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1
Gherardini, Rachele. "P35 ARTERIAL STIFFNESS AND CHRONIC STRESS: ROLE OF GENDER – RIGIDITà ARTERIOSA E STRESS CRONICO: RUOLO DEL GENERE." Artery Research 24, no. C (2018): 89. http://dx.doi.org/10.1016/j.artres.2018.10.088.
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Ikemura, Tsukasa, Nobuhiro Nakamura, and Naoyuki Hayashi. "Impact of acute dynamic exercise on vascular stiffness in the retinal arteriole in healthy subjects." Journal of Applied Physiology 132, no. 2 (February 1, 2022): 459–68. http://dx.doi.org/10.1152/japplphysiol.00507.2021.
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Acute dynamic exercise is well known to improve vascular stiffness in the conduit artery while its effect on the retinal arterioles has been unknown. This study showed that an acute dynamic exercise does not change vascular stiffness in the retinal arteriole in healthy humans. Different responses to acute dynamic exercise in vascular stiffness in retinal arterioles and conduit arteries are suggested.
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Jahn, Linda A., Lee Hartline, Nagashree Rao, Brent Logan, Justin J. Kim, Kevin Aylor, Li-Ming Gan, Helena U. Westergren, and Eugene J. Barrett. "Insulin Enhances Endothelial Function Throughout the Arterial Tree in Healthy But Not Metabolic Syndrome Subjects." Journal of Clinical Endocrinology & Metabolism 101, no. 3 (March 1, 2016): 1198–206. http://dx.doi.org/10.1210/jc.2015-3293.
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Abstract Context: Insulin reportedly impairs endothelial function in conduit arteries but improves it in resistance and microvascular arterioles in healthy humans. No studies have assessed endothelial function at three arterial levels in healthy or metabolic syndrome (METSYN) subjects. Objective: The objective of the study was to compare endothelial responsiveness of conduit arteries, resistance, and microvascular arterioles to insulin in healthy and METSYN subjects. Design: We assessed conduit, resistance, and microvascular arterial function in the postabsorptive and postprandial states and during euglycemic hyperinsulinemia (insulin clamp). Setting: The study was conducted at a clinical research unit. Participants: Age-matched healthy and METSYN subjects participated in the study. Interventions: We used brachial flow-mediated dilation, forearm postischemic flow velocity, and contrast-enhanced ultrasound to assess the conduit artery, resistance arteriole, and microvascular arteriolar endothelial function, respectively. We also assessed the conduit artery stiffness (pulse wave velocity and augmentation index) and measured the plasma concentrations of 92 cardiovascular disease biomarkers at baseline and after the clamp. Results: Postabsorptive and postprandial endothelial function was similar in controls and METSYN in all tested vessels. METSYN subjects were metabolically insulin resistant (P < .005). In controls, but not METSYN subjects, during euglycemic hyperinsulinemia, endothelial function improved at each level of arterial vasculature (P < .05 or less for each). Conduit vessel stiffness (pulse wave velocity) was increased in the METSYN group. Twelve of 92 biomarkers differed at baseline (P < .001) and remained different at the end of the insulin clamp. Conclusions: We conclude that insulin enhances arterial endothelial function in health but not in METSYN, and this vascular insulin resistance may underlie its increased cardiovascular disease risk.
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Sander, Ruth. "Swollen arteries and stiffness." Nursing Older People 23, no. 7 (September 2011): 11. http://dx.doi.org/10.7748/nop.23.7.11.s8.
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Eiken, O., A. Elia, H. Sköldefors, P. Sundblad, M. E. Keramidas, and R. Kölegård. "Adaptation to 5 weeks of intermittent local vascular pressure increments; mechanisms to be considered in the development of primary hypertension?" American Journal of Physiology-Heart and Circulatory Physiology 320, no. 4 (April 1, 2021): H1303—H1312. http://dx.doi.org/10.1152/ajpheart.00763.2020.
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Adaptive responses to arterial/arteriolar pressure elevation have typically been investigated in cross-sectional studies in hypertensive patients or in longitudinal studies in experimental animals. The present investigation shows that in healthy individuals, fifteen 40-min, carefully controlled, moderate transmural pressure elevations markedly increase in vivo stiffness (i.e. reduce pressure distension) in arteries and arterioles. The response is mediated via local mechanisms, and it appears that endothelin-1, angiotensin-II, and matrix metalloproteinase 7 may have key roles.
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Morales-Quinones, Mariana, Francisco I. Ramirez-Perez, Christopher A. Foote, Thaysa Ghiarone, Larissa Ferreira-Santos, Maria Bloksgaard, Nicole Spencer, et al. "LIMK (LIM Kinase) Inhibition Prevents Vasoconstriction- and Hypertension-Induced Arterial Stiffening and Remodeling." Hypertension 76, no. 2 (August 2020): 393–403. http://dx.doi.org/10.1161/hypertensionaha.120.15203.
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Increased arterial stiffness and vascular remodeling precede and are consequences of hypertension. They also contribute to the development and progression of life-threatening cardiovascular diseases. Yet, there are currently no agents specifically aimed at preventing or treating arterial stiffening and remodeling. Previous research indicates that vascular smooth muscle actin polymerization participates in the initial stages of arterial stiffening and remodeling and that LIMK (LIM kinase) promotes F-actin formation and stabilization via cofilin phosphorylation and consequent inactivation. Herein, we hypothesize that LIMK inhibition is able to prevent vasoconstriction- and hypertension-associated arterial stiffening and inward remodeling. We found that small visceral arteries isolated from hypertensive subjects are stiffer and have greater cofilin phosphorylation than those from nonhypertensives. We also show that LIMK inhibition prevents arterial stiffening and inward remodeling in isolated human small visceral arteries exposed to prolonged vasoconstriction. Using cultured vascular smooth muscle cells, we determined that LIMK inhibition prevents vasoconstrictor agonists from increasing cofilin phosphorylation, F-actin volume, and cell cortex stiffness. We further show that localized LIMK inhibition prevents arteriolar inward remodeling in hypertensive mice. This indicates that hypertension is associated with increased vascular smooth muscle cofilin phosphorylation, cytoskeletal stress fiber formation, and heightened arterial stiffness. Our data further suggest that pharmacological inhibition of LIMK prevents vasoconstriction-induced arterial stiffening, in part, via reductions in vascular smooth muscle F-actin content and cellular stiffness. Accordingly, LIMK inhibition should represent a promising therapeutic means to stop the progression of arterial stiffening and remodeling in hypertension.
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Pannier, Bruno, Alain P. Guérin, Sylvain J. Marchais, Michel E. Safar, and Gérard M. London. "Stiffness of Capacitive and Conduit Arteries." Hypertension 45, no. 4 (April 2005): 592–96. http://dx.doi.org/10.1161/01.hyp.0000159190.71253.c3.
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Obeid, Hasan, Catherine Fortier, Charles-Antoine Garneau, Mathilde Pare, Pierre Boutouyrie, Rosa Maria Bruno, Hakim Khettab, Rémi Goupil, and Mohsen Agharazii. "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 (April 1, 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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Hanna, Mina A., Curtis R. Taylor, Bei Chen, Hae-Sun La, Joshua J. Maraj, Cody R. Kilar, Bradley J. Behnke, Michael D. Delp, and Judy M. Muller-Delp. "Structural remodeling of coronary resistance arteries: effects of age and exercise training." Journal of Applied Physiology 117, no. 6 (September 15, 2014): 616–23. http://dx.doi.org/10.1152/japplphysiol.01296.2013.
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Age is known to induce remodeling and stiffening of large-conduit arteries; however, little is known of the effects of age on remodeling and mechanical properties of coronary resistance arteries. We employed a rat model of aging to investigate whether 1) age increases wall thickness and stiffness of coronary resistance arteries, and 2) exercise training reverses putative age-induced increases in wall thickness and stiffness of coronary resistance arteries. Young (4 mo) and old (21 mo) Fischer 344 rats remained sedentary or underwent 10 wk of treadmill exercise training. Coronary resistance arteries were isolated for determination of wall-to-lumen ratio, effective elastic modulus, and active and passive responses to changes in intraluminal pressure. Elastin and collagen content of the vascular wall were assessed histologically. Wall-to-lumen ratio increased with age, but this increase was reversed by exercise training. In contrast, age reduced stiffness, and exercise training increased stiffness in coronary resistance arteries from old rats. Myogenic responsiveness was reduced with age and restored by exercise training. Collagen-to-elastin ratio (C/E) of the wall did not change with age and was reduced with exercise training in arteries from old rats. Thus age induces hypertrophic remodeling of the vessel wall and reduces the stiffness and myogenic function of coronary resistance arteries. Exercise training reduces wall-to-lumen ratio, increases wall stiffness, and restores myogenic function in aged coronary resistance arteries. The restorative effect of exercise training on myogenic function of coronary resistance arteries may be due to both changes in vascular smooth muscle phenotype and expression of extracellular matrix proteins.
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Safar, Michel E., and P. Lacolley. "Disturbance of macro- and microcirculation: relations with pulse pressure and cardiac organ damage." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (July 2007): H1—H7. http://dx.doi.org/10.1152/ajpheart.00063.2007.
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Whereas large arteries dampen oscillations resulting from intermittent ventricular ejection, small arteries steadily deliver optimal blood flow to various organs as the heart. The transition from pulsatile to steady pressure is influenced by several factors as wave travel, damping, and reflections, which are mainly determined by the impedance mismatch between large vessels and arteriolar bifurcations. The mechanism(s) behind the dampening of pressure wave in the periphery and the links between central and peripheral pulsatile pressure (PP) may determine cardiac damage. Active pathways participate to pulse widening and changes in pulse amplitude in microvessels. Steady and cyclic stresses operate through different transduction mechanisms, the former being focal adhesion kinase and the latter being free radicals and oxidative stress. Independently of mechanics, calcifications and attachment molecules contribute to enhance vessel wall stiffness through changes in collagen cross-links, proteoglycans, integrins, and fibronectin. Enhanced PP transmission may thus occur and precipitate organ damage at each time that autoregulatory mechanisms, normally protecting the heart from vascular injury, are blunted. Such circumstances, observed in old subjects with systolic hypertension and/or Type 2 diabetes mellitus, particularly under high-sodium diet, cause cardiac damage and explain why increased PP and arterial stiffness are significant predictors of morbidity and mortality in the elderly.
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Niwa, Koichiro. "Landmark lecture: Perloff lecture: Tribute to Professor Joseph Kayle Perloff and lessons learned from him: aortopathy in adults with CHD." Cardiology in the Young 27, no. 10 (December 2017): 1959–65. http://dx.doi.org/10.1017/s1047951117002116.
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AbstractMarfan syndrome, bicuspid aortic valve, and/or coarctation of the aorta are associated with medial abnormalities of the ascending aortic or para-coarctation aorta. Medial abnormalities in the ascending aorta are prevalent in other type of patients with a variety of CHDs such as single ventricle, persistent truncus arteriosus, transposition of the great arteries, hypoplastic left heart syndrome, and tetralogy of Fallot, encompassing a wide age range and may predispose to dilatation, aneurysm, and rapture necessitating aortic valve and root surgery. These CHDs exhibit ongoing dilatation of the aortic root and reduced aortic elasticity and increased aortic stiffness that may relate to intrinsic properties of the aortic root. These aortic dilatation and increased stiffness can induce aortic aneurysm, rapture of the aorta, and aortic regurgitation, but also provoke left ventricular hypertrophy, reduced coronary artery flow, and left ventricular failure. Therefore, a new clinical entity can be used to call this association of aortic pathophysiological abnormality, aortic dilation, and aorto-left ventricular interaction – “aortopathy”.
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Gajnitdinova, V. V., A. B. Bakirov, E. Kh Akhmetzyanova, N. F. Berdikaeva, and V. B. Zakirova. "Arterial stiffness of peripheral vasculature in patients with chronic obstructive pulmonary disease and its association with arterial hypertension." Kazan medical journal 94, no. 6 (December 15, 2013): 808–12. http://dx.doi.org/10.17816/kmj1795.
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Aim. To study the structural and functional state of vascular wall, arterial stiffness of large peripheral arteries (common carotid arteries, renal arteries) in patients with severe chronic obstructive pulmonary disease and its association with arterial hypertension. Methods. The study included 67 patients of working age, mainly males, having chronic obstructive pulmonary disease. Among them, 52 patients had severe chronic obstructive pulmonary disease (defined by GOLD III, 2011), 15 had concomitant arterial hypertension of I and II stage. Structural and functional status of common carotid arteries, renal arteries was assessed by measurement of intima-media thickness, arterial stiffness indexes were calculated. Arterial elasticity indices: arterial compliance, elastic index, Young’s elastic modulus were calculated based on the results of ultrasonography of main arterial wall parameters (diameter, arterial wall thickness) and blood pressure measurement. Results. A decrease in common carotid arteries and renal arteries wall elasticity was revealed in patients with chronic obstructive pulmonary disease. Increase of stiffness index in patients with severe chronic obstructive pulmonary disease associated with arterial hypertension, marking the decreased arterial wall elasticity, was registered both in common carotid arteries and renal arteries. Conclusion. In common carotid arteries vascular wall thickness contribute the most in vascular wall stiffness increase, compared to altered hemodynamics in renal arteries. Development of arterial hypertension in these patients is a predicting factor for further large vessel remodeling associated with hypoxia.
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London, Gerard M., Michel E. Safar, and Bruno Pannier. "The Age–Stiffness Relationships of Elastic and Muscular Arteries in a Control Population and in End-Stage Renal Disease Patients." Kidney and Dialysis 3, no. 1 (January 3, 2023): 36–45. http://dx.doi.org/10.3390/kidneydial3010003.
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Arterial dysfunction is major risk factor for cardiovascular complications, and arterial stiffness is an independent risk factor in end-stage renal disease patients. As the distance from the heart increases, arterial stiffness (pulse wave velocity) becomes progressively more marked. This generates a centrifugal stiffness gradient, which leads to partial, continuous local wave reflections, which in turn attenuate the transmission of pulsatile pressure into the microcirculation, thus limiting the potentially deleterious outcomes both upstream (on the heart: left-ventricular hypertrophy and coronary perfusion) and downstream (on the renal and cerebral microcirculation: reduced glomerular filtration and impaired cognitive functions). The impact of arterial aging is greater on the aorta and central capacitive arteries, and it is characterized by a loss or reversal of the physiological stiffness gradient between central and peripheral arteries. Recently, however, in contrast to observations on the aorta, several studies have shown less pronounced, absent, or even negative associations between muscular peripheral arteries and age–stiffness relationships, which may be associated with a decrease in or reversal of the stiffness gradient. These findings point to a potential benefit of assessing the muscular peripheral arteries to predict the risk of cardiovascular disease and suggest that reversal of the stiffness gradient may be an independent risk factor for all-cause mortality.
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Genkel, V. V., A. O. Salachenko, O. A. Alekseeva, and I. I. Shaposhnik. "Endothelial shear rate, local and regional vascular stiffness in patients in different stages of atherogenesis." Regional blood circulation and microcirculation 15, no. 3 (September 30, 2016): 50–56. http://dx.doi.org/10.24884/1682-6655-2016-15-3-50-56.
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Introduction and purpose. Endothelial cells are subjected to biomechanical stress produced by the bloodstream and tunica media of the vessel. Vascular stiffness and endothelial shear stress have cooperative effects on the endothelial structure and function. However, the relationship of shear stress and arterial stiffness is still poorly understood. The purpose of the study was to assess the relationship of endothelial shear rate and both local and regional vascular stiffness in patients at different stages of the development of atherosclerosis. Methods. The study included 60 patients, 33 men and 27 women. The average age of patients was 54.8±11.7 years. Regional arterial stiffness was assessed by measurement of the pulse wave velocity in the arteries of elastic and muscular types. Local stiffness of the carotid arteries was characterized by Peterson elastic modulus, Young's modulus, stiffness index β, the deformation of the common carotid artery. Endothelial shear rate was measured at the site of the common carotid artery. Results. Average values of carotid endothelial shear rate were equal to 433±127 s-1. Reduced endothelial shear rate in the carotid arteries was associated with an increased Peterson modulus (r = -0.289; p = 0.025) and the stiffness index β (r = -0.280; p = 0.037), and moreover - with decreasing vascular distensibility (r = 0.288; p = 0.026) and deformation (r = 0.296; p = 0.024). Assessment of the relationship between endothelial shear rate and regional vascular stiffness showed weak statistically significant negative correlation of shear rate and PWVcf (r = -0.367; p = 0.014). Conclusion. In study subjects endothelial shear rate reduction in the area of the common carotid artery was associated with an increased Peterson modulus, stiffness index β, decreasing deformation of carotid arteries and increase in aortic stiffness.
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Yu, Shikai, and Carmel M. McEniery. "Central Versus Peripheral Artery Stiffening and Cardiovascular Risk." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 5 (May 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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Hamilton, Paul K., Christopher J. Lockhart, Cathy E. Quinn, and Gary E. Mcveigh. "Arterial stiffness: clinical relevance, measurement and treatment." Clinical Science 113, no. 4 (July 13, 2007): 157–70. http://dx.doi.org/10.1042/cs20070080.
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Most traditional cardiovascular risk factors alter the structure and/or function of arteries. An assessment of arterial wall integrity could therefore allow accurate prediction of cardiovascular risk in individuals. The term ‘arterial stiffness’ denotes alterations in the mechanical properties of arteries, and much effort has focused on how best to measure this. Pulse pressure, pulse wave velocity, pulse waveform analysis, localized assessment of blood vessel mechanics and other methods have all been used. We review the methodology underlying each of these measures, and present an evidence-based critique of their relative merits and limitations. An overview is also given of the drug therapies that may prove useful in the treatment of patients with altered arterial mechanics.
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Ogola, Benard O., Margaret A. Zimmerman, Gabrielle L. Clark, Caleb M. Abshire, Kaylee M. Gentry, Kristin S. Miller, and Sarah H. Lindsey. "New insights into arterial stiffening: does sex matter?" American Journal of Physiology-Heart and Circulatory Physiology 315, no. 5 (November 1, 2018): H1073—H1087. http://dx.doi.org/10.1152/ajpheart.00132.2018.
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This review discusses sexual dimorphism in arterial stiffening, disease pathology interactions, and the influence of sex on mechanisms and pathways. Arterial stiffness predicts cardiovascular mortality independent of blood pressure. Patients with increased arterial stiffness have a 48% higher risk for developing cardiovascular disease. Like other cardiovascular pathologies, arterial stiffness is sexually dimorphic. Young women have lower stiffness than aged-matched men, but this sex difference reverses during normal aging. Estrogen therapy does not attenuate progressive stiffening in postmenopausal women, indicating that currently prescribed drugs do not confer protection. Although remodeling of large arteries is a protective adaptation to higher wall stress, arterial stiffening increases afterload to the left ventricle and transmits higher pulsatile pressure to smaller arteries and target organs. Moreover, an increase in aortic stiffness may precede or exacerbate hypertension, particularly during aging. Additional studies are needed to elucidate the mechanisms by which females are protected from arterial stiffness to provide insight into its mechanisms and, ultimately, therapeutic targets for treating this pathology.
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Holwerda, Seth W., Randy H. Kardon, Ryuya Hashimoto, Jan M. Full, Julie K. Nellis, Lyndsey E. DuBose, Jess G. Fiedorowicz, and Gary L. Pierce. "Aortic stiffness is associated with changes in retinal arteriole flow pulsatility mediated by local vasodilation in healthy young/middle-age adults." Journal of Applied Physiology 129, no. 1 (July 1, 2020): 84–93. http://dx.doi.org/10.1152/japplphysiol.00252.2020.
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By using the human retinal microvasculature as an end-organ in vivo model, we confirm that aortic stiffness and related increases in central pulse pressure are inversely correlated with retinal arteriole lumen diameter and increased microvascular resistance among heathy young/middle-age adults. Additionally, higher aortic stiffness is not associated with excessive flow pulsatility in the retinal microvasculature under tonic conditions but may be related to limited reductions in retinal arteriole flow pulsatility in response to local vasodilation.
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Aizawa, Kunihiko, and Robert J. Petrella. "Acute and Chronic Impact of Dynamic Exercise on Arterial Stiffness in Older Hypertensives." Open Cardiovascular Medicine Journal 2, no. 1 (February 12, 2008): 3–8. http://dx.doi.org/10.2174/1874192400802010003.
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Arterial stiffness increases with ageing and hypertension. Regular physical activity has been recommended as an important management component of hypertension. The purpose of this study was to examine the acute impact of maximal dynamic exercise and the effect of 20 weeks of aerobic exercise on arterial stiffness of the carotid and brachial arteries in older hypertensives. Nine previously sedentary and treated older hypertensives (2 men and 7 women, age 68.2 ± 5.4 yrs) performed maximal treadmill exercise to volitional fatigue while arterial stiffness indices (arterial distensibility and β stiffness index) were measured prior to, immediately (about 10 min) following, and 24 h following maximal exercise. These measurements were repeated following 20 weeks of moderate intensity aerobic exercise training. Maximal exercise had no impact on arterial stiffness indices immediately and 24 h following exercise intervention. Following 20 weeks of training, arterial stiffness indices remained unchanged at rest and following maximal exercise. These data show that, in older hypertensives, 1) acute maximal dynamic exercise had no impact on arterial stiffness of the carotid and brachial arteries, and 2) 20 weeks of moderate intensity aerobic exercise training failed to modify arterial stiffness.
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Salih, Saba F., Najeeb H. Mohammed, Abbas N. Muslim, and Sarab H. Al-Misebawi. "Arterial stiffness index as a marker for the occurrence of atherosclerotic cardiovascular disease." Journal of the Faculty of Medicine Baghdad 58, no. 1 (April 3, 2016): 94–97. http://dx.doi.org/10.32007/jfacmedbagdad.581209.
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Background: Arterial functional changes reflected by vascular stiffness might occur at early stages of cardiovascular disease before the morphological alterations reflected by increasing the intima media thickness and it is widely used as a very sensitive indicator of functional vascular damage.Objectives: This study is aimed to correlate ultrasound detected vascular functional changes with the severity and extent of coronary artery disease.Patients and methods: Sonographic scans were performed on 100 Patients (61males, 39 females) with an age range of (40-65years) for measuring carotid and brachial arteries end diastolic and end systolic diameters to calculate vascular stiffness index . Coronary CT angiography has been used to visualize the atherosclerotic plaque to define the degree of luminal stenosis by creation of high-quality images which are obtained by the multislice CT spiral scanners.Results: A positive statistical correlation was observed between the stiffness index of both carotid and brachial arteries in single coronary lesion (SCL), multiple coronary lesion (MCL) and control groups in addition to the significant positive correlation between both arteries stiffness index with the percentage of coronary artery stenosis in SCL group. Significant difference between the arterial stiffness index among the study groups is only noticed for carotid artery between the control and MCL groups (p<0.05).Conclusion: Conduit arterial stiffness index is a good indicator of the severity and extent of coronary artery disease.
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Genkel, Vadim V., Alexey O. Salashenko, Tatyana N. Shamaeva, Veronika A. Sumerkina, and Igor I. Shaposhnik. "Association between Carotid Wall Shear Rate and Arterial Stiffness in Patients with Hypertension and Atherosclerosis of Peripheral Arteries." International Journal of Vascular Medicine 2018 (August 1, 2018): 1–8. http://dx.doi.org/10.1155/2018/6486234.
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Aim. To evaluate carotid wall shear rate (WSR) in association with local and regional vascular stiffness in patients with hypertension (HTN) and atherosclerosis of peripheral arteries and to study the pattern of change of WSR in patients with HTN with increasing severity of peripheral artery atherosclerosis. Materials and Methods. Study involved 133 patients with HTN, 65 men and 48 women, aged in average 57.9±10.8 years. All patients were divided into four groups in accordance with ultrasound morphologic classification of vessel wall. Duplex scanning of carotid and lower limb arteries was performed. Carotid-femoral (cfPWV) and carotid-radial (crPWV) pulse wave velocity (PWV) were measured. Local carotid stiffness was evaluated by carotid ultrasound. Results. WSR of patients with plaques without and with hemodynamic disturbance was 416±128 s−1 and 405±117 s−1, respectively, which was significantly less than the WSR in patients with intact peripheral arteries – 546±112 s−1. Decreased carotid WSR was associated with increased crPVW, cfPWV, Peterson’s elastic modulus, decreased distensibility, and distensibility coefficient. Conclusion. In patients with HTN and atherosclerotic lesions of peripheral arteries, it is registered that the carotid WSR decreased with increasing severity of atherosclerosis. Decreased carotid WSR is associated with increased local carotid stiffness, regional vascular stiffness of muscular, and elastic vessels.
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Du, Bing, An Ouyang, Jason S. Eng, and Bradley S. Fleenor. "Aortic perivascular adipose-derived interleukin-6 contributes to arterial stiffness in low-density lipoprotein receptor deficient mice." American Journal of Physiology-Heart and Circulatory Physiology 308, no. 11 (June 1, 2015): H1382—H1390. http://dx.doi.org/10.1152/ajpheart.00712.2014.
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We tested the hypothesis that aortic perivascular adipose tissue (PVAT) from young low-density lipoprotein receptor-deficient (LDLr−/−) mice promotes aortic stiffness and remodeling, which would be mediated by greater PVAT-derived IL-6 secretion. Arterial stiffness was assessed by aortic pulse wave velocity and with ex vivo intrinsic mechanical properties testing in young (4–6 mo old) wild-type (WT) and LDLr−/− chow-fed mice. Compared with WT mice, LDLr−/− mice had increased aortic pulse wave velocity (407 ± 18 vs. 353 ± 13 cm/s) and intrinsic mechanical stiffness (5,308 ± 623 vs. 3,355 ± 330 kPa) that was associated with greater aortic protein expression of collagen type I and advanced glycation end products (all P < 0.05 vs. WT mice). Aortic segments from LDLr−/− compared with WT mice cultured in the presence of PVAT had greater intrinsic mechanical stiffness (6,092 ± 480 vs. 3,710 ± 316 kPa), and this was reversed in LDLr−/− mouse arteries cultured without PVAT (3,473 ± 577 kPa, both P < 0.05). Collagen type I and advanced glycation end products were increased in LDLr−/− mouse arteries cultured with PVAT ( P < 0.05 vs. WT mouse arteries), which was attenuated when arteries were cultured in the absence of PVAT ( P < 0.05). PVAT from LDLr−/− mice secreted larger amounts of IL-6 (3.4 ± 0.1 vs. 2.3 ± 0.7 ng/ml, P < 0.05), and IL-6 neutralizing antibody decreased intrinsic mechanical stiffness in LDLr−/− aortic segments cultured with PVAT ( P < 0.05). Collectively, these data provide evidence for a role of PVAT-derived IL-6 in the pathogenesis of aortic stiffness and remodeling in chow-fed LDLr−/− mice.
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Namba, Takayuki, Nobuyuki Masaki, Bonpei Takase, and Takeshi Adachi. "Arterial Stiffness Assessed by Cardio-Ankle Vascular Index." International Journal of Molecular Sciences 20, no. 15 (July 26, 2019): 3664. http://dx.doi.org/10.3390/ijms20153664.
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Arterial stiffness is an age-related disorder. In the medial layer of arteries, mechanical fracture due to fatigue failure for the pulsatile wall strain causes medial degeneration vascular remodeling. The alteration of extracellular matrix composition and arterial geometry result in structural arterial stiffness. Calcium deposition and other factors such as advanced glycation end product-mediated collagen cross-linking aggravate the structural arterial stiffness. On the other hand, endothelial dysfunction is a cause of arterial stiffness. The biological molecular mechanisms relating to aging are known to involve the progression of arterial stiffness. Arterial stiffness further applies stress on large arteries and also microcirculation. Therefore, it is closely related to adverse outcomes in cardiovascular and cerebrovascular system. Cardio-ankle vascular index (CAVI) is a promising diagnostic tool for evaluating arterial stiffness. The principle is based on stiffness parameter β, which is an index intended to assess the distensibility of carotid artery. Stiffness parameter β is a two-dimensional technique obtained from changes of arterial diameter by pulse in one section. CAVI applied the stiffness parameter β to all of the arterial segments between heart and ankle using pulse wave velocity. CAVI has been commercially available for a decade and the clinical data of its effectiveness has accumulated. The characteristics of CAVI differ from other physiological tests of arterial stiffness due to the independency from blood pressure at the time of examination. This review describes the pathophysiology of arterial stiffness and CAVI. Molecular mechanisms will also be covered.
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Boutouyrie, Pierre, Phil Chowienczyk, Jay D. Humphrey, and Gary F. Mitchell. "Arterial Stiffness and Cardiovascular Risk in Hypertension." Circulation Research 128, no. 7 (April 2, 2021): 864–86. http://dx.doi.org/10.1161/circresaha.121.318061.
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Arterial stiffness, a leading marker of risk in hypertension, can be measured at material or structural levels, with the latter combining effects of the geometry and composition of the wall, including intramural organization. Numerous studies have shown that structural stiffness predicts outcomes in models that adjust for conventional risk factors. Elastic arteries, nearer to the heart, are most sensitive to effects of blood pressure and age, major determinants of stiffness. Stiffness is usually considered as an index of vascular aging, wherein individuals excessively affected by risk factor exposure represent early vascular aging, whereas those resistant to risk factors represent supernormal vascular aging. Stiffness affects the function of the brain and kidneys by increasing pulsatile loads within their microvascular beds, and the heart by increasing left ventricular systolic load; excessive pressure pulsatility also decreases diastolic pressure, necessary for coronary perfusion. Stiffness promotes inward remodeling of small arteries, which increases resistance, blood pressure, and in turn, central artery stiffness, thus creating an insidious feedback loop. Chronic antihypertensive treatments can reduce stiffness beyond passive reductions due to decreased blood pressure. Preventive drugs, such as lipid-lowering drugs and antidiabetic drugs, have additional effects on stiffness, independent of pressure. Newer anti-inflammatory drugs also have blood pressure independent effects. Reduction of stiffness is expected to confer benefit beyond the lowering of pressure, although this hypothesis is not yet proven. We summarize different steps for making arterial stiffness measurement a keystone in hypertension management and cardiovascular prevention as a whole.
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Sugawara, Jun, Tsubasa Tomoto, Hsin-Fu Lin, Chen-Huan Chen, and Hirofumi Tanaka. "Aortic reservoir function of Japanese female pearl divers." Journal of Applied Physiology 125, no. 6 (December 1, 2018): 1901–5. http://dx.doi.org/10.1152/japplphysiol.00466.2018.
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Female pearl divers in Japan, called “ Ama,” engage in repeated breath-hold free-diving maneuvers for collecting pearls, seaweeds, and shellfish in the cold sea. We previously reported that they have lower systemic arterial stiffness than age-matched sedentary peers. As a follow-up study, we evaluated their segmental arterial stiffness and aortic reservoir function. A total of 120 non-medicated women living in the same fishing villages (mean age: 65 ± 11 yr), including 88 Ama and 32 age-matched sedentary peers, were studied. Pulse wave velocity from the heart to the brachial artery (hbPWV; partly reflecting proximal aortic stiffness) and between the brachial artery and the ankle (baPWV; reflecting stiffness of abdominal aorta and leg arteries) were measured. Aortic hemodynamic variables were estimated from applanation tonometry carotid arterial pressure waveforms via general transfer function. Carotid artery impedance was calculated from blood flow velocity and blood pressure of contralateral common carotid arteries. baPWV was not different between the groups ( P = 0.117), whereas hbPWV was significantly lower in pearl divers than sedentary peers ( P = 0.004). Additionally, Ama had significantly lower aortic reservoir pressure integral ( P = 0.029) and carotid artery impedance modulus in frequency ranges from 0.78 to 4.0 Hz ( P = 0.011~0.019) than in sedentary peers. Collectively, these findings indicate that lifelong female pearl divers have superior reservoir function in central elastic arteries (e.g., the proximal aorta and carotid artery) in comparison with age-matched sedentary women living in the same fishing village. NEW & NOTEWORTHY We previously reported that lifelong female pearl divers in Japan, called “ Ama,” have lower systemic arterial stiffness than age-matched sedentary peers. As a follow-up study, we evaluated their segmental arterial stiffness and aortic reservoir function. In comparison with age-matched sedentary women living in the same fishing village, Ama demonstrated significantly lower arterial stiffness in more proximal and elastic arterial segments and superior reservoir function in central elastic arteries.
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Bender, Shawn B., Jorge A. Castorena-Gonzalez, Mona Garro, Constantino C. Reyes-Aldasoro, James R. Sowers, Vincent G. DeMarco, and Luis A. Martinez-Lemus. "Regional variation in arterial stiffening and dysfunction in Western diet-induced obesity." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 4 (August 15, 2015): H574—H582. http://dx.doi.org/10.1152/ajpheart.00155.2015.
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Increased central vascular stiffening, assessed in vivo by determination of pulse wave velocity (PWV), is an independent predictor of cardiovascular event risk. Recent evidence demonstrates that accelerated aortic stiffening occurs in obesity; however, little is known regarding stiffening of other disease-relevant arteries or whether regional variation in arterial stiffening occurs in this setting. We addressed this gap in knowledge by assessing femoral PWV in vivo in conjunction with ex vivo analyses of femoral and coronary structure and function in a mouse model of Western diet (WD; high-fat/high-sugar)-induced obesity and insulin resistance. WD feeding resulted in increased femoral PWV in vivo. Ex vivo analysis of femoral arteries revealed a leftward shift in the strain-stress relationship, increased modulus of elasticity, and decreased compliance indicative of increased stiffness following WD feeding. Confocal and multiphoton fluorescence microscopy revealed increased femoral stiffness involving decreased elastin/collagen ratio in conjunction with increased femoral transforming growth factor-β (TGF-β) content in WD-fed mice. Further analysis of the femoral internal elastic lamina (IEL) revealed a significant reduction in the number and size of fenestrae with WD feeding. Coronary artery stiffness and structure was unchanged by WD feeding. Functionally, femoral, but not coronary, arteries exhibited endothelial dysfunction, whereas coronary arteries exhibited increased vasoconstrictor responsiveness not present in femoral arteries. Taken together, our data highlight important regional variations in the development of arterial stiffness and dysfunction associated with WD feeding. Furthermore, our results suggest TGF-β signaling and IEL fenestrae remodeling as potential contributors to femoral artery stiffening in obesity.
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Vitols, A., and M. Vitola. "STIFFNESS AND HEMODYNAMIC RESISTANCE OF ARTERIES AT ESSENTIAL HYPERTENSION." Journal of Hypertension 22, Suppl. 2 (June 2004): S201. http://dx.doi.org/10.1097/00004872-200406002-00698.
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Zhang, Yi, Patrick Lacolley, Athanase D. Protogerou, and Michel E. Safar. "Arterial Stiffness in Hypertension and Function of Large Arteries." American Journal of Hypertension 33, no. 4 (February 15, 2020): 291–96. http://dx.doi.org/10.1093/ajh/hpz193.
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Abstract BACKGROUND Arterial stiffness—typically assessed from non-invasive measurement of pulse wave velocity along a straight portion of the vascular tree between the right common carotid and femoral arteries—is a reliable predictor of cardiovascular risk in patients with essential hypertension. METHODS We reviewed how carotid-femoral pulse wave velocity increases with age and is significantly higher in hypertension (than in age- and gender-matched individuals without hypertension), particularly when hypertension is associated with diabetes mellitus. RESULTS From the elastic aorta to the muscular peripheral arteries of young healthy individuals, there is a gradual but significant increase in stiffness, with a specific gradient. This moderates the transmission of pulsatile pressure towards the periphery, thus protecting the microcirculatory network. The heterogeneity of stiffness between the elastic and muscular arteries causes the gradient to disappear or be inversed with aging, particularly in long-standing hypertension. CONCLUSIONS In hypertension therefore, pulsatile pressure transmission to the microcirculation is augmented, increasing the potential risk of damage to the brain, the heart, and the kidney. Furthermore, elevated pulse pressure exacerbates end-stage renal disease, particularly in older hypertensive individuals. With increasing age, the elastin content of vessel walls declines throughout the arterial network, and arterial stiffening increases further due to the presence of rigid wall material such as collagen, but also fibronectin, proteoglycans, and vascular calcification. Certain genes, mainly related to angiotensin and/or aldosterone, affect this aging process and contribute to the extent of arterial stiffness, which can independently affect both forward and reflected pressure waves.
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Owen, Aaron L., and J. Mikhail Kellawan. "Upstream stiffness, downstream problems: not all arteries are equal." Journal of Physiology 593, no. 20 (October 14, 2015): 4517–18. http://dx.doi.org/10.1113/jp271236.
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Frisbee, Jefferson C. "Reduced nitric oxide bioavailability contributes to skeletal muscle microvessel rarefaction in the metabolic syndrome." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 2 (August 2005): R307—R316. http://dx.doi.org/10.1152/ajpregu.00114.2005.
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This study tested the hypothesis that chronically elevated oxidant stress contributes to impaired active hyperemia in skeletal muscle of obese Zucker rats (OZR) vs. lean Zucker rats (LZR) through progressive deteriorations in microvascular structure. Twelve-week-old LZR and OZR were given 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (tempol) in the drinking water for ∼4 wk. Subsequently, perfusion of in situ gastrocnemius muscle was determined during incremental elevations in metabolic demand, while a contralateral skeletal muscle arteriole and the gastrocnemius muscle was removed to determine dilator reactivity, vessel wall mechanics, and microvessel density. Under control conditions, active hyperemia was impaired at all levels of metabolic demand in OZR, and this was correlated with a reduced microvessel density, increased arteriolar stiffness, and impaired dilator reactivity. Chronic tempol ingestion improved perfusion during moderate to high metabolic demand only and was associated with improved arteriolar reactivity and microvessel density; passive vessel mechanics were unaltered. Combined antioxidant therapy and nitric oxide synthase inhibition in OZR prevented much of the restored perfusion and microvessel density. In LZR, treatment with Nω-nitro-l-arginine methyl ester (l-NAME) hydrochloride and hydralazine (to prevent hypertension) impaired active hyperemia, dilator reactivity, and microvessel density, although arteriolar distensibility was not altered. These results suggest that with the development of the metabolic syndrome, chronic reductions in nitric oxide bioavailability, in part via the scavenging actions of oxidative free radicals, contribute to a loss of skeletal muscle microvessels, leading to impaired muscle perfusion with elevated metabolic demand.
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Gandley, R. E., K. C. Griggs, K. P. Conrad, and M. K. McLaughlin. "Intrinsic tone and passive mechanics of isolated renal arteries from virgin and late-pregnant rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 1 (July 1, 1997): R22—R27. http://dx.doi.org/10.1152/ajpregu.1997.273.1.r22.
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The purpose of this study was to investigate whether there are alterations in the intrinsic properties of renal interlobar arteries during pregnancy. Renal interlobar arteries (internal diameter approximately 250 microns) from virgin and late-pregnant rats were mounted in a pressurized arteriograph system. Intrinsic tone was quantified as the percent difference in luminal diameter of each artery in the presence of physiological saline solution and while pharmacologically relaxed with papaverine. At pressures between 75 and 125 mmHg, tone was 35-50% less in arteries from pregnant rats (P < 0.05). Endothelial removal reduced tone in arteries from virgin rats but had no effect on arteries from pregnant rats. Analysis of stress-strain curves (rate constants: pregnant, 6.31 +/- 0.38; virgin, 7.81 +/- 0.78; P < 0.05) indicate that there is a decrease in arterial stiffness in gestation. Thus pregnancy is associated with a reduced intrinsic tone, possibly because of a reduction in an endothelial constrictor influence on the vascular smooth muscle in isolated rat renal interlobar arteries. This effect, coupled with the decreased arterial stiffness, demonstrates the significant arterial adaptation occurring during pregnancy.
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Ferreira, Isabel, Marieke B. Snijder, Jos W. R. Twisk, Willem van Mechelen, Han C. G. Kemper, Jacob C. Seidell, and Coen D. A. Stehouwer. "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 (June 1, 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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Zarrinkoob, Laleh, Khalid Ambarki, Anders Wåhlin, Richard Birgander, Bo Carlberg, Anders Eklund, and Jan Malm. "Aging alters the dampening of pulsatile blood flow in cerebral arteries." Journal of Cerebral Blood Flow & Metabolism 36, no. 9 (July 20, 2016): 1519–27. http://dx.doi.org/10.1177/0271678x16629486.
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Excessive pulsatile flow caused by aortic stiffness is thought to be a contributing factor for several cerebrovascular diseases. The main purpose of this study was to describe the dampening of the pulsatile flow from the proximal to the distal cerebral arteries, the effect of aging and sex, and its correlation to aortic stiffness. Forty-five healthy elderly (mean age 71 years) and 49 healthy young (mean age 25 years) were included. Phase-contrast magnetic resonance imaging was used for measuring blood flow pulsatility index and dampening factor (proximal artery pulsatility index/distal artery pulsatility index) in 21 cerebral and extra-cerebral arteries. Aortic stiffness was measured as aortic pulse wave velocity. Cerebral arterial pulsatility index increased due to aging and this was more pronounced in distal segments of cerebral arteries. There was no difference in pulsatility index between women and men. Dampening of pulsatility index was observed in all cerebral arteries in both age groups but was significantly higher in young subjects than in elderly. Pulse wave velocity was not correlated with cerebral arterial pulsatility index. The increased pulsatile flow in elderly together with reduced dampening supports the pulse wave encephalopathy theory, since it implies that a higher pulsatile flow is reaching distal arterial segments in older subjects.
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Lacolley, Patrick, Véronique Regnault, Patrick Segers, and Stéphane Laurent. "Vascular Smooth Muscle Cells and Arterial Stiffening: Relevance in Development, Aging, and Disease." Physiological Reviews 97, no. 4 (October 1, 2017): 1555–617. http://dx.doi.org/10.1152/physrev.00003.2017.
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The cushioning function of large arteries encompasses distension during systole and recoil during diastole which transforms pulsatile flow into a steady flow in the microcirculation. Arterial stiffness, the inverse of distensibility, has been implicated in various etiologies of chronic common and monogenic cardiovascular diseases and is a major cause of morbidity and mortality globally. The first components that contribute to arterial stiffening are extracellular matrix (ECM) proteins that support the mechanical load, while the second important components are vascular smooth muscle cells (VSMCs), which not only regulate actomyosin interactions for contraction but mediate also mechanotransduction in cell-ECM homeostasis. Eventually, VSMC plasticity and signaling in both conductance and resistance arteries are highly relevant to the physiology of normal and early vascular aging. This review summarizes current concepts of central pressure and tensile pulsatile circumferential stress as key mechanical determinants of arterial wall remodeling, cell-ECM interactions depending mainly on the architecture of cytoskeletal proteins and focal adhesion, the large/small arteries cross-talk that gives rise to target organ damage, and inflammatory pathways leading to calcification or atherosclerosis. We further speculate on the contribution of cellular stiffness along the arterial tree to vascular wall stiffness. In addition, this review provides the latest advances in the identification of gene variants affecting arterial stiffening. Now that important hemodynamic and molecular mechanisms of arterial stiffness have been elucidated, and the complex interplay between ECM, cells, and sensors identified, further research should study their potential to halt or to reverse the development of arterial stiffness.
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Aguirre, Nicolas, Leandro J. Cymberknop, Edith Grall-Maës, Eugenia Ipar, and Ricardo L. Armentano. "Central Arterial Dynamic Evaluation from Peripheral Blood Pressure Waveforms Using CycleGAN: An In Silico Approach." Sensors 23, no. 3 (February 1, 2023): 1559. http://dx.doi.org/10.3390/s23031559.
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Arterial stiffness is a major condition related to many cardiovascular diseases. Traditional approaches in the assessment of arterial stiffness supported by machine learning techniques are limited to the pulse wave velocity (PWV) estimation based on pressure signals from the peripheral arteries. Nevertheless, arterial stiffness can be assessed based on the pressure–strain relationship by analyzing its hysteresis loop. In this work, the capacity of deep learning models based on generative adversarial networks (GANs) to transfer pressure signals from the peripheral arterial region to pressure and area signals located in the central arterial region is explored. The studied signals are from a public and validated virtual database. Compared to other works in which the assessment of arterial stiffness was performed via PWV, in the present work the pressure–strain hysteresis loop is reconstructed and evaluated in terms of classical machine learning metrics and clinical parameters. Least-square GAN (LSGAN) and Wasserstein GAN with gradient penalty (WGAN-GP) adversarial losses are compared, yielding better results with LSGAN. LSGAN mean ± standard deviation of error for pressure and area pulse waveforms are 0.8 ± 0.4 mmHg and 0.1 ± 0.1 cm2, respectively. Regarding the pressure–strain elastic modulus, it is achieved a mean absolute percentage error of 6.5 ± 5.1%. GAN-based deep learning models can recover the pressure–strain loop of central arteries while observing pressure signals from peripheral arteries.
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De Bruyne, Tess, Bieke Steenput, Lynn Roth, Guido De Meyer, Claudia Santos, Kateřina Valentová, Maija Dambrova, and Nina Hermans. "Dietary Polyphenols Targeting Arterial Stiffness: Interplay of Contributing Mechanisms and Gut Microbiome-Related Metabolism." Nutrients 11, no. 3 (March 8, 2019): 578. http://dx.doi.org/10.3390/nu11030578.
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Increased arterial stiffness is a degenerative vascular process, progressing with age that leads to a reduced capability of arteries to expand and contract in response to pressure changes. This progressive degeneration mainly affects the extracellular matrix of elastic arteries and causes loss of vascular elasticity. Recent studies point to significant interference of dietary polyphenols with mechanisms involved in the pathophysiology and progression of arterial stiffness. This review summarizes data from epidemiological and interventional studies on the effect of polyphenols on vascular stiffness as an illustration of current research and addresses possible etiological factors targeted by polyphenols, including pathways of vascular functionality, oxidative status, inflammation, glycation, and autophagy. Effects can either be inflicted directly by the dietary polyphenols or indirectly by metabolites originated from the host or microbial metabolic processes. The composition of the gut microbiome, therefore, determines the resulting metabolome and, as a consequence, the observed activity. On the other hand, polyphenols also influence the intestinal microbial composition, and therefore the metabolites available for interaction with relevant targets. As such, targeting the gut microbiome is another potential treatment option for arterial stiffness.
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Schutte, Aletta E., Ruan Kruger, Lebo F. Gafane-Matemane, Yolandi Breet, Michél Strauss-Kruger, and J. Kennedy Cruickshank. "Ethnicity and Arterial Stiffness." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 5 (May 2020): 1044–54. http://dx.doi.org/10.1161/atvbaha.120.313133.
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Early vascular aging reflects increased arterial stiffness of central blood vessels at young chronological ages and powerfully predicts cardiovascular events and mortality, independent of routine brachial blood pressure and other risk factors. Since ethnic disparities exist in routine blood pressure, in hypertension and cardiovascular outcomes, this review evaluates major studies comparing arterial stiffness through the life course between different ethnic groups or races (which have no biological definition)—in children, adolescents, young, and middle-aged adults and the very elderly. Most report that compared with white European-origin samples, populations of black African descent have increased central arterial stiffness throughout different life stages, as well as a more rapid increase in arterial stiffness at young ages. Exceptions may include African Caribbean origin people in Europe. Differences in vascular structure and function are clearest, where obesity, socioeconomic, and psychosocial factors are most marked. Few studies evaluate a wider spectrum of ethnic groups or factors contributing to these ethnic disparities. Genetic effects are not obvious; maternal risk and intergenerational studies are scarce. Nevertheless, across all ethnic groups, for given levels of blood pressure and age, some people have stiffer central arteries than others. These individuals are most at risk of vascular events and mortality and, therefore, may benefit from early, as yet untested, preventive action and treatment.
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Rapant, Cvečková, Fajčíková, Hajdúk, Hiller, and Stehlíková. "Hard Water, More Elastic Arteries: A Case Study from Krupina District, Slovakia." International Journal of Environmental Research and Public Health 16, no. 9 (April 29, 2019): 1521. http://dx.doi.org/10.3390/ijerph16091521.
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The protective role of hard drinking water against cardiovascular diseases is well documented by numerous studies. This article describes the impact of Ca and Mg contents in the drinking water with different water hardness on the cardiovascular system (arterial stiffness, arterial age) of residents of the Krupina district, the Slovak Republic. The research was based on the measurements of arterial stiffness, including the measurements of aortic pulse wave velocity (PWVao) and the calculation of the arterial age of the residents. In total, 144 randomly selected residents were included in measurements, divided into the two groups according to Ca and Mg contents in drinking water (water hardness). The first group was supplied with soft drinking water (total dissolved solids (TDS): 200–300 mg·L−1, Ca: 20–25 mg·L−1, Mg: 5–10 mg·L−1). The second group of residents was supplied with harder drinking water (TDS: 500–600 mg·L−1, Ca: 80–90 mg·L−1, Mg: 25–30 mg·L−1). Differences in arterial stiffness between the two groups of respondents were documented. Higher arterial stiffness (low flexibility of arteries) was determined for a group of residents supplied with soft drinking water. This was reflected in higher PWVao levels, higher number of pathological cases (PWVao > 10 m·s−1), and arterial age of respondents compared to their actual age. The “absolute” difference between the arterial and actual age between the two evaluated groups of residents (soft vs. harder water) was nearly 5 years on average. The higher arterial stiffness and age of residents that consumed soft drinking water indicate the health significance of lower contents of Ca and Mg in drinking water as an environmental risk factor of cardiovascular diseases. Measuring arterial stiffness of residents in the areas supplied with soft drinking water can be used as a non-invasive approach in the prevention of cardiovascular risks.
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Léránt, Brigitta, Christina Straesser, Réka Katalin Kovács, László Oláh, László Kardos, and László Csiba. "Morphological, hemodynamic and stiffness changes in arteries of young smokers." Perspectives in Medicine 1, no. 1-12 (September 2012): 152–55. http://dx.doi.org/10.1016/j.permed.2012.02.061.
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Liu, Yanan, Mengke Li, Xue Lv, Kaiwen Bao, Xiao Yu Tian, Lei He, Lei Shi, Yi Zhu, and Ding Ai. "Yes-Associated Protein Targets the Transforming Growth Factor β Pathway to Mediate High-Fat/High-Sucrose Diet-induced Arterial Stiffness." Circulation Research 130, no. 6 (March 18, 2022): 851–67. http://dx.doi.org/10.1161/circresaha.121.320464.
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Background: Metabolic syndrome is related to cardiovascular diseases, which is attributed in part, to arterial stiffness; however, the mechanisms remain unclear. The present study aimed to investigate the molecular mechanisms of metabolic syndrome–induced arterial stiffness and to identify new therapeutic targets. Methods: Arterial stiffness was induced by high-fat/high-sucrose diet in mice, which was quantified by Doppler ultrasound. Four-dimensional label-free quantitative proteomic analysis, affinity purification and mass spectrometry, and immunoprecipitation and GST (glutathione S-transferase) pull-down experiments were performed to explore the mechanism of YAP (Yes-associated protein)-mediated TGF (transforming growth factor) β pathway activation. Results: YAP protein was upregulated in the aortic tunica media of mice fed a high-fat/high-sucrose diet for 2 weeks and precedes arterial stiffness. Smooth muscle cell–specific YAP knockdown attenuated high-fat/high-sucrose diet–induced arterial stiffness and activation of TGFβ-Smad2/3 signaling pathway in arteries. By contrast, Myh11Cre ERT2 -Yap Tg mice exhibited exacerbated high-fat/high-sucrose diet–induced arterial stiffness and enhanced TGFβ-activated Smad2/3 phosphorylation in arteries. PPM1B (protein phosphatase, Mg 2+ /Mn 2+ -dependent 1B) was identified as a YAP-bound phosphatase that translocates into the nucleus to dephosphorylate Smads (mothers against decapentaplegic homologs) in response to TGFβ. This process was inhibited by YAP through removal of the K63-linked ubiquitin chain of PPM1B at K326. Conclusions: This study provides a new mechanism by which smooth muscle cell YAP regulates the TGFβ pathway and a potential therapeutic target in metabolic syndrome–associated arterial stiffness.
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Snijder, M. B., A. Flyvbjerg, C. D. A. Stehouwer, J. Frystyk, R. M. A. Henry, J. C. Seidell, R. J. Heine, and J. M. Dekker. "Relationship of adiposity with arterial stiffness as mediated by adiponectin in older men and women: the Hoorn Study." European Journal of Endocrinology 160, no. 3 (March 2009): 387–95. http://dx.doi.org/10.1530/eje-08-0817.
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ObjectiveTo investigate whether adiponectin is associated with arterial stiffness, and whether adiponectin explains the association between body composition and arterial stiffness.DesignCross-sectional cohort study.MethodsSubjects were participants (n=456, mean age 68.9±6.1 years; age range 60–86 years) of the third follow-up examination of the Hoorn Study. Trunk fat, leg fat, trunk lean, and leg lean mass were measured by dual-energy X-ray absorptiometry. Ultrasound was used to measure distensibility and compliance of the carotid, femoral, and brachial arteries, and carotid Young's elastic modulus (as estimates of peripheral arterial stiffness).ResultsTrunk fat mass was negatively associated with (ln-transformed) adiponectin (standardizedβ=−0.49,P<0.001), while leg fat mass was positively associated with adiponectin (β=0.44,P<0.001), after adjustment for each other, age, and lean mass. After adjustment for age, sex, mean arterial pressure, and estimated glomerular filtration rate, higher adiponectin was associated with decreased peripheral arterial stiffness (βof meanZ-scores of all three arteries=0.14,P=0.001). However, the associations of trunk fat (β=−0.26,P<0.001) and leg fat (β=0.16,P=0.006) with peripheral arterial stiffness were only minimally explained by adiponectin levels.ConclusionTrunk fat and leg fat are oppositely associated with adiponectin. Although low adiponectin was a determinant of increased peripheral arterial stiffness, it only explained a small part of the association between body fat and peripheral arterial stiffness. This indicated that factors other than adiponectin may be more important in the pathophysiological mechanisms by which abdominal obesity leads to arterial stiffness.
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Christensen, T., and B. Neubauer. "Increased Arterial Wall Stiffness and Thickness in Medium-Sized Arteries in Patients with Insulin-Dependent Diabetes Mellitus." Acta Radiologica 29, no. 3 (May 1988): 299–302. http://dx.doi.org/10.1177/028418518802900308.
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By means of ultrasonography, arterial wall stiffness, arterial wall thickness, and the elastic modulus of the common femoral artery were estimated in a group of 19 young insulin-dependent diabetics. The ultrasound technique for determination of these parameters is described as well as the echo-anatomy of the arterial wall. In accordance with a previous investigation a significant rise in arterial wall stiffness was found. Furthermore, there was a highly significant correlation between the stiffness and the thickness of the arterial wall. The elastic modulus also correlated to the stiffness. It is concluded that the diabetic macroangiopathy is characterized by an increased stiffness of the arterial wall caused by increased thickness as well as by progressive alterations of the elastic characteristics of the wall tissue. Possible pathogenetic reasons are discussed.
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Dodson, R. Blair, Matthew R. Morgan, Csaba Galambos, Kendall S. Hunter, and Steven H. Abman. "Chronic intrauterine pulmonary hypertension increases main pulmonary artery stiffness and adventitial remodeling in fetal sheep." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 11 (December 1, 2014): L822—L828. http://dx.doi.org/10.1152/ajplung.00256.2014.
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Persistent pulmonary hypertension of the newborn (PPHN) is a clinical syndrome that is characterized by high pulmonary vascular resistance due to changes in lung vascular growth, structure, and tone. PPHN has been primarily considered as a disease of the small pulmonary arteries (PA), but proximal vascular stiffness has been shown to be an important predictor of morbidity and mortality in other diseases associated with pulmonary hypertension (PH). The objective of this study is to characterize main PA (MPA) stiffness in experimental PPHN and to determine the relationship of altered biomechanics of the MPA with changes in extracellular matrix (ECM) content and orientation of collagen and elastin fibers. MPAs were isolated from control and PPHN fetal sheep model and were tested by planar biaxial testing to measure stiffness in circumferential and axial vessel orientations. Test specimens were fixed for histological assessments of the vascular wall ECM constituents collagen and elastin. MPAs from PPHN sheep had increased mechanical stiffness ( P < 0.05) and altered ECM remodeling compared with control MPA. A constitutive mathematical model and histology demonstrated that PPHN vessels have a smaller contribution of elastin and a greater role for collagen fiber engagement compared with the control arteries. We conclude that exposure to chronic hemodynamic stress in late-gestation fetal sheep increases proximal PA stiffness and alters ECM remodeling. We speculate that proximal PA stiffness further contributes to increased right ventricular impedance in experimental PPHN, which contributes to abnormal transition of the pulmonary circulation at birth.
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Sementsova, N. A., A. I. Chesnikova, V. A. Safronenko, and N. S. Skarzhinskaya. "Arterial stiffness in hypertensive patients with peripheral artery disease." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 28, no. 4 (July 7, 2022): 386–95. http://dx.doi.org/10.18705/1607-419x-2022-28-4-386-395.
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Objective. To identify features of arterial stiffness, to establish relationships with indicators of the daily blood pressure profile and peripheral artery disease in patients with hypertension (HTN) in combination with subclinical and manifested atherosclerotic lesions of the arteries of the lower extremities. Design and methods. 120 patients were divided into 3 groups: group 1-46 patients with HTN and clinically manifested AALE, group 2-39 patients with HTN and asymptomatic AALE, group 3-35 HTN patients without AALE. All patients underwent general clinical laboratory and instrumental research methods, including 24-hour blood pressure ambulatory monitoring (24h-ABPM) with the assessment of 24-hour blood pressure profile and arterial stiffness parameters, ultrasonic triplex scanning (USTS) of the arteries of the lower extremities. Statistical data processing was carried out using Microsoft Office Excel 16 (2015, Microsoft, USA), Statistica 10.0 (StatSoft, USA), IBM SPSS Statistica 26.0 (IBM, USA). Results. Higher values of pulse wave velocity (PWVao), augmentation index (AIx) and ambulatory arterial stiffness index (AASI) were found in the 1st group in comparison to the 2nd and 3rd groups (p < 0,05). Lower reflected wave transit time (RWTT) (119,5 [112;127] ms) was found in the 1st group (128 [122;132], p = 0,001 and 126 [121;129] ms, p = 0,03 in the 2nd and and 3rd groups, respectively) groups. The maximum rate of blood pressure increase (dP/dtmax) in patients of the 1st (550 [466;666] mm Hg/s) and 2nd (634 [511;695] mm Hg/s) groups was significantly lower than in patients of the 3rd group (655 [526;806] mm Hg/s, p < 0,05). A direct correlation was found between AASI values and SBP (r = 0,291, p = 0,049) and its variability (r = 0,301, p = 0,042), AASI and PBP (r = 0,518, p < 0,001), its variability (r = 0,596, r < 0,001) in group 1, as well as AASI and PBP (r = 0,514, p < 0,001) and PBP variability (r = 0,632, p < 0,001) in group 2. A correlation between AIx and the degree of stenosis (%) of the arteries of the lower extremities was found in patients with AH and AALE of varying severity (r = 0,310, p = 0,004). Conclusions. In patients with subclinical course of AALE, lower values of dP/dtmax in comparison with HTN patients without AALE indicate an increase in arterial stiffness at the initial stages of peripheral atherosclerosis. Clinically manifested atherosclerotic lesions of the arteries of the lower extremities in HTN patients are associated with a more pronounced increase in arterial stiffness, which contributes to a higher cardiovascular risk.
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Ku, David N., Marvin N. Zeigler, and J. Micah Downing. "One-Dimensional Steady Inviscid Flow Through a Stenotic Collapsible Tube." Journal of Biomechanical Engineering 112, no. 4 (November 1, 1990): 444–50. http://dx.doi.org/10.1115/1.2891209.
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A one-dimensional inviscid solution for flow through a compliant tube with a stenosis is presented. The model is used to represent an artery with an atherosclerotic plaque and to investigate a range of conditions for which arterial collapse may occur. The coupled equations for flow through collapsible tubes are solved using a Runge-Kutta finite difference scheme. Quantitative results are given for specific physiological parameters including inlet and outlet pressure, flow rate, stenosis size, length and stiffness. The results suggest that high-grade stenotic arteries may exhibit collapse with typical physiological pressures. Critical stenoses may cause choking of flow at the throat followed by a transition to supercritical flow with tube collapse downstream. Greater amounts of stenosis produced a linear reduction of flow rate and a shortening of the collapsed region. Changes in stenosis length created proportional changes in the length of collapse. Increasing the stiffness of the stenosis to a value greater than the nominal tube stiffness caused a greater amount of flow limitation and more negative pressures, compared to a stenosis with constant stiffness. These findings assist in understanding the clinical consequences of flow through atherosclerotic arteries.
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Panfilova, Viktoriya Nikolaevna, A. Ya Panfilov, S. N. Doroshchenko, and T. E. Taranushenko. "Ultrasonographic study of common carotid arteries in adolescents with type 1 diabetes mellitus." Diabetes mellitus 12, no. 1 (March 15, 2009): 36–38. http://dx.doi.org/10.14341/2072-0351-5419.
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Aim. To elucidate sonographic characteristics of common carotid arteries in adolescents with type1 diabetes mellitus (DM1) depending on the duration of the disease and thepresence of chronic complications. Materials and methods. A total of 56 adolescents having DM1 of different duration were examined to evaluate conditions of common carotid arteries (CA) in the systole anddiastole during at least 3 cardiac cycles. The following parameters were measured: CA diameter, intima-media thickness (IMT), estimated stretch and stiffness coefficients, Youngsmodulus. The control group comprised 16 healthy adolescents. Results. Bilateral increase of IMT was recorded in patients with DM duration over 5 years. Youngs modulus, stretch and stiffness coefficients were virtually unrelated to diseaseduration. In patients having DM for more than 10 years, stretch coefficient was 5.38 (95% DI 4.82-5.8) compared with 5.82 (95% DI 5.63-7.38) in those with DM for less than 3years (p = 0.04). The level of albuminuria correlated with IMT (r=0.32, p=0.03), stiffness coefficient (r = 0.43, p=0.001), stretch coefficient (r= -0.48, p
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Kondiboyina, Avinash, Joseph J. Smolich, Michael M. H. Cheung, Berend E. Westerhof, and Jonathan P. Mynard. "Conduit arterial wave reflection promotes pressure transmission but impedes hydraulic energy transmission to the microvasculature." American Journal of Physiology-Heart and Circulatory Physiology 319, no. 1 (July 1, 2020): H66—H75. http://dx.doi.org/10.1152/ajpheart.00733.2019.
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With aging, a reduction in the stiffness gradient between elastic and muscular arteries is thought to reduce wave reflection in conduit arteries, leading to increased pulsatile pressure transmission into the microvasculature. This assumes that wave reflection limits pressure transmission in arteries. However, using a computational model, we showed that wave reflection promotes pulsatile pressure transmission, although it does limit hydraulic energy transmission. Increased microvascular pulse pressure with aging is instead related to decreasing arterial compliance.
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Åström Malm, Ida, Rachel De Basso, Peter Blomstrand, and Dick Wågsäter. "Association of IL-10 and CRP with Pulse Wave Velocity in Patients with Abdominal Aortic Aneurysm." Journal of Clinical Medicine 11, no. 5 (February 23, 2022): 1182. http://dx.doi.org/10.3390/jcm11051182.
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Background: Markers of inflammation and arterial stiffness are predictors of cardiovascular morbidity and events, but their roles in the mechanisms and progression of abdominal aortic aneurysm (AAA) in males have not been fully investigated. This study explored possible associations between inflammatory marker levels and arterial stiffness in males with AAA. Methods: A total of 270 males (191 AAA and 79 controls) were included in the study. Arterial stiffness was assessed using non-invasive applanation tonometry to measure the regional pulse wave velocity between the carotid and femoral arteries and the carotid and radial arteries. Blood samples were obtained, and interleukin-10 (IL-10) and CRP levels were analysed. Results: Subjects with an AAA had higher levels of IL-10 (21.5 ± 14.0 ng/mL versus 16.6 ± 9.3 ng/mL) compared to controls (p = 0.007). In the AAA cohort, subjects with T2DM showed higher levels of IL-10 (26.4 ± 17.3 versus 20.4 ± 13.0, p = 0.036). We observed a positive correlation between PWVcf and CRP in the control group (r = 0.332) but not the AAA group. PWVcf and CRP were negatively correlated (r = 0.571) in the T2DM subjects treated with metformin in the AAA group. Conclusion: Arterial stiffness is related to the degree of inflammation reflected by CRP and IL-10 levels in males with an AAA. IL-10 is negatively correlated with arterial stiffness in these subjects. This finding suggests that IL-10 may decrease arterial stiffness in males with AAA. The negative correlation between CRP and PWVcf in males with T2DM treated with metformin may indicate that metformin influences the arterial wall to decrease stiffness in subjects with AAA.
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Okada, Yoshiyuki, Shigeki Shibata, Naoki Fujimoto, Stuart A. Best, Benjamin D. Levine, and Qi Fu. "Long-term effects of a renin inhibitor versus a thiazide diuretic on arterial stiffness and left ventricular diastolic function in elderly hypertensive patients." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 313, no. 4 (October 1, 2017): R400—R409. http://dx.doi.org/10.1152/ajpregu.00125.2017.
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Arterial stiffness and cardiac function are important predictors of cardiovascular events in patients with hypertension, even with adequate blood pressure (BP) control. We evaluated whether a direct renin inhibitor, aliskiren, reduces arterial stiffness and modulates left ventricular function compared with a diuretic, hydrochlorothiazide, in elderly hypertensive patients. Twenty-one hypertensive patients [67 ± 14 (SD) yr] were randomly assigned to receive 6-mo aliskiren ( n = 11) or hydrochlorothiazide ( n = 10)-based therapy. We assessed β-stiffness of the local arteries, arterial elastance ( Ea), and echocardiographic variables, including early ( E) and late ( A) mitral inflow velocity, deceleration time of E, early ( E′) and late ( A′) diastolic mitral annular velocity, and left ventricular end-systolic elastance ( Ees) before and after treatment. BP decreased similarly ( P < 0.001) after both therapies. β-Stiffness of the carotid artery decreased after aliskiren but increased after hydrochlorothiazide treatment (aliskiren: 6.42 ± 2.34 pre vs. 5.07 ± 1.29 post; hydrochlorothiazide: 5.05 ± 1.78 vs. 7.25 ± 2.68, P = 0.001 for interaction). β-Stiffness of the femoral and radial arteries were not different after either treatment. Different from aliskiren, E decreased (73 ± 16 vs. 67 ± 14 cm/s, P = 0.026), and the deceleration time was prolonged (218 ± 40 vs. 236 ± 35 ms, P = 0.032) after hydrochlorothiazide therapy, whereas the E/ A, and E′ remained unchanged after both treatments. Ea and Ees decreased after aliskiren therapy (both P < 0.05), whereas the Ea/ Ees (ventricular-arterial coupling) was maintained after both treatments. Thus, aliskiren decreased the stiffness of carotid artery and left ventricular end-systolic elastance with maintenance of ventricular-arterial coupling without any effects on diastolic filling, while hydrochlorothiazide increased carotid arterial stiffness and slowed early diastolic filling in elderly hypertensive patients.
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Chang, Stephen KY, Joel WL Lau, and Chee Kong Chui. "Changes in Mechanical, Structural Integrity and Microbiological Properties Following Cryopreservation of Human Cadaveric Iliac Arteries." Annals of the Academy of Medicine, Singapore 43, no. 10 (October 15, 2014): 492–98. http://dx.doi.org/10.47102/annals-acadmedsg.v43n10p492.
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Introduction: The study seeks to investigate how the duration of storage of cryopreserved human cadaveric iliac arteries impacts their mechanical, structural and microbiological properties as compared to their fresh sample. Materials and Methods: Iliac arteries were harvested from 12 human cadavers and divided into 2 groups. One group underwent mechanical stress-strain assessment immediately and another was cryopreserved for a pre-determined time-period (range, 29 to 364 days). Mechanical functionality was assessed with a customised clamping mechanism. The arteries’ microbiological properties were studied pre- and post-cryopreservation. The post-thawed arteries were also assessed histologically for structural integrity. Results: Of the 12 pairs, only 7 (58, 119, 150, 252, 300, 332 and 364 days) iliac arteries were included in the final analysis. The other 5 pairs (29, 90, 188, 205 and 270 days) had abundant local calcification and their stress-strain curves could not be characterised. From the curves, pre- and post-cryopreserved arteries had the most similar mechanical properties when stored for 119 days. A trend of increasing relative stiffness with increased duration of storage was noted. The post-thawed arteries demonstrated minimal fragmentation except in atherosclerotic areas. Majority of the arteries were not contaminated by bacterial or fungal infection pre- and post-cryopreservation. Also, 2 arteries (364 and 332 days) which had initial bacterial colonisation showed no bacterial growth on their post-thawed sample. Conclusion: Mechanically, non-atherosclerotic cryopreserved arteries can be a good substitute to their corresponding fresh arterial graft. However, the length of cryopreservation has an effect on the relative stiffness of the pre- and post-cryopreserved arteries. Histological and microbiological findings suggest that cryopreservation have little impact on an artery structural integrity and may possibly have a role in maintaining sterility and sterilising the arteries. Key words: Arterial allograft, Human arteries, Stress-strain curves, Vascular cryopreservation