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      Relations of Microvascular Function, Cardiovascular Disease Risk Factors, and Aortic Stiffness in Blacks: The Jackson Heart Study

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          Abstract

          Background

          Blacks have more severe endothelial dysfunction and aortic stiffening as compared with whites. We aimed to investigate the association between aortic stiffness and microvascular function in the black community.

          Methods and Results

          We assessed the association between forearm vascular reactive hyperemia (an indicator of microvascular function) and aortic stiffness in 1458 black participants (N=965 [66% women]; mean age: 66±11 years) in the Jackson Heart Study. We evaluated 2 measures of aortic stiffness: brachial pulse pressure and carotid‐femoral pulse wave velocity. Using high‐resolution ultrasound and Doppler, we evaluated brachial blood flow at baseline and during reactive hyperemia after 5 minutes of forearm ischemia. Multiple cardiovascular risk factors were significantly related to baseline and hyperemic brachial flow velocity. Women had lower baseline flow across the entire age spectrum. During hyperemia, we observed a significant age‐sex interaction for flow velocity ( P=0.02). Female sex was protective against microvascular dysfunction among younger participants, but older women exhibited a greater attenuation of the hyperemic flow reserve. In multivariable models that adjusted for cardiovascular disease risk factors and mean arterial pressure, higher carotid‐femoral pulse wave velocity (β=−0.106±0.033; P=0.001 was related to lower baseline flow. However, during reactive hyperemia, elevated brachial pulse pressure (β=−0.070±0.031; P=0.03) and carotid‐femoral pulse wave velocity (β=−0.128±0.030; P<0.001) were both related to attenuated brachial flow velocity.

          Conclusions

          In a sample of blacks, higher aortic stiffness and pressure pulsatility were associated with lower flow reserve during reactive hyperemia, beyond changes attributable to traditional cardiovascular disease risk factors alone.

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          Most cited references27

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          Arterial stiffness, pressure and flow pulsatility and brain structure and function: the Age, Gene/Environment Susceptibility--Reykjavik study.

          Aortic stiffness increases with age and vascular risk factor exposure and is associated with increased risk for structural and functional abnormalities in the brain. High ambient flow and low impedance are thought to sensitize the cerebral microcirculation to harmful effects of excessive pressure and flow pulsatility. However, haemodynamic mechanisms contributing to structural brain lesions and cognitive impairment in the presence of high aortic stiffness remain unclear. We hypothesized that disproportionate stiffening of the proximal aorta as compared with the carotid arteries reduces wave reflection at this important interface and thereby facilitates transmission of excessive pulsatile energy into the cerebral microcirculation, leading to microvascular damage and impaired function. To assess this hypothesis, we evaluated carotid pressure and flow, carotid-femoral pulse wave velocity, brain magnetic resonance images and cognitive scores in participants in the community-based Age, Gene/Environment Susceptibility--Reykjavik study who had no history of stroke, transient ischaemic attack or dementia (n = 668, 378 females, 69-93 years of age). Aortic characteristic impedance was assessed in a random subset (n = 422) and the reflection coefficient at the aorta-carotid interface was computed. Carotid flow pulsatility index was negatively related to the aorta-carotid reflection coefficient (R = -0.66, P<0.001). Carotid pulse pressure, pulsatility index and carotid-femoral pulse wave velocity were each associated with increased risk for silent subcortical infarcts (hazard ratios of 1.62-1.71 per standard deviation, P<0.002). Carotid-femoral pulse wave velocity was associated with higher white matter hyperintensity volume (0.108 ± 0.045 SD/SD, P = 0.018). Pulsatility index was associated with lower whole brain (-0.127 ± 0.037 SD/SD, P<0.001), grey matter (-0.079 ± 0.038 SD/SD, P = 0.038) and white matter (-0.128 ± 0.039 SD/SD, P<0.001) volumes. Carotid-femoral pulse wave velocity (-0.095 ± 0.043 SD/SD, P = 0.028) and carotid pulse pressure (-0.114 ± 0.045 SD/SD, P = 0.013) were associated with lower memory scores. Pulsatility index was associated with lower memory scores (-0.165 ± 0.039 SD/SD, P<0.001), slower processing speed (-0.118 ± 0.033 SD/SD, P<0.001) and worse performance on tests assessing executive function (-0.155 ± 0.041 SD/SD, P<0.001). When magnetic resonance imaging measures (grey and white matter volumes, white matter hyperintensity volumes and prevalent subcortical infarcts) were included in cognitive models, haemodynamic associations were attenuated or no longer significant, consistent with the hypothesis that increased aortic stiffness and excessive flow pulsatility damage the microcirculation, leading to quantifiable tissue damage and reduced cognitive performance. Marked stiffening of the aorta is associated with reduced wave reflection at the interface between carotid and aorta, transmission of excessive flow pulsatility into the brain, microvascular structural brain damage and lower scores in various cognitive domains.
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            Local shear stress and brachial artery flow-mediated dilation: the Framingham Heart Study.

            Endothelium-dependent flow-mediated dilation is a homeostatic response to short-term increases in local shear stress. Flow-mediated dilation of the brachial artery in response to postischemic reactive hyperemia is impaired in patients with cardiovascular disease risk factors and may reflect local endothelial dysfunction in the brachial artery. However, previous studies have largely neglected the effect of risk factors on evoked shear stress, which is the stimulus for dilation. We evaluated brachial artery percent dilation and evoked diastolic shear stress during reactive hyperemia using high-resolution ultrasound and Doppler in 2045 participants (1107 women, mean age 61 years) in the Framingham Offspring Study. In age- and sex-adjusted models, baseline and hyperemic shear stress were related to brachial artery percent dilation. In stepwise multivariable analyses examining clinical correlates of percent dilation (without shear stress in the model), age, sex, mean arterial pressure, pulse pressure, heart rate, body mass index, lipid medication use, and hormone replacement therapy were related to percent dilation (R2=0.189; P<0.001). When hyperemic shear stress was incorporated, the overall R2 improved (R2=0.335; P<0.001), but relationships between risk factors and percent dilation were attenuated (age and mean arterial pressure) or no longer significant (all others). In contrast, risk factors were related to baseline and hyperemic shear stress in multivariable analyses. Evoked hyperemic shear stress is a major correlate of brachial artery flow-mediated dilation. The associations between many risk factors and brachial artery flow-mediated dilation may be attributable to reduced stimulus for dilation rather than impaired local conduit artery response during hyperemia.
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              Cross-sectional relations of peripheral microvascular function, cardiovascular disease risk factors, and aortic stiffness: the Framingham Heart Study.

              Aortic stiffness and small-artery structure and function share various risk factors; however, relations between these 2 measures of vascular function are complex and incompletely understood. We examined hyperemic forearm blood flow, an indicator of microvascular structure and function, and aortic stiffness in 2045 participants (1107 women, mean age 61+/-9 years) in the Framingham Heart Study offspring cohort. Using arterial tonometry, we evaluated 3 measures of aortic stiffness: brachial pulse pressure; carotid-femoral pulse wave velocity (CFPWV), which is related directly to aortic wall stiffness; and forward pressure wave amplitude (Pf), which is related directly to aortic wall stiffness and inversely to aortic diameter. Using high-resolution ultrasound and Doppler, we evaluated brachial artery diameter, blood flow, and forearm vascular resistance (FVR) at baseline and during reactive hyperemia after 5 minutes of forearm ischemia. In multivariable models that adjusted for cardiovascular disease risk factors, local brachial pulse pressure, CFPWV, and Pf, considered separately, were associated with increased baseline and hyperemic FVR (P<0.001). In models that further adjusted for mean arterial pressure, each measure of aortic stiffness was associated with reduced hyperemic flow (P<0.001). In risk factor-adjusted models that simultaneously considered CFPWV and Pf, both were associated with increased FVR at baseline (P<0.01) and during hyperemia (P<0.001). Our findings indicate that abnormal aortic stiffness and increased pressure pulsatility are associated with blunted microvascular reactivity to ischemic stress that is in excess of changes attributable to conventional cardiovascular disease risk factors alone, including mean arterial pressure.
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                Author and article information

                Contributors
                lcooper@vassar.edu
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                14 October 2018
                16 October 2018
                : 7
                : 20 ( doiID: 10.1002/jah3.2018.7.issue-20 )
                : e009515
                Affiliations
                [ 1 ] Biology Department Vassar College Poughkeepsie NY
                [ 2 ] Division of Cardiovascular Diseases Department of Medicine University of Mississippi Medical Center Jackson MS
                [ 3 ] Washington University School of Arts and Sciences St. Louis MO
                [ 4 ] Institute of Molecular Cardiology University of Louisville KY
                [ 5 ] Boston University and NHLBI's Framingham Heart Study Framingham MA
                [ 6 ] Cardiovascular Division Department of Medicine Beth Israel Deaconess Medical Center and Harvard Medical School Boston MA
                [ 7 ] Evans Department of Medicine Boston University School of Medicine Boston MA
                [ 8 ] Whitaker Cardiovascular Institute Boston University School of Medicine Boston MA
                [ 9 ] Sections of Cardiology, Preventive Medicine and Epidemiology Department of Medicine Boston University Schools of Medicine Boston MA
                [ 10 ] Department of Epidemiology Boston University School of Public Health Boston MA
                [ 11 ] Cardiovascular Engineering, Inc. Norwood MA
                Author notes
                [*] [* ] Correspondence to: Leroy L. Cooper, PhD, MPH, Biology Department, Vassar College, 124 Raymond Ave., Box 70, Poughkeepsie, NY 12604. E‐mail: lcooper@ 123456vassar.edu
                Article
                JAH33524
                10.1161/JAHA.118.009515
                6474961
                30371273
                df701d6c-01e2-429d-898f-defdf0b0df9f
                © 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                : 03 July 2018
                : 10 August 2018
                Page count
                Figures: 1, Tables: 3, Pages: 8, Words: 5976
                Funding
                Funded by: Jackson State University
                Award ID: HHSN268201300049C
                Award ID: HHSN268201300050C
                Funded by: Tougaloo College
                Award ID: HHSN268201300048C
                Funded by: University of Mississippi Medical Center
                Award ID: HHSN268201300046C
                Award ID: HHSN268201300047C
                Funded by: National Heart, Lung, and Blood Institute
                Funded by: National Institute for Minority Health and Health Disparities
                Funded by: National Institutes of Health
                Award ID: HL094898
                Award ID: DK082447
                Award ID: HL107385
                Award ID: HL104184
                Award ID: HL126136
                Categories
                Original Research
                Original Research
                Epidemiology
                Custom metadata
                2.0
                jah33524
                October 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.5.0.1 mode:remove_FC converted:16.10.2018

                Cardiovascular Medicine
                aortic stiffness,endothelium,health disparities,microvascular dysfunction,pulse wave velocity,cardiovascular disease,epidemiology,race and ethnicity,risk factors,ultrasound

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