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      Comparison of peripheral and cerebral vascular function between premenopausal, early and late postmenopausal females

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          Abstract

          The risk of cardiovascular and cerebrovascular disease increases in ageing females, coinciding with the onset of menopause. Differences in peripheral and cerebrovascular function across menopausal stages, however, are poorly characterized. The aim of this study was to compare peripheral and cerebrovascular function between healthy premenopausal (PRE), early (1–6 years after final menstrual period; E‐POST) and late (>6 years after final menstrual period; L‐POST) postmenopausal females. We also explored the association between reproductive hormones, NO bioavailability and cerebrovascular function. In 39 females (40–65 years of age), we measured arterial stiffness, brachial artery flow‐mediated dilatation, and cerebrovascular reactivity (CVR) to hypercapnia in the middle (MCAv) and internal (ICA) carotid arteries. Follicle‐stimulating hormone, estradiol, progesterone and plasma nitrate and nitrite concentrations were also measured. Years since final menstrual period (PRE, 0 ± 0 years; E‐POST, 3 ± 1 years; L‐POST, 11 ± 4 years; P < 0.001) and estradiol levels (PRE, 145.5 ± 65.6 pg ml −1; E‐POSTm 30.2 ± 81.2 pg ml −1; L‐POST, 7.7 ± 11.3 pg ml −1; P < 0.001) were different between groups. All groups exceeded the guidelines for recommended physical activity. There were no group differences in blood pressure ( P = 0.382), arterial stiffness ( P = 0.129), flow‐mediated dilatation ( P = 0.696) or MCAv CVR ( P = 0.442). The ICA CVR blood flow response was lower in PRE compared with L‐POST (26.5 ± 19.2 vs. 47.8 ± 12.6%; P = 0.010), but after adjusting for age these differences were no longer present. Flow‐mediated dilatation ( r = 0.313, P = 0.105) and ICA CVR ( r = −0.154, P = 0.495) were not associated with the estradiol concentration. There were no associations between the estradiol concentration and NO bioavailability. These results suggest that in healthy, physically active early and late postmenopausal females, vascular and cerebrovascular function is generally well preserved.

          Abstract

          • What is the central question of this study?

            We sought to investigate whether peripheral and cerebrovascular function are impaired in early and late postmenopausal females compared with premenopausal females, while also accounting for nitric oxide and estradiol levels.

          • What is the main finding and its importance?

            We observed no differences in peripheral vascular and cerebrovascular function between healthy and physically active premenopausal females and early and late postmenopausal females. Our findings contradict previous cross‐sectional observations of vascular and cerebrovascular dysfunction across menopause. Longitudinal studies assessing vascular and cerebrovascular outcomes across the menopausal transition are warranted.

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          Most cited references55

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          General cardiovascular risk profile for use in primary care: the Framingham Heart Study.

          Separate multivariable risk algorithms are commonly used to assess risk of specific atherosclerotic cardiovascular disease (CVD) events, ie, coronary heart disease, cerebrovascular disease, peripheral vascular disease, and heart failure. The present report presents a single multivariable risk function that predicts risk of developing all CVD and of its constituents. We used Cox proportional-hazards regression to evaluate the risk of developing a first CVD event in 8491 Framingham study participants (mean age, 49 years; 4522 women) who attended a routine examination between 30 and 74 years of age and were free of CVD. Sex-specific multivariable risk functions ("general CVD" algorithms) were derived that incorporated age, total and high-density lipoprotein cholesterol, systolic blood pressure, treatment for hypertension, smoking, and diabetes status. We assessed the performance of the general CVD algorithms for predicting individual CVD events (coronary heart disease, stroke, peripheral artery disease, or heart failure). Over 12 years of follow-up, 1174 participants (456 women) developed a first CVD event. All traditional risk factors evaluated predicted CVD risk (multivariable-adjusted P<0.0001). The general CVD algorithm demonstrated good discrimination (C statistic, 0.763 [men] and 0.793 [women]) and calibration. Simple adjustments to the general CVD risk algorithms allowed estimation of the risks of each CVD component. Two simple risk scores are presented, 1 based on all traditional risk factors and the other based on non-laboratory-based predictors. A sex-specific multivariable risk factor algorithm can be conveniently used to assess general CVD risk and risk of individual CVD events (coronary, cerebrovascular, and peripheral arterial disease and heart failure). The estimated absolute CVD event rates can be used to quantify risk and to guide preventive care.
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            Expert consensus and evidence-based recommendations for the assessment of flow-mediated dilation in humans

            Endothelial dysfunction is involved in the development of atherosclerosis, which precedes asymptomatic structural vascular alterations as well as clinical manifestations of cardiovascular disease (CVD). Endothelial function can be assessed non-invasively using the flow-mediated dilation (FMD) technique. Flow-mediated dilation represents an endothelium-dependent, largely nitric oxide (NO)-mediated dilatation of conduit arteries in response to an imposed increase in blood flow and shear stress. Flow-mediated dilation is affected by cardiovascular (CV) risk factors, relates to coronary artery endothelial function, and independently predicts CVD outcome. Accordingly, FMD is a tool for examining the pathophysiology of CVD and possibly identifying subjects at increased risk for future CV events. Moreover, it has merit in examining the acute and long-term impact of physiological and pharmacological interventions in humans. Despite concerns about its reproducibility, the available evidence shows that highly reliable FMD measurements can be achieved when specialized laboratories follow standardized protocols. For this purpose, updated expert consensus guidelines for the performance of FMD are presented, which are based on critical appraisal of novel technical approaches, development of analysis software, and studies exploring the physiological principles underlying the technique. Uniformity in FMD performance will (i) improve comparability between studies, (ii) contribute to construction of reference values, and (iii) offer an easy accessible and early marker of atherosclerosis that could complement clinical symptoms of structural arterial disease and facilitate early diagnosis and prediction of CVD outcomes.
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              The influence of heart rate on augmentation index and central arterial pressure in humans.

              Arterial stiffness is an important determinant of cardiovascular risk. Augmentation index (AIx) is a measure of systemic arterial stiffness derived from the ascending aortic pressure waveform. The aim of the present study was to assess the effect of heart rate on AIx. We elected to use cardiac pacing rather than chronotropic drugs to minimize confounding effects on the systemic circulation and myocardial contractility. Twenty-two subjects (13 male) with a mean age of 63 years and permanent cardiac pacemakers in situ were studied. Pulse wave analysis was used to determine central arterial pressure waveforms, non-invasively, during incremental pacing (from 60 to 110 beats min-1), from which AIx and central blood pressure were calculated. Peripheral blood pressure was recorded non-invasively from the brachial artery. There was a significant, inverse, linear relationship between AIx and heart rate (r = -0.76; P < 0.001). For a 10 beats min-1 increment, AIx fell by around 4 %. Ejection duration and heart rate were also inversely related (r = -0. 51; P < 0.001). Peripheral systolic, diastolic and mean arterial pressure increased significantly during incremental pacing. Although central diastolic pressure increased significantly with pacing, central systolic pressure did not. There was a significant increase in the ratio of peripheral to central pulse pressure (P < 0.001), which was accounted for by the observed change in central pressure augmentation. These results demonstrate an inverse, linear relationship between AIx and heart rate. This is likely to be due to alterations in the timing of the reflected pressure wave, produced by changes in the absolute duration of systole. Consideration of wave reflection and aortic pressure augmentation may explain the lack of rise in central systolic pressure during incremental pacing despite an increase in peripheral pressure.
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                Author and article information

                Contributors
                s.ruediger@uq.edu.au
                Journal
                Exp Physiol
                Exp Physiol
                10.1111/(ISSN)1469-445X
                EPH
                expphysiol
                Experimental Physiology
                John Wiley and Sons Inc. (Hoboken )
                0958-0670
                1469-445X
                09 January 2023
                March 2023
                : 108
                : 3 ( doiID: 10.1113/eph.v108.3 )
                : 518-530
                Affiliations
                [ 1 ] Physiology and Ultrasound Laboratory in Science and Exercise Centre for Research on Exercise, Physical Activity and Health School of Human Movement and Nutrition Sciences The University of Queensland Brisbane Queensland Australia
                [ 2 ] Children's Health and Exercise Research Centre, Sport and Health Sciences College of Life and Environmental Sciences University of Exeter Exeter UK
                [ 3 ] VasoActive Research Group School of Health University of the Sunshine Coast Sippy Downs Queensland Australia
                [ 4 ] Sunshine Coast Health Institute Sunshine Coast Hospital and Health Service Birtinya Queensland Australia
                [ 5 ] School of Nursing Midwifery and Social Work The University of Queensland Brisbane Queensland Australia
                Author notes
                [*] [* ] Correspondence

                Stefanie L. Ruediger, Physiology and Ultrasound Laboratory in Science and Exercise, Centre for Research on Exercise, Physical Activity and Health, School of Human Movement and Nutrition Sciences, The University of Queensland, Brisbane, QLD 4072, Australia.

                Email: s.ruediger@ 123456uq.edu.au

                Author information
                https://orcid.org/0000-0001-6339-6506
                https://orcid.org/0000-0001-7632-7956
                https://orcid.org/0000-0003-4137-6840
                https://orcid.org/0000-0002-6990-3596
                https://orcid.org/0000-0001-8076-8789
                https://orcid.org/0000-0001-8531-2780
                Article
                EPH13291
                10.1113/EP090813
                10103882
                36621779
                887e883f-7694-45f7-8c60-37b7ff260ad1
                © 2022 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 01 September 2022
                : 06 December 2022
                Page count
                Figures: 1, Tables: 4, Pages: 13, Words: 8865
                Funding
                Funded by: University of Queensland Research Training Stipend and Sports Medicine Australia
                Categories
                Research Article
                RESEARCH ARTICLES
                VASCULAR
                Editor's Pick
                Custom metadata
                2.0
                1 March 2023
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.4.0 mode:remove_FC converted:02.04.2024

                Anatomy & Physiology
                arterial stiffness,cerebrovascular reactivity,internal carotid artery,menopause,oestrogen,vascular function

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