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Articles de revues sur le sujet « Large artery stiffness »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 10 mars 2023

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1

Benetos, Athanase, Stéphane Laurent, Roland G. Asmar, and Patrick Lacolley. "Large artery stiffness in hypertension." Journal of Hypertension 15 (1997): S89—S97. http://dx.doi.org/10.1097/00004872-199715022-00009.

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2

McEniery, C. M., and I. B. Wilkinson. "Large artery stiffness and inflammation." Journal of Human Hypertension 19, no. 7 (2005): 507–9. http://dx.doi.org/10.1038/sj.jhh.1001814.

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3

Blacher, J., Athanase Protogerou, and M. Safar. "Large Artery Stiffness and Antihypertensive Agents." Current Pharmaceutical Design 11, no. 25 (2005): 3317–26. http://dx.doi.org/10.2174/138161205774424654.

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4

Chirinos, Julio A. "Echocardiographic Assessment of Large Artery Stiffness." Journal of the American Society of Echocardiography 29, no. 11 (2016): 1117–21. http://dx.doi.org/10.1016/j.echo.2016.09.004.

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5

Chirinos, Julio A. "Large Artery Stiffness and New-Onset Diabetes." Circulation Research 127, no. 12 (2020): 1499–501. http://dx.doi.org/10.1161/circresaha.120.318317.

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6

Kingwell, Bronwyn A., Tanya L. Medley, Tamara K. Waddell, Timothy J. Cole, Anthony M. Dart, and Garry L. Jennings. "Large Artery Stiffness: Structural And Genetic Aspects." Clinical and Experimental Pharmacology and Physiology 28, no. 12 (2001): 1040–43. http://dx.doi.org/10.1046/j.1440-1681.2001.03580.x.

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7

Butlin, Mark, and Ahmad Qasem. "Large Artery Stiffness Assessment Using SphygmoCor Technology." Pulse 4, no. 4 (2016): 180–92. http://dx.doi.org/10.1159/000452448.

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8

Tan, Isabella, Bart Spronck, Hosen Kiat, et al. "Heart Rate Dependency of Large Artery Stiffness." Hypertension 68, no. 1 (2016): 236–42. http://dx.doi.org/10.1161/hypertensionaha.116.07462.

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9

Chirinos, Julio A., Patrick Segers, Timothy Hughes, and Raymond Townsend. "Large-Artery Stiffness in Health and Disease." Journal of the American College of Cardiology 74, no. 9 (2019): 1237–63. http://dx.doi.org/10.1016/j.jacc.2019.07.012.

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10

Wagenseil, Jessica E., and Robert P. Mecham. "Elastin in Large Artery Stiffness and Hypertension." Journal of Cardiovascular Translational Research 5, no. 3 (2012): 264–73. http://dx.doi.org/10.1007/s12265-012-9349-8.

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11

Alivon, Maureen, Julie Giroux, Marie Briet, François Goldwasser, Stéphane Laurent, and Pierre Boutouyrie. "Large artery stiffness and hypertension after antiangiogenic drugs." Journal of Hypertension 33, no. 6 (2015): 1310–17. http://dx.doi.org/10.1097/hjh.0000000000000550.

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12

MORCET, J. "Influence of heart rate on large artery stiffness." American Journal of Hypertension 12, no. 4 (1999): 174. http://dx.doi.org/10.1016/s0895-7061(99)80629-3.

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13

van den Meiracker, Anton H., and Francesco US Mattace-Raso. "Large artery stiffness and microalbuminuria: a causal relationship?" Journal of Hypertension 27, no. 7 (2009): 1355–57. http://dx.doi.org/10.1097/hjh.0b013e32832d2149.

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14

Alivon, M., K. T. Ong, H. Khettab, et al. "6.2 LARGE ARTERY STIFFNESS ASSESSMENT WITH ARTERIOGRAPH DEVICE." Artery Research 4, no. 4 (2010): 149. http://dx.doi.org/10.1016/j.artres.2010.10.179.

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15

Stróżecki, Paweł, Zbigniew Serafin, Andrzej Adamowicz, Mariusz Flisiński, Zbigniew Włodarczyk, and Jacek Manitius. "Coronary artery calcification and large artery stiffness in renal transplant recipients." Advances in Medical Sciences 60, no. 2 (2015): 240–45. http://dx.doi.org/10.1016/j.advms.2015.04.002.

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16

Korhonen, Päivi, Kari Syvänen, and Pertti Aarnio. "Surrogates of Large Artery versus Small Artery Stiffness and Ankle-Brachial Index." International Journal of Angiology 20, no. 03 (2011): 167–72. http://dx.doi.org/10.1055/s-0031-1284200.

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17

Kingwell, Bronwyn A., Tamara K. Waddell, Tanya L. Medley, James D. Cameron, and Anthony M. Dart. "Large artery stiffness predicts ischemic threshold in patients with coronary artery disease." Journal of the American College of Cardiology 40, no. 4 (2002): 773–79. http://dx.doi.org/10.1016/s0735-1097(02)02009-0.

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18

Premužić, Vedran, Ana Jelaković, Lea Katalinić, et al. "Large artery stiffness and sexual dysfunction in hemodialysis patients." Cardiologia Croatica 12, no. 3 (2017): 74. http://dx.doi.org/10.15836/ccar2017.74.

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19

Kingwell, Bronwyn, A. M. Dart, J. D. Cameron, et al. "CHOLESTEROL AND LARGE ARTERY STIFFNESS IN A HYPERTENSIVE POPULATION." Journal of Hypertension 22, Suppl. 1 (2004): S168. http://dx.doi.org/10.1097/00004872-200402001-00715.

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20

Kotsis, Vasilios, and Stella Stabouli. "Arterial Stiffness, Vascular Aging, and Intracranial Large Artery Disease." American Journal of Hypertension 24, no. 3 (2011): 252. http://dx.doi.org/10.1038/ajh.2010.251.

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21

Wilkinson, Ian B., Stanley S. Franklin, and John R. Cockcroft. "Nitric Oxide and the Regulation of Large Artery Stiffness." Hypertension 44, no. 2 (2004): 112–16. http://dx.doi.org/10.1161/01.hyp.0000138068.03893.40.

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22

Chan, William, and Anthony M. Dart. "Vascular stiffness and aging in HIV." Sexual Health 8, no. 4 (2011): 474. http://dx.doi.org/10.1071/sh10160.

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Large artery stiffening is a biological index of vascular aging. Vascular aging and atherosclerosis are two closely linked processes that develop in parallel and in synergy, sharing common aetiological determinants. Vascular stiffening increases left ventricular work and can lead to diminished coronary perfusion, and may therefore contribute to the development of cardiovascular disease. There is emerging evidence that large artery stiffness and vascular aging are accelerated in HIV infection because of the high prevalence of cardiovascular risk factors among HIV-infected patients. Moreover, the biological effects of HIV and the metabolic perturbations associated with antiretroviral therapies appear to accelerate vascular stiffening in HIV-infected patients. Further studies evaluating the effects of general and targeted therapies and various combinations of antiretroviral therapies on measures of large artery stiffness are urgently needed.

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23

Nardone, Massimo, John S. Floras, and Philip J. Millar. "Sympathetic neural modulation of arterial stiffness in humans." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 6 (2020): H1338—H1346. http://dx.doi.org/10.1152/ajpheart.00734.2020.

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Elevated large-artery stiffness is recognized as an independent predictor of cardiovascular and all-cause mortality. The mechanisms responsible for such stiffening are incompletely understood. Several recent cross-sectional and acute experimental studies have examined whether sympathetic outflow, quantified by microneurographic measures of muscle sympathetic nerve activity (MSNA), can modulate large-artery stiffness in humans. A major methodological challenge of this research has been the capacity to evaluate the independent neural contribution without influencing the dynamic blood pressure dependence of arterial stiffness. The focus of this review is to summarize the evidence examining 1) the relationship between resting MSNA and large-artery stiffness, as determined by carotid-femoral pulse wave velocity or pulse wave reflection characteristics (i.e., augmentation index) in men and women; 2) the effects of acute sympathoexcitatory or sympathoinhibitory maneuvers on carotid-femoral pulse wave velocity and augmentation index; and 3) the influence of sustained increases or decreases in sympathetic neurotransmitter release or circulating catecholamines on large-artery stiffness. The present results highlight the growing evidence that the sympathetic nervous system is capable of modulating arterial stiffness independent of prevailing hemodynamics and vasomotor tone.

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24

Ahimastos, Anna A., Melissa Formosa, Anthony M. Dart, and Bronwyn A. Kingwell. "Gender Differences in Large Artery Stiffness Pre- and Post Puberty." Journal of Clinical Endocrinology & Metabolism 88, no. 11 (2003): 5375–80. http://dx.doi.org/10.1210/jc.2003-030722.

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Abstract Age-related large artery stiffening is more pronounced in women compared with men and is an important cause of isolated systolic hypertension. This study aimed to investigate whether such gender differences are inherent or the result of sex steroid influences. Healthy children prepuberty [26 female (10.3 ± 0.1 yr), 32 male (10.3 ± 0.1 yr), mean age ± sd] and post puberty [30 female (15.9 ± 0.2 yr), 22 male (15.9 ± 0.4 yr)] were studied. Large artery stiffness was assessed globally via systemic arterial compliance and regionally via pulse wave velocity. Prepubertal males and females did not differ in body size, cardiac output, or heart rate. Prepubertal females had stiffer large arteries and higher pulse pressure than age-matched males (P &lt; 0.05). Postpubertal males were taller and heavier and had a greater cardiac output and lower heart rate compared with similarly aged females. In relation to pubertal status, females developed more distensible large arteries post puberty whereas males developed stiffer large vessels (P &lt; 0.05). These changes where such that central large artery stiffness was similar between genders in the postpubertal group. Together these data suggest that large artery stiffness varies intrinsically between genders but is also modulated by both male and female sex steroids.

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25

Rey-García, Jimena, and Raymond R. Townsend. "Large Artery Stiffness: A Companion to the 2015 AHA Science Statement on Arterial Stiffness." Pulse 9, no. 1-2 (2021): 1–10. http://dx.doi.org/10.1159/000518613.

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Large artery stiffness (LAS) has proven to be an independent risk factor for cardiovascular disease and mortality. Nevertheless, the position of current hypertension guidelines regarding the usefulness of assessing LAS differs across different continents. In general, European Guidelines recognize pulse wave velocity (PWV) as a marker of target organ damage but do not recommend its systematic use in general population. Asian guidelines consider PWV as a recommended test at diagnosis of hypertension, in contrast to North American guidelines that do not state any position about its usefulness. However, PWV predicts cardiovascular events, and several studies have shown that it improves risk classification adjusting for established risk factors especially for intermediate-risk patients. Finally, some advances have been made related to treatments affecting LAS. Dietary interventions such as sodium restriction and exercise-based interventions have a modest effect in reducing LAS. Pharmacological interventions, such as statins, or more recent advances with mineralocorticoid blocker seem to have a beneficial effect. Last, controversial effects of renal denervation on LAS have been found. Our goal here is to update the reader on LAS on these areas since the 2015 American Heart Association Scientific Statement.

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26

Bank, Alan J. "Physiologic Aspects of Drug Therapy and Large Artery Elastic Properties." Vascular Medicine 2, no. 1 (1997): 44–50. http://dx.doi.org/10.1177/1358863x9700200107.

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Vasoactive drugs alter smooth muscle tone not only in arterial resistance vessels, but also in large conduit arteries. The resultant changes in smooth muscle tone alter both conduit vessel size and stiffness and hence influence pulsatile components of left ventricular afterload. The effects of smooth muscle relaxation and contraction on arterial elastic properties are complex and have not been fully characterized. Several recent studies have utilized a new intravascular ultrasound technique to study the effects of changes in smooth muscle tone on brachial artery elastic mechanics in normal human subjects in vivo. Smooth muscle relaxation with nitroglycerin improves isobaric brachial artery compliance without significantly altering arterial wall stiffness as measured by incremental elastic modulus ( Einc). The improvement in compliance with smooth muscle relaxation is the net result of factors that: (1) increase wall stiffness (increased tension in parallel elastin and collagen fibers); (2) decrease wall stiffness (decreased tension in the smooth muscle and its associated series elastic component); and (3) increase vessel lumen size. Using a modified Maxwell model for the arterial wall, smooth muscle relaxation is also shown to shift the predominant elements contributing to wall stress and EInc from smooth muscle and the collagen fibers in series with the smooth muscle to collagen fibers in parallel with the smooth muscle. A better understanding of the mechanisms contributing to changes in arterial elastic mechanics following alterations in smooth muscle tone will help in developing pharmacologic therapies aimed at reducing pulsatile components of left ventricular afterload.

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27

Gupta, Shresth, Anurag Singh, and Abhishek Sharma. "Dynamic Large Artery Stiffness Index for Cuffless Blood Pressure Estimation." IEEE Sensors Letters 6, no. 3 (2022): 1–4. http://dx.doi.org/10.1109/lsens.2022.3157060.

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28

Iannarelli, Nathaniel J., Kylie S. Dempster, Aindriu R. R. Maguire, et al. "Serum MMP‐3 and its Association with Large Artery Stiffness." FASEB Journal 34, S1 (2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.01878.

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29

Wohlfahrt, Peter, Alena Krajcoviechova, Marie Jozifova, et al. "Large artery stiffness and carotid flow pulsatility in stroke survivors." Journal of Hypertension 32, no. 5 (2014): 1097–103. http://dx.doi.org/10.1097/hjh.0000000000000137.

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30

Blacher, Jacques, and Michel E. Safar. "Large-artery stiffness, hypertension and cardiovascular risk in older patients." Nature Clinical Practice Cardiovascular Medicine 2, no. 9 (2005): 450–55. http://dx.doi.org/10.1038/ncpcardio0307.

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31

Palombo, C., C. Morizzo, F. Vittone, et al. "Visceral Adiposity and Large Artery Stiffness in Healthy Obese Subjects." High Blood Pressure & Cardiovascular Prevention 12, no. 3 (2005): 176. http://dx.doi.org/10.2165/00151642-200512030-00109.

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32

Kingwell, Bronwyn A. "Large Artery Stiffness: Implications For Exercise Capacity And Cardiovascular Risk." Clinical and Experimental Pharmacology and Physiology 29, no. 3 (2002): 214–17. http://dx.doi.org/10.1046/j.1440-1681.2002.03622.x.

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33

Strauss, Michél, Wayne Smith, Wen Wei, Alexei Y. Bagrov, Olga V. Fedorova, and Aletta E. Schutte. "Large artery stiffness is associated with marinobufagenin in young adults." Journal of Hypertension 36, no. 12 (2018): 2333–39. http://dx.doi.org/10.1097/hjh.0000000000001866.

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34

Aoun, S., J. Blacher, ME Safar, and JJ Mourad. "Diabetes mellitus and renal failure: effects on large artery stiffness." Journal of Human Hypertension 15, no. 10 (2001): 693–700. http://dx.doi.org/10.1038/sj.jhh.1001253.

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35

van den Bogaard, B., C. Spaan, K. Lieve, G. A. van Montfrans, and B. J. H. van den Born. "P8.08HEMODYNAMICS AND LARGE ARTERY STIFFNESS IN YOUNG PREHYPERTENSIVE MEDICAL STUDENTS." Artery Research 3, no. 4 (2009): 188. http://dx.doi.org/10.1016/j.artres.2009.10.114.

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36

Hickler, R. B. "Aortic and large artery stiffness: Current methodology and clinical correlations." Clinical Cardiology 13, no. 5 (1990): 317–22. http://dx.doi.org/10.1002/clc.4960130504.

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37

Vehkavaara, Satu, Jukka Westerbacka, Tiina Hakala-Ala-Pietilä, Antti Virkamäki, Outi Hovatta, and Hannele Yki-Järvinen. "Effect of Estrogen Replacement Therapy on Insulin Sensitivity of Glucose Metabolism and Preresistance and Resistance Vessel Function in Healthy Postmenopausal Women1." Journal of Clinical Endocrinology & Metabolism 85, no. 12 (2000): 4663–70. http://dx.doi.org/10.1210/jcem.85.12.7034.

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In the present study, we hypothesized that estradiol, via its ability to vasodilate in an endothelium-dependent manner, might enhance vascular effects of insulin. Basal and insulin-stimulated peripheral blood flow and resistance, arterial stiffness, and glucose metabolism were determined in 27 healthy postmenopausal women before and after 12 weeks of treatment with either transdermal or oral estradiol or corresponding placebo preparations. Whole body insulin sensitivity was determined using the euglycemic insulin clamp technique (rate of continuous insulin infusion 1 mU/kg·min), forearm blood flow with a strain-gauge plethysmography, and arterial stiffness using pulse wave analysis. Estradiol therapy increased basal peripheral blood flow (1.5 ± 0.1 vs. 1.9 ± 0.1 mL/dL·min, 0 vs. 12 weeks; P &lt; 0.01), decreased peripheral vascular resistance (65 ± 3 vs. 52± 3 mm Hg/mL/dL·min, respectively; P &lt; 0.01), and diastolic blood pressure (78 ± 2 vs. 75± 2 mm Hg, respectively; P &lt; 0.05) but had no effect on large artery stiffness. Infusion of insulin did not acutely alter peripheral blood flow but diminished large artery stiffness significantly both before and after the 12-week period of estradiol therapy. No measure of acute insulin action (glucose metabolism, blood flow, or large artery stiffness) was altered by estradiol or placebo treatment. These data demonstrate that insulin and estradiol have distinct hemodynamic effects. Physiological doses of estradiol increase peripheral blood flow but have no effects on large artery stiffness, whereas physiological concentrations of insulin acutely decrease stiffness without changing peripheral blood flow. Putative vasculoprotection by estradiol is, thus, not mediated via alterations in arterial stiffness or insulin sensitivity.

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38

Schillaci, Giuseppe, and Giacomo Pucci. "Is ambulatory arterial stiffness index a marker of large-artery stiffness? Evidence from intervention studies." Hypertension Research 38, no. 12 (2015): 799–801. http://dx.doi.org/10.1038/hr.2015.101.

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39

MILLASSEAU, S. C., R. P. KELLY, J. M. RITTER, and P. J. CHOWIENCZYK. "Determination of age-related increases in large artery stiffness by digital pulse contour analysis." Clinical Science 103, no. 4 (2002): 371–77. http://dx.doi.org/10.1042/cs1030371.

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The stiffness of the aorta can be determined by measuring carotid–femoral pulse wave velocity (PWVcf). PWV may also influence the contour of the peripheral pulse, suggesting that contour analysis might be used to assess large artery stiffness. An index of large artery stiffness (SIDVP) derived from the digital volume pulse (DVP) measured by transmission of IR light (photoplethysmography) was examined. SIDVP was obtained from subject height and from the time delay between direct and reflected waves in the DVP. The timing of these components of the DVP is determined by PWV in the aorta and large arteries. SIDVP was, therefore, expected to provide a measure of stiffness similar to PWV. SIDVP was compared with PWVcf obtained by applanation tonometry in 87 asymptomatic subjects (21–68 years; 29 women). The reproducibility of SIDVP and PWVcf and the response of SIDVP to glyceryl trinitrate were assessed in subsets of subjects. The mean within-subject coefficient of variation of SIDVP, for measurements at weekly intervals, was 9.6%. SIDVP was correlated with PWVcf (r = 0.65, P<0.0001). SIDVP and PWVcf were each independently correlated with age and mean arterial blood pressure (MAP) with similar regression coefficients: SIDVP = 0.63+0.086×age+0.042×MAP (r = 0.69, P<0.0001); PWVcf = 0.76+0.080×age+0.053×MAP (r = 0.71, P<0.0001). Administration of glyceryl trinitrate (3, 30 and 300 μg/min intravenous; each dose for 15 min) in nine healthy men produced similar changes in SIDVP and PWVcf. Thus contour analysis of the DVP provides a simple, reproducible, non-invasive measure of large artery stiffness.

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Briet, Marie. "Mineralocorticoid Receptor, the Main Player in Aldosterone-Induced Large Artery Stiffness." Hypertension 63, no. 3 (2014): 442–43. http://dx.doi.org/10.1161/hypertensionaha.113.02581.

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41

Saito, M., H. Okayama, K. Nishimura, et al. "Possible link between large artery stiffness and coronary flow velocity reserve." Heart 94, no. 6 (2008): e20-e20. http://dx.doi.org/10.1136/hrt.2007.126128.

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42

Chirinos, Julio A., Mayank Sardana, Amer Ahmed Syed, et al. "Aldosterone, inactive matrix gla-protein, and large artery stiffness in hypertension." Journal of the American Society of Hypertension 12, no. 9 (2018): 681–89. http://dx.doi.org/10.1016/j.jash.2018.06.018.

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43

Halabi, Carmen M., Thomas J. Broekelmann, Russell H. Knutsen, Li Ye, Robert P. Mecham, and Beth A. Kozel. "Chronic antihypertensive treatment improves pulse pressure but not large artery mechanics in a mouse model of congenital vascular stiffness." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 5 (2015): H1008—H1016. http://dx.doi.org/10.1152/ajpheart.00288.2015.

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Increased arterial stiffness is a common characteristic of humans with Williams-Beuren syndrome and mouse models of elastin insufficiency. Arterial stiffness is associated with multiple negative cardiovascular outcomes, including myocardial infarction, stroke, and sudden death. Therefore, identifying therapeutic interventions that improve arterial stiffness in response to changes in elastin levels is of vital importance. The goal of this study was to determine the effect of chronic pharmacologic therapy with different classes of antihypertensive medications on arterial stiffness in elastin insufficiency. Elastin-insufficient mice 4–6 wk of age and wild-type littermates were subcutaneously implanted with osmotic micropumps delivering a continuous dose of one of the following: vehicle, losartan, nicardipine, or propranolol for 8 wk. At the end of treatment period, arterial blood pressure and large artery compliance and remodeling were assessed. Our results show that losartan and nicardipine treatment lowered blood pressure and pulse pressure in elastin-insufficient mice. Elastin and collagen content of abdominal aortas as well as ascending aorta and carotid artery biomechanics were not affected by any of the drug treatments in either genotype. By reducing pulse pressure and shifting the working pressure range of an artery to a more compliant region of the pressure-diameter curve, antihypertensive medications may mitigate the consequences of arterial stiffness, an effect that is drug class independent. These data emphasize the importance of early recognition and long-term management of hypertension in Williams-Beuren syndrome and elastin insufficiency.

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44

Et-taouil, Karima, Pierre Schiavi, Bernard I. Lévy, and Gérard E. Plante. "Sodium Intake, Large Artery Stiffness, and Proteoglycans in the Spontaneously Hypertensive Rat." Hypertension 38, no. 5 (2001): 1172–76. http://dx.doi.org/10.1161/hy1101.96740.

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45

Sasha, S., J. Warren, P. Ngu, A. Dart, and J. Shaw. "Vitamin D Levels Do Not Correlate with Measures of Large Artery Stiffness." Heart, Lung and Circulation 22 (January 2013): S29. http://dx.doi.org/10.1016/j.hlc.2013.05.067.

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46

Schillaci, Giuseppe, Giacomo Pucci, Matteo Pirro, et al. "Large-artery stiffness: A reversible marker of cardiovascular risk in primary hyperparathyroidism." Atherosclerosis 218, no. 1 (2011): 96–101. http://dx.doi.org/10.1016/j.atherosclerosis.2011.05.010.

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47

Yu, Shikai, and Carmel M. McEniery. "Central Versus Peripheral Artery Stiffening and Cardiovascular Risk." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 5 (2020): 1028–33. http://dx.doi.org/10.1161/atvbaha.120.313128.

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The large elastic arteries fulfill an important role in buffering the cyclical changes in blood pressure, which result from intermittent ventricular ejection. With aging and accrual of cardiovascular risk factors, the elastic arteries stiffen, and this process holds a number of deleterious consequences for the cardiovascular system and major organs. Indeed, arterial stiffness is now recognized as an important, independent determinant of cardiovascular disease risk. Additional, important information concerning the mechanisms underlying arterial stiffening has come from longitudinal studies of arterial stiffness. More recently, attention has focused on the role of peripheral, muscular arteries in cardiovascular disease risk prediction and, in particular, the clinical consequences of reversal of the normal gradient of arterial stiffness between central and peripheral arteries, with aging and disease.

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48

Seals, Douglas R., Christopher A. DeSouza, Anthony J. Donato, and Hirofumi Tanaka. "Habitual exercise and arterial aging." Journal of Applied Physiology 105, no. 4 (2008): 1323–32. http://dx.doi.org/10.1152/japplphysiol.90553.2008.

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Aging affects the function and structure of arteries and increases the risk of cardiovascular diseases (CVD). In healthy sedentary adults, aging is associated with increased stiffness (reduced compliance) of large elastic arteries; impaired vascular endothelial function, including reductions in endothelium-dependent dilation (EDD), release of tissue-type plasminogen activator (fibrinolytic capacity) and endothelial progenitor cell number and function; increased intima-media wall thickness (IMT); and peripheral vasoconstriction (decreased basal leg blood flow). Habitual physical activity/increased aerobic exercise capacity is associated with reduced risk of CVD. Compared with their sedentary peers, adults who regularly perform aerobic exercise demonstrate smaller or no age-associated increases in large elastic artery stiffness, reductions in vascular endothelial function, and increases in femoral artery IMT. A short-term, moderate-intensity aerobic exercise intervention (brisk daily walking for 12 wk) improves carotid artery compliance and can restore vascular endothelial function in previously sedentary middle-aged and older adults. Reduced oxidative stress may be an important mechanism contributing to these effects. Habitual resistance exercise increases (high-intensity) or does not affect (moderate-intensity) large elastic artery stiffness, and prevents/restores the age-associated reduction in basal leg blood flow independent of changes in leg fat-free mass. Habitual exercise favorably modulates several expressions of arterial aging, thus preserving vascular function and possibly reducing the risk of CVD.

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Obeid, Hasan, Catherine Fortier, Charles-Antoine Garneau, et al. "Radial-digital pulse wave velocity: a noninvasive method for assessing stiffness of small conduit arteries." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 4 (2021): H1361—H1369. http://dx.doi.org/10.1152/ajpheart.00551.2020.

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Aortic stiffness, a cardiovascular risk factor and a marker of arterial aging, is assessed by pulse wave velocity (PWV) over this arterial segment. The interaction between the stiffness of various arterial segments is important in understanding the behavior of pressure and flow waves along the arterial tree. However, PWV assessment has been limited to large elastic vessels (aorta) or medium-sized arteries (i.e., brachial artery). In this paper, we provide a novel and noninvasive method of assessing the regional stiffness of small conduit arteries using the same piezoelectric sensors used for determination of PWV over large and medium-sized arteries. This development allows for an integrated approach to arterial stiffness from large to medium-sized arteries and now to small conduit arteries in humans.

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Ferreira, Isabel, Marieke B. Snijder, Jos W. R. Twisk, et al. "Central Fat Mass Versus Peripheral Fat and Lean Mass: Opposite (Adverse Versus Favorable) Associations with Arterial Stiffness? The Amsterdam Growth and Health Longitudinal Study." Journal of Clinical Endocrinology & Metabolism 89, no. 6 (2004): 2632–39. http://dx.doi.org/10.1210/jc.2003-031619.

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Abstract Central and peripheral fatness seem to confer opposite (i.e. adverse vs. protective) effects on cardiovascular risk, but how this occurs is not clear. In addition, the role of peripheral lean mass needs to be elucidated. We therefore investigated, in 336 (175 women) 36-yr-old and apparently healthy adults, the relationship between trunk fat, peripheral fat, and peripheral lean mass on the one hand, and estimates of stiffness of three large arteries on the other. Body composition was assessed by dual-energy x-ray absorptiometry. Arterial properties were assessed by ultrasound imaging. We found that 1) trunk fat was positively (i.e. adversely) associated with stiffness of the carotid and femoral arteries, whereas peripheral fat was inversely (i.e. favorably) associated with stiffness of the brachial and the carotido-femoral segment; 2) peripheral lean mass was positively associated with arterial diameter and carotid compliance and inversely associated with stiffness of the carotido-femoral segment; and 3) after adjustment for the other body composition variables, the above-mentioned associations remained, but peripheral fat in addition became, if anything, favorably associated with stiffness of the femoral artery. We conclude that trunk fat is adversely associated with large artery stiffness, whereas some degree of protection is conferred by peripheral fat and lean mass.

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