood pressure ( P = 0.040) were increased in men but not women. We concluded that a 1-h SHS exposure at bar/restaurant levels is accompanied by decrements in gonadal hormones in both sexes and marked increases in thyroid hormone secretion, IL-1β production, and systolic blood pressure in men.


2006 ◽  
Vol 291 (6) ◽  
pp. E1365-E1371 ◽  
Author(s):  
Savitha Subramanian ◽  
Michael A. DeRosa ◽  
Carlos Bernal-Mizrachi ◽  
Nicholas Laffely ◽  
William T. Cade ◽  
...  

Fibrates, activators of the nuclear receptor PPARα, improve dyslipidemia, but their effects on insulin resistance and vascular disease are unresolved. To test the hypothesis that PPARα activation improves insulin resistance and vascular function, we determined the effects of fenofibrate in healthy adults with insulin resistance induced by short-term glucocorticoid administration. Eighteen normal-weight subjects were studied in four stages: at baseline, after 21 days of fenofibrate (160 mg/day) alone, after 3 days of dexamethasone (8 mg/day) added to fenofibrate, and after 3 days of dexamethasone added to placebo (dexamethasone alone). Dexamethasone alone caused hyperinsulinemia, increased glucose, decreased glucose disposal, and reduced insulin-induced suppression of hepatic glucose production as determined by hyperinsulinemic euglycemic clamp and increased systolic blood pressure as determined by ambulatory monitoring, features associated with an insulin-resistant state. Fenofibrate improved fasting LDL and total cholesterol in the setting of dexamethasone treatment but had no significant effect on levels of insulin or glucose, insulin-stimulated glucose disposal, or insulin suppression of glucose production during clamps, or ambulatory monitored blood pressure. In the absence of dexamethasone, fenofibrate lowered fasting triglycerides and cholesterol but unexpectedly increased systolic blood pressure by ambulatory monitoring. These data suggest that PPARα activation in humans does not correct insulin resistance induced by glucocorticoids and may adversely affect blood pressure.


BMJ Open ◽  
2019 ◽  
Vol 9 (Suppl 3) ◽  
pp. 34-43 ◽  
Author(s):  
Freya K Kahn ◽  
Melissa Wake ◽  
Kate Lycett ◽  
Susan Clifford ◽  
David P Burgner ◽  
...  

ObjectivesTo describe the epidemiology and parent–child concordance of vascular function in a population-based sample of Australian parent–child dyads at child age 11–12 years.DesignCross-sectional study (Child Health CheckPoint), nested within a prospective cohort study, the Longitudinal Study of Australian Children (LSAC).SettingAssessment centres in seven major Australian cities and eight regional towns or home visits, February 2015–March 2016.ParticipantsOf all participating CheckPoint families (n=1874), 1840 children (49% girls) and 1802 parents (88% mothers) provided vascular function data. Survey weights and methods were applied to account for LSAC’s complex sample design and clustering within postcodes and strata.Outcome measuresThe SphygmoCor XCEL assessed vascular function, generating estimates of brachial and central systolic blood pressure and diastolic blood pressure, central pulse pressure, augmentation index and carotid–femoral pulse wave velocity. Pearson’s correlation coefficients and multivariable linear regression models estimated parent–child concordance.ResultsHypertension was present in 3.9% of children and 9.0% of parents. Mean child and parent values for augmentation index were 4.5% (SD 11.6) and 21.3% (SD 12.3), respectively, and those for carotid–femoral pulse wave velocity were 4.48 m/s (SD 0.59) and 6.85 m/s (SD 1.14), respectively. Parent–child correlation for brachial systolic blood pressure was 0.20 (95% CI 0.15 to 0.24), brachial diastolic blood pressure 0.21 (95% CI 0.16 to 0.26), central systolic blood pressure 0.21 (95% CI 0.16 to 0.25), central diastolic blood pressure 0.21 (95% CI0.17 to 0.26), central pulse pressure 0.19 (95% CI 0.14 to 0.24), augmentation index 0.28 (95% CI 0.23 to 0.32) and pulse wave velocity 0.22 (95% CI 0.18 to 0.27).ConclusionsWe report Australian values for traditional and more novel vascular function markers, providing a reference for future population studies. Cross-generational concordance in multiple vascular function markers is already established by age 11–12 years, with mechanisms of heritability remaining to be explored.


2017 ◽  
Vol 6 (1) ◽  
pp. 1-8
Author(s):  
Thomas K. Pellinger ◽  
Catherine B. Pearce ◽  
Grant H. Simmons ◽  
Jack L. Snitzer

Background: For individuals with type 2 diabetes (T2D), the hemodynamic response to regular exercise is critical for regulating blood glucose, protecting vascular function, and reducing cardiovascular disease risk, but the hemodynamic responses to differing doses of acute exercise in T2D are unclear. We aimed to compare postexercise (PE) hemodynamics in patients with T2D in response to 4 doses of dynamic exercise. Methods: Eight subjects with well-controlled T2D (42–64 years old.; hemoglobin A1c: 6.6% ± 0.9%) participated in 4 study days, during which they exercised on a cycle ergometer at 4 different combinations of exercise duration and intensity: 30 min at 40% V˙O2peak (30@40), 30 min at 60% V˙O2peak (30@60), 60 min at 40% V˙O2peak (60@40), and 60 min at 60% V˙O2peak (60@60). Heart rate, arterial pressure, and femoral blood flow (Doppler ultrasound) were measured pre-exercise and every 15 min through 120 min PE. Femoral vascular conductance was calculated as flow/pressure. Results: Compared with pre-exercise baseline, femoral blood flow and femoral vascular conductance were higher through at least 105 min of recovery in all conditions (all P &lt; .05), except for the 30@40 trial. Compared with the pre-exercise measures, systolic blood pressure was lower through at least 75 min of recovery in all conditions (all P &lt; .05), except for the 30@40 trial. Conclusion: These results suggest that exercise must be at least moderate in intensity or prolonged in duration (&gt;30 min) to promote sustained PE elevations in skeletal muscle blood flow and reductions in systolic blood pressure in patients with T2D.


Heart ◽  
2008 ◽  
Vol 94 (7) ◽  
pp. 919-924 ◽  
Author(s):  
S S M Chen ◽  
A E Donald ◽  
C Storry ◽  
J P Halcox ◽  
P Bonhoeffer ◽  
...  

Author(s):  
Jhana O. Hendrickx ◽  
Sofie De Moudt ◽  
Debby Van Dam ◽  
Peter Paul De Deyn ◽  
Paul Fransen ◽  
...  

Alzheimer's disease (AD) has long been considered a brain-specific dementia syndrome. However, in recent decades the occurrence of cardiovascular (CV) disease in the progression of AD has been confirmed by increasing epidemiological evidence. In this study, we conducted an in-depth cardiovascular characterization of a humanized APP overexpressing mouse model (hAPP23+/-), which overexpresses the Swedish mutation (KM670/671NL). At the age of 6 months, hAPP23+/- mice had a lower survival, lower body weight and increased corticosterone and VMA levels compared to C57BL/6 littermates. Systolic blood pressure was increased in hAPP23+/- animals compared to C57BL/6 littermates, but diastolic blood pressure was not statistically different. Pulse pressure remained unchanged but abdominal and carotid pulse wave velocity (aPWV and cPWV) were increased in hAPP23+/- compared to C57BL/6 mice. Echocardiography showed no differences in systolic or diastolic cardiac function. Ex vivo evaluation of vascular function showed decreased adreno-receptor dependent vasoconstriction of hAPP23+/- aortic segments, although the isobaric biomechanics of the aortic wall were similar to C57BL/6 aortic segments. In conclusion, hAPP23+/- mice exhibited high serum corticosterone levels, elevated systolic blood pressure and increased arterial stiffness in vivo. However, ex vivo aortic stiffness of hAPP23+/- aortic segments was not changed and vascular reactivity to α1-adrenoceptor stimulation was attenuated. These findings highlight the need for more frequent assessment of circulating stress hormone levels and PWV measurements in daily clinical practice for people at risk of AD.


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