Relevant bibliographies by topics / Stiffness arteriosa

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Stiffness arteriosa'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Stiffness arteriosa"

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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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Dissertations / Theses on the topic "Stiffness arteriosa"

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Rastelli, Stefania. "Struttura e funzione arteriosa nelle malattie infiammatorie croniche intestinali." Doctoral thesis, Università di Catania, 2015. http://hdl.handle.net/10761/4023.

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Le malattie infiammatorie croniche intestinali (IBD) sono associate ad un aumentato rischio cardiovascolare non completamente spiegabile con la prevalenza dei fattori di rischio cardiovascolare tradizionali. L'infiammazione e l'aumento della rigidità arteriosa ad essa correlata potrebbero avere un ruolo importante nella valutazione del rischio cardiovascolare di questi soggetti. In questa tesi ho studiato la correlazione tra infiammazione e rigidità arteriosa nelle IBD. Per la prima volta ho riportato che i soggetti con IBD hanno un'aumentata rigidità arteriosa che può essere normalizzata dall'uso di farmaci anti TNF-alfa.
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BIANCHI, FRANCESCA CARLA MARIA. "Effetti della terapia antiretrovirale sulla struttura e funzionalità arteriosa in una popolazione affetta da HIV." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/83623.

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L’introduzione dalla terapia antiretrovirale (ART ) ha determinato una notevole riduzione della morbidità e mortalità nei pazienti HIV positivi. È però stato evidenziato un aumento degli eventi cardiovascolari in questi soggetti. Scopo del nostro studio è stato valutare l’effetto su parametri arteriosi di due differenti protocolli di terapia antiretrovirale su soggetti HIV positivi naive ovvero mai sottoposti precedentemente a terapia antiretrovirale. Abbiamo studiato 40 pazienti HIV positivi naive prima (tempo 0) e dopo 6 mesi (tempo 1) durante i quali i pazienti, suddivisi in 2 gruppi, sono stati sottoposti a 2 differenti protocolli di terapia antiretrovirale. I pazienti del gruppo A (19 soggetti) sono stati sottoposti a terapia con 2 Inibitori nucleosidici della trascrittasi inversa -NRTI+ 1 Inibitori non nucleosidici della trascrittasi inversa -NNRTI. I pazienti del gruppo B (21 soggetti) ) sono stati invece sottoposti a terapia con 2 Inibitori nucleosidici della trascrittasi inversa -NRTI+ 1 Inibitore delle Proteasi-PI. Utilizzando la metodica di echotracking con Esaote Gold 60® abbiamo analizzato la distensibilità carotidea (Dist), lo spessore miointimale e la funzione endoteliale mediante la Flow Mediated Dilation (FMD); grazie al Complior System® abbiamo invece valutato la Pulse Wave Velocity (PWV). I due gruppi (A e B) erano sovrapponibili per età (38.2 ± 9.4 vs 40.2± 9.1 anni); sesso (femmine 15.7% vs 19%) , pressione arteriosa, BMI, conta dei CD4 e titolo HIV-RNA, glicemia e profilo lipidico. Alla prima valutazione (tempo 0) i parametri da noi analizzati sulla struttura e funzionalità arteriosa (Distensibilità carotidea, spessore miointimale, PWV e FMD) presentavano valori di normalità in entrambi i gruppi. Alla seconda valutazione (tempo1) come ci si aspettava abbiamo osservato un incremento dei CD4 e una diminuzione del titolo HIV-RNA; abbiamo inoltre osservato un incremento dei valori di colesterolemia totale, LDL e HDL in entrambi i gruppi mentre i parametri arteriosi non hanno subito modificazioni statisticamente significative sia per quanto riguarda i 2 differenti gruppi sia per quanto concerne le misurazioni effettuate all’interno dello stesso gruppo prima di iniziare la terapia antiretrovirale e dopo 6 mesi di terapia. Durante il periodo osservazionale di 6 mesi i due protocolli antiretrovirali messi a confronto e in particolare l’NNRTI e PI non sembrano modificare i parametri utilizzati per la valutazione della struttura e la funzionalità arteriosa. È possibile che occorra un periodo più lungo perché si determinino tali alterazioni.
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Vedam, Hima. "Short-term hypoxia and arterial stiffness." Thesis, The University of Sydney, 2007. https://hdl.handle.net/2123/28093.

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The studies in this thesis assess the ventilatory and vascular effects of short-term awake isocapnic hypoxia in healthy subjects and those with obstructive sleep apnoea (OSA). The particular focus of this thesis is the impact of the hypoxic stimulus on indices of arterial stiffness, in particular the augmentation index (AIx) and time to reflection (Tr). The role of nitric oxide in this response in healthy subjects is also examined.
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Butlin, Mark Graduate School of Biomedical Engineering Faculty of Engineering UNSW. "Structural and functional effects on large artery stiffness: an in-vivo experimental investigation." Awarded by:University of New South Wales. Graduate School of Biomedical Engineering, 2007. http://handle.unsw.edu.au/1959.4/29479.

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Large artery stiffness is predictive of adverse cardiovascular events and all cause mortality. Artery structure and function are determinants of artery stiffness. This thesis presents a series of in-vivo experimental studies of effect of structural and functional changes on large artery stiffness. Improved analysis methods were developed for measurement of arterial stiffness indexes, Pulse Wave Velocity (PWV) and pressure wave re ection. These were applied in studies of acute in ammation, active and passive changes in systemic pressures, aortic elastic laminae defects, and aortic calcification in rats using a novel, high fidelity, dual pressure sensing technique of measuring aortic rat PWV. Findings indicated that acute in ammation does not increase large artery stiffness, and that localised effects altering arterial structure do not manifest in in-vivo changes in large artery stiffness. The functional component of stiffness was investigated using graded systemic infusion of vasoconstrictor agents (angiotensin-II, noradrenaline, and Endothelin-1 (ET-1)) in the in-vivo ovine iliac artery. There was a markedly greater dose dependency of pressure independent change in PWV (angiotensin-II) compared to direct endothelial effects (ET-1), although blocking of ET-1 receptors produced marked changes in iliac blood ow. A similar experiment in the human iliac artery found that the B-antagonist and nitric oxide (NO) donor, x Structural and functional effects on large artery stiffness nebivolol, potentially causes a decrease in regional functional stiffness. An additional study in human subjects directly measured the decrease in forearm arterial stiffness during reactive hyperaemia following different periods of ischaemia. The findings precluded the use of this method in measuring brachial artery structural stiffness with maximal smooth muscle relaxation. Increasing periods of ischaemia had a bi-phasic relationship with changes in arterial stiffness, the first phase linked to endogenous nitric oxide release. This finding is of importance in the clinical quantification of endothelial dysfunction. These findings in basic research of arterial haemodynamics provide new quantitative contributions to the in-vivo experimental investigation of the aetiology of large artery stiffness related to structure and function of endothelial and medial wall properties. This can lead to potential clinical applications and techniques for assessment of cardiovascular risk.
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Berry, Karen L. (Karen Louise) 1972. "The structural basis of arterial stiffness and its relationship to cardiovascular outcome." Monash University, Dept. of Medicine, 2003. http://arrow.monash.edu.au/hdl/1959.1/7919.

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Walton, Lucy Anne. "From molecules to tissues : characterising the relationship between structure and function in ageing arteries." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/from-molecules-to-tissues-characterising-the-relationship-between-structure-and-function-in-ageing-arteries(b06aab9a-6845-41d2-ac97-0aac85e71e1a).html.

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Increased arterial stiffness is a predictor of cardiovascular events and mortality across a diverse range of populations. Although gross-mechanical stiffness can be measured in vivo, in order to understand the pathological mechanisms it will be necessary to identify which local micro-structural remodelling events are the prime drivers of altered macro-mechanical function. However, characterisation of arterial structure by conventional histological approaches: i) commonly induces artefacts as a consequence of the sectioning process, ii) provides no insight into the three dimensional structure of the tissue and iii) is performed on unpressurised tissue. This project has set out to address these limitations by developing new micro computed x-ray tomography (micro-CT) methodologies which are capable of visualising the three dimensional structure of rat arteries. This new methodology was then been applied in combination with gross-and micro-mechanical testing and atomic force microscopy imaging to characterise the effects of both intra-luminal pressure and age on arterial structure and function. From these investigations it was clear that micro-CT could readily distinguish discrete tissue sub-structures in paraffin embedded tissues, including skin and arteries and that this imaging approach was compatible with complimentary histological and immunohistochemical analyses. Characterisation of the structure and mechanical function of carotid arteries in aged rats demonstrated localised stiffening in the adventitial layer and a change in the molecular structure of adventitial collagen. The effects of intra-luminal pressure on structure using micro-CT revealed changes in artery cross-sectional area, which suggest the artery wall may be compressible. Investigations into the effects of pressure on the molecular structure of adventitial collagen revealed an increase in periodicity at mean pressure. These findings together demonstrate that the adventitial layer has an important role in the development of arterial stiffness. Micro-CT can reveal novel information that improves our understating of artery structure and how artery structure changes during ageing.
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Xie, Bingjiao, and 謝冰姣. "Association of arterial stiffness and blood pressure variability with silent brain lesions in healthy hypertensive elderly Chinese." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2015. http://hdl.handle.net/10722/212629.

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Kölegård, Roger. "Distensibility in Arteries, Arterioles and Veins in Humans : Adaptation to Intermittent or Prolonged Change in Regional Intravascular Pressure." Doctoral thesis, KTH, Omgivningsfysiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-25965.

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The present series of in vivo experiments in healthy subjects, were performed to investigate wall stiffness in peripheral vessels and how this modality adapts to iterative increments or sustained reductions in local intravascular pressures. Vascular stiffness was measured as changes in arterial and venous diameters, and in arterial flow, during graded increments in distending pressures in the vasculature of an arm or a lower leg. In addition, effects of intravascular pressure elevation on flow characteristics in veins, and on limb pain were elucidated. Arteries and veins were stiffer (i.e. pressure distension was less) in the lower leg than in the arm. The pressure-induced increase in arterial flow was substantially greater in the arm than in the lower leg, indicating a greater stiffness in the arterioles of the lower leg. Prolonged reduction of intravascular pressures in the lower body, induced by 5 wks of sustained horizontal bedrest (BR), decreased stiffness in the leg vasculature. BR increased pressure distension in the tibial artery threefold and in the tibial vein by 86 %. The pressure-induced increase in tibial artery flow was greater post bedrest, indicating reduced stiffness in the arterioles of the lower leg. Intermittent increases of intravascular pressures in one arm (pressure training; PT) during a 5-wk period decreased vascular stiffness. Pressure distension and pressure-induced flow in the brachial artery were reduced by about 50 % by PT. PT reduced pressure distension in arm veins by 30 to 50 %. High intravascular pressures changed venous flow to arterial-like pulsatile patterns, reflecting propagation of pulse waves from the arteries to the veins either via the capillary network or through arteriovenous anastomoses. High vascular pressures induced pain, which was aggravated by BR and attenuated by PT; the results suggest that the pain was predominantly caused by vascular overdistension. In conclusion, vascular wall stiffness constitutes a plastic modality that adapts to meet demands imposed by a change in the prevailing local intravascular pressure. That increased intravascular pressure leads to increased arteriolar wall stiffness supports the notion that local pressure load may serve as a “prime mover” in the development of vascular changes in hypertension.
medicine doktorsexamen QC 20101109
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Chen, Hay-son Robin, and 陳羲舜. "Left ventricular contractile reserve and stiffness of the neoaorta after arterial switch operation for complete transposition of thegreat arteries: a stress echocardiographystudy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48333578.

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Adamopoulos, Dionysios. "Environmental determinants of arterial stiffness and wave reflection: pathophysiological mechanisms and clinical implications." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209744.

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Introduction – Objectives. The cardiovascular system is in direct and constant interaction with its environment. Exposure to various environmental parameters, such as low temperature, air pollution and tobacco smoke, has been strongly associated with serious or even fatal cardiovascular outcomes. Arterial stiffening and greater wave reflection are age-related vascular modifications that lead to an increased risk of cardiovascular events. The aim of this work was to explore the relationship between selected environmental factors and arterial elastic properties in an effort to elucidate the underlying mechanisms that link these factors to increased cardiovascular mortality.

Study 1: Effects of cold exposure on central and peripheral vascular tone. Our first study explored the effects of cold exposure on aortic stiffness and peripheral microvascular tone. We observed that cold exposure, in addition to its chronotropic effects, provoked an increase in aortic stiffness, as assessed by aortic pulse wave velocity, as well as significant vasoconstriction of peripheral arterioles in the microcirculation. Moreover, we explored the magnitude of this effect in a different population (Black subjects of African origin), which is traditionally characterized by exaggerated reactions to adrenergic stimuli. We noted that the vascular reactions, in terms of both aortic stiffness and microvascular vasoconstriction, were more profound in Black Africans than in age-matched Caucasian-Whites. These results argue for a direct effect of cold exposure on arterial stiffness and peripheral vascular tone, probably through activation of the orthosympathetic system.

Study 2: Exposure to ambient particulate matter and arterial stiffness. We explored the effects of acute exposure to outdoor particulate matter on aortic stiffness and aortic wave reflection. We studied the relationship between central hemodynamic parameters and ambient concentration of particulate matter in a population of patients who attended the Hypertension Clinics of Athens University. After statistical correction for a number of potential confounders, we did not observe an association between ambient concentrations of particulate matter and aortic stiffness. However, in men, particulate matter concentration was related to the amplitude of the reflected wave reaching the aorta from the periphery. These results suggest a direct acute interaction between particulate matter concentration and vascular tone, leading to an enhanced arterial wave reflection.

Study 3: The role of nicotine on the vascular effects of environmental tobacco smoke. Environmental tobacco smoke is considered as the most important source of particulate matter in the indoor environment. We recently demonstrated that exposure to tobacco smoke augmented wave reflection, an effect that was not seen after equivalent exposure to the smoke of non-tobacco, herbal cigarettes. We also noticed that the increased wave reflection was proportional to the plasma concentrations of nicotine. However, a direct causal effect between nicotine, arterial wave reflection and aortic stiffness has never been clearly demonstrated. We observed that increasing nicotine plasma concentration to levels comparable to those seen after extensive exposure to environmental tobacco smoke, provoked an increase in both aortic stiffness and arterial wave reflection after correction for heart rate and blood pressure changes. These results confirm the significant participation of nicotine in the vascular effects of passive smoking.

Conclusions. Globally, our results reveal the deleterious effects of cold, particulate matter exposure, and nicotinic stimulation on arterial stiffness, peripheral microcirculation and aortic wave reflection. The hemodynamic modifications associated with these effects may at least partially explain the causal relation between cold exposure, ambient air pollution and cardiovascular mortality.

Introduction-Objectifs. Le système cardiovasculaire est en relation directe et constante avec l’environnement. L’exposition au froid, la pollution atmosphérique et le tabagisme passif sont associés à des événements cardiovasculaires aigus graves et même fatals. La rigidification des artères et l’intensification de la réflexion de l’onde de pouls au niveau de l’aorte accompagnent le vieillissement et prédisent un risque cardiovasculaire accru. Nous avons testés l’hypothèse que les effets cardiovasculaires délétères des facteurs environnementaux comportent une altération des propriétés élastiques artérielles. Ceci pourrait être un des mécanismes physiopathologiques qui lie la mortalité cardiovasculaire aux variables environnementales.

Étude 1 :Exposition au froid ;effets centraux et périphériques. Notre première étude portait sur l’effet de l’exposition au froid sur la rigidité aortique et le tonus vasculaire des artérioles périphériques. Nous avons démontré que l’exposition au froid, hormis ses effets chronotropes, provoquait une augmentation de la rigidité artérielle – mesuré par la vitesse de l’onde de pouls au niveau de l’aorte - ainsi qu’une vasoconstriction importante au niveau des artérioles de la microcirculation. Nous avons ensuite déterminé l’amplitude de cet effet dans une autre population (sujets Africains-Noirs) qui se caractérise par des réactions plus prononcées aux différentes stimulations adrénergiques. Nous avons observé que les réactions vasculaires, tant au niveau de la rigidité aortique qu’au niveau de la microcirculation, étaient plus marquées chez les Africains-Noirs que chez les Caucasiens. Ces résultats révèlent un effet délétère de l’exposition au froid sur la rigidité aortique et le tonus vasculaire des artères périphériques, probablement via une activation du système orthosympathique.

Étude 2 :Exposition aux microparticules atmosphériques et rigidité artérielle. Nous avons ensuite investigué les effets de la pollution atmosphérique sur la rigidité artérielle et la réflexion de l’onde de pouls vers l’aorte. Nous avons étudié la relation entre les paramètres hémodynamiques centraux et la concentration atmosphérique de microparticules dans une population de patients qui ont consulté la Clinique Universitaire d’Hypertension Artérielle d’Athènes. Après correction statistique pour les facteurs confondants, nous n’avons pas observé de corrélation entre la rigidité artérielle et le taux de microparticules atmosphériques dans l’ensemble de la population investiguée. Par contre, si on restreint l’analyse aux résultats obtenus chez les sujets masculins, on s’aperçoit que la concentration atmosphérique de microparticules était associée de façon significative avec l’amplitude de l’onde réfléchie par la périphérie vers l’aorte et la pression pulsée aortique. Ces résultants suggèrent un effet direct des microparticules au niveau de la microcirculation. L’augmentation de l’amplitude de l’onde réfléchie consécutive à une vasoconstriction périphérique, modifie vraisemblablement les pressions au niveau de l’aorte chez le sujet masculin lors de pics de pollution.

Etude 3 :Le rôle de la nicotine dans les effets vasculaires du tabagisme passif. Le tabagisme passif est considéré comme la source la plus importante d’émission de microparticules au niveau domestique. Cependant, la composition chimique des particules semble jouer un rôle essentiel sur les ondes de réflexion. Nous avons démontré récemment que l’exposition passive à la fumée des cigarettes du tabac augmente l’intensité de la réflexion de l’onde de pouls. Ceci n’a pas été observé avec l’exposition à la fumée des cigarettes non tabagiques, en dépit d’une concentration ambiante tout à fait comparable de microparticules. Par ailleurs, nous avons observé que l’augmentation de l’incidence de l’onde de pouls au niveau de l’aorte était fortement associée à la concentration plasmatique de la nicotine. Un lien causal entre la nicotine, réflexion de l’onde de pouls et rigidité artérielle n’avait jamais clairement été établi. Nous avons testé cette hypothèse en administrant la nicotine pure chez des sujets sains. Nous avons observé que l’augmentation des taux plasmatiques de la nicotine à des valeurs comparables à celles qui surviennent après une exposition intensive au tabagisme passif, intensifiait la réflexion de l’onde de pouls et augmentait la rigidité artérielle. La correction statistique pour l’augmentation de la fréquence cardiaque et l’augmentation de la pression artérielle en réponse à la nicotine ne modifiait pas ces conclusions. Nos résultats démontrent ainsi les effets cardiovasculaires importants de faibles concentrations de nicotine, similaires à ceux qui sont atteints en cas d’exposition à un tabagisme passif.

Conclusions. Nos résultats révèlent les effets néfastes de l’exposition au froid et aux microparticules atmosphériques sur la rigidité artérielle, la microcirculation périphérique et la réflexion de l’onde de pouls. Nous avons pu également démontrer le rôle de la stimulation nicotinique dans les effets vasculaires aigus du tabagisme passif, comme en témoigne l’augmentation de la réflexion de l’onde de pouls au niveau aortique. Ces modifications hémodynamiques favorisent l’ischémie myocardique, et constituent un des mécanismes par lesquels l’exposition au froid et à la pollution atmosphérique favorisent la pathologie cardiovasculaire.


Doctorat en Sciences médicales
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Books on the topic "Stiffness arteriosa"

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Fleenor, Bradley S., and Adam J. Berrones. Arterial Stiffness: Implications and Interventions. Springer London, Limited, 2015.

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Fleenor, Bradley S. S., and Adam J. Berrones. Arterial Stiffness: Implications and Interventions. Springer, 2015.

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Arterial stiffness in hypertension. Edinburgh: Elsevier, 2006.

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Safar, Michel, and Michael F. O'Rourke. Arterial Stiffness in Hypertension: Handbook of Hypertension Series (Handbook of Hypertension). Elsevier, 2006.

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Montgomery, Hugh, and Rónan Astin. Normal physiology of the cardiovascular system. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0128.

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Preload modulates contractile performance, and is determined by end-diastolic volume (EDV) and ventricular compliance. Compliance falls with increasing preload, muscle stiffness or ventricular hypertrophy, making central venous pressure (CVP) a poor surrogate for EDV. Responsiveness to fluid loading can be identified by seeking a change in stroke volume (SV) with changes in cardiac loading. Afterload, the force to be overcome before cardiac muscle can shorten to eject blood, rises with transmural pressure and end-diastolic radius, and inversely with wall thickness. Afterload, being the tension across the ventricular wall, is influenced by pleural pressure. Reductions in afterload increase SV for any cardiac work, as do reductions in vascular resistance. Resistance is modified by changes in arteriolar cross-sectional area. A rise in resistance increases blood pressure and microvascular flow velocity. Increased resistance may reduce CO if cardiac work cannot be augmented sufficiently. Flow autoregulationis the ability of vascular beds to maintain constant flow across varied pressures by adjusting local resistance.
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Raggi, Paolo, and Luis D’Marco. Imaging for detection of vascular disease in chronic kidney disease patients. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0116.

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The well-known severity of cardiovascular disease in patients suffering from chronic kidney disease (CKD) requires an accurate risk stratification of these patients in several clinical situations. Imaging has been used successfully for such purpose in the general population and it has demonstrated excellent potential among CKD patients as well. Two main forms of arterial pathology develop in patients with CKD: atherosclerosis, with accumulation of inflammatory cells, lipids, fibrous tissue and calcium in the subintimal space, and arteriosclerosis. The latter is characterized by accumulation of deposits of hydroxyapatite and amorphous calcium crystals in the muscular media of the vessel wall, and is believed to be more closely associated with alterations of mineral metabolism than with traditional atherosclerosis risk factors. The result is the development of what appears to be premature arterial ageing, with loss of elastic properties, increased stiffness, and increased overall fragility of the arterial system. Despite intensifying research and increasing awareness of these issues, the underlying pathophysiology of the aggressive vasculopathy of CKD remains largely unknown. As a consequence, there are currently very limited pathways to prevent progression of vascular damage in CKD. The indications, strengths and weaknesses of several imaging modalities employed to evaluate vascular disease in CKD are described, focusing on coronary arterial circulation and the peripheral arteries, with the exclusion of the intracranial arteries.
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Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.

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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.
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Book chapters on the topic "Stiffness arteriosa"

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Fleenor, Bradley S., and Adam J. Berrones. "Interventions to Destiffen Arteries." In Arterial Stiffness, 43–57. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-24844-8_4.

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Díez, Javier. "Arterial Stiffness and Extracellular Matrix." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 76–95. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096722.

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Atkinson, Jeffrey. "Animal Models of Arterial Stiffness." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 96–116. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096723.

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Mackey, Rachel H., Lakshmi Venkitachalam, and Kim Sutton-Tyrrell. "Calcifications, Arterial Stiffness and Atherosclerosis." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 234–44. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096744.

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Wilkinson, Ian, and John R. Cockcroft. "Cholesterol, Lipids and Arterial Stiffness." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 261–77. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096747.

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Kingwell, Bronwyn A., and Anna A. Ahimastos. "Arterial Stiffness and Coronary Ischemic Disease." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 125–38. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096725.

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Safar, Michel E. "Arterial Stiffness and Peripheral Arterial Disease." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 199–211. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096731.

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McEniery, Carmel M., and John R. Cockcroft. "Does Arterial Stiffness Predict Atherosclerotic Coronary Events?" In Atherosclerosis, Large Arteries and Cardiovascular Risk, 160–72. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096728.

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Agabiti-Rosei, Enrico, and Maria Lorenza Muiesan. "Carotid Atherosclerosis, Arterial Stiffness and Stroke Events." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 173–86. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096729.

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Yki-Järvinen, Hannele, and Jukka Westerbacka. "Insulin Resistance, Arterial Stiffness and Wave Reflection." In Atherosclerosis, Large Arteries and Cardiovascular Risk, 252–60. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096746.

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Conference papers on the topic "Stiffness arteriosa"

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Kiran, V. Raj, Abhidev V.V., Nabeel P.M., Jayaraj Joseph, Mohanasankar Sivaprakasam, and Malay Ilesh Shah. "Arterial Stiffness in Elastic and Muscular Arteries: Measurement using ARTSENS Pen." In 2019 IEEE International Symposium on Medical Measurements and Applications (MeMeA). IEEE, 2019. http://dx.doi.org/10.1109/memea.2019.8802225.

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Ota, Shinichiro, Toshitaka Yasuda, and Takashi Saito. "Quantification of Arterial Stiffness Reduced Effect of Vessel Geometry." In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-67086.

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Arteriosclerosis is such as phenomena hardening of arteries, with thickening and loss of elasticity. Previous indexes include effect of geometric and mechanical factors as the radius, the wall thickness and mechanical properties of arteries. In this study, we proposed viscoelasticity indexes formulated by thin cylindrical shell theory estimated dynamic strain, and this index was independent of wall thickness and radius of arterial vessels. To confirm the validity of these indexes, we evaluated the parameters of viscoelasticity using the latex tube with different wall thickness of blood vessel model. We measured a radius of the latex tube and an inner pressure maintained by a pulsatile pump in a mock circuit filled with the water. Estimating the parameters of elasticity using these measured values, we concluded that a proposal index was independent of the wall thickness of the artery.
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Stephen, Beth, Theresa A. Good, and L. D. Timmie Topoleski. "Change in Mechanical Response of Arterial Elastin due to Glycation." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80087.

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Collagen and elastin are the primary load-bearing components of arteries. Elastin is a low strength, highly elastic, fibrous material and collagen is a stiffer material, generally present as wavy fibers when unstretched. Together, they account for the material response of arteries under tensile load. Arteries, and other soft tissues, exhibit a two-part material response to tensile load. There is an initial low stiffness response at low stretch followed by a high stiffness response at higher stretch. It has been proposed that the low stiffness response is dominated by the elastin in the material and the high stiffness response is dominated by collagen [1]. The elastin accounts for the initial low stiffness response of the material, until the wavy collagen fibers straighten and become engaged, at which point the material transitions to its higher stiffness response. It is important to understand the role of the individual collagen and elastin components and how they contribute to the overall mechanical response of the arteries. Further, it is important to understand how specific biochemical processes that occur with age and disease affect the mechanical response of the individual collagen and elastin components and consequently the overall mechanical response of the arteries. This knowledge will increase our understanding of arterial mechanical response and how this response changes arterial function in health and disease.
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Hoffman, Allen H., Zhongzhao Teng, Calvin Mui, Jie Zheng, Pamela K. Woodard, and Dalin Tang. "Stiffness Comparisons Between Adventitia, Media and Full Thickness Specimens From Human Atherosclerotic Carotid Arteries." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206401.

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Arteries display highly nonlinear, anisotropic material behavior and can be considered to be a layered composite of fiber oriented materials composed of three layers: intima, media and adventitia. The intima does not affect the material properties of the artery. Thus, the mechanical properties of an artery result from the combined interaction of the media and adventitia with each layer displaying different material properties. It has been widely accepted that atherosclerosis changes the material properties of the arterial wall. However, little experimental data exists relating the properties of the media and adventitia of atherosclerotic vessels to the overall properties of the artery. Knowledge of the properties of human atherosclerotic tissues is essential for an improved understanding the effects of atherosclerosis and also for creating more accurate computational models for predicting the effects of the disease [1]. A prior study of bovine carotid arteries determined the properties of the adventitia and media using a deductive method [2]. This paper focuses on directly measuring and comparing the stiffness of paired samples of adventitia, media and full thickness specimens from human atherosclerotic carotid arteries.
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Bennetts, Craig J., Ahmet Erdemir, and Melissa Young. "Surface Stiffness of Patient-Specific Arterial Segments With Varying Plaque Compositions." In ASME 2013 Conference on Frontiers in Medical Devices: Applications of Computer Modeling and Simulation. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/fmd2013-16132.

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Peripheral arterial disease (PAD), resulting from the accumulation of plaque, causes obstruction of blood flow in the large arteries in the arm and leg. In the United States, approximately 8.4 million people over the age of 40 have PAD [1]. If not treated, PAD can cause ischemic ulcerations and gangrene, which could eventually lead to amputation. Approximately, 25% of patients with PAD have worsening limb symptoms over 5 years, 7% requiring revascularization, and 4% requiring amputation [2].
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Espinosa, Gabriela, Lisa Bennett, William Gardner, and Jessica Wagenseil. "The Effects of Extracellular Matrix Protein Insufficiency and Treatment on the Stiffness of Arterial Smooth Muscle Cells." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14131.

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Increased arterial stiffness is directly correlated with hypertension and cardiovascular disease. Stiffness of the conducting arteries is largely determined by the extracellular matrix (ECM) proteins in the wall, such as collagen and elastin, produced by the smooth muscle cells (SMCs) found in the medial layer. Elastin is deposited as soluble tropoelastin and is later crosslinked into elastin fibers. Newborn mice lacking the elastin protein ( Eln−/−) have increased arterial wall stiffness and SMCs with altered proliferation, migration and morphology [1]. Vessel elasticity is also mediated by other ECM proteins, such as fibulin-4. Elastic tissue, such as lung, skin, and arteries, from fibulin-4 deficient ( Fbln4−/−) mice show no decrease in elastin content, but have reduced elasticity due to disrupted elastin fibers [2]. Arteries from both elastin and fibulin-4 deficient mice have been previously studied, but the mechanical properties of their SMCs have not been investigated. Recent experiments comparing arterial SMCs from old and young animals suggest that mechanical properties of the SMCs themselves may contribute to changes in wall stiffness [3]. Hence, we investigated the stiffness of isolated arterial SMCs from elastin and fibulin-4 deficient mice using atomic force microscopy (AFM). In addition, we studied the effects of two elastin treatments on the mechanical properties of SMCs from Eln+/+ and Eln−/− mice. Differences between the treatments may elucidate the importance of soluble versus crosslinked elastin on single cell stiffness.
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Zhang, Xiaoming, and James F. Greenleaf. "Measurement of the Propagation Velocity of Pulse Wave Generated by Ultrasound in Arteries." In ASME 2005 International Mechanical Engineering Congress and Exposition. ASMEDC, 2005. http://dx.doi.org/10.1115/imece2005-79619.

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Arterial wall stiffness can be associated with various diseases. The stiffness of an artery can be assessed by measurement of the pulse wave velocity (PWV). Usually, PWV is estimated using the foot-to-foot method. However, the foot of the pressure wave is not very clear due to reflected waves. Also, the blood pressure wave generated by the heart is normally a low frequency wave, hence the time resolution is low. PWV is an average indicator of artery stiffness between two measuring locations, therefore, it is not easy to identify local stiffness. In this paper a short external pulse is generated in an artery by the radiation force of ultrasound. The propagation velocity of the pulse wave is measured along the artery. The temporal resolution of this method, which is in the range of microseconds, is much higher than the conventional pressure PWV method, and therefore allows the wave velocity to be measured accurately over a few millimeters.
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Forsblad-d’Elia, Helena, Lucy Law, Karin Bengtsson, Stefan Söderberg, and Per Lindqvist. "SAT0325 REDUCED STRAIN AND INCREASED STIFFNESS OF COMMON CAROTID ARTERIES IN PATIENTS WITH ANKYLOSING SPONDYLITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.4587.

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Canton, Gador, Dalin Tang, Daniel S. Hippe, and Chun Yuan. "Distensibility of the Atherosclerotic Carotid Artery: Relationship With Plaque Burden and Composition?" In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80845.

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Arterial distensibility is a marker that can measure vessel wall functional and structural changes resulting from atherosclerosis [5] with applications including estimation of mechanical properties of the wall for biomechanical models. Although arterial segments affected by atherosclerosis are characterized by marked stiffening [2], little is known about the relationship between local specific atherosclerotic plaque features and wall stiffness. In particular, calcification has been shown to be associated with greater wall stiffness, however, this relationship is not consistent in different arterial segments [1,6]. For the carotid arteries, a more thorough understanding of the role of plaque features in determining wall stiffness might be offered by magnetic resonance imaging (MRI). Multi-contrast, high resolution MRI is an established imaging tool to quantify the components of carotid lesions, as well as plaque burden [8,9]. In addition, CINE MRI has been proven to be a reliable tool to measure arterial distensibility [3], an index frequently used to measure stiffness. In this study, our goals were to use MRI to characterize subject-specific wall stiffness in vivo in atherosclerotic carotid arteries, and to analyze the relation between stiffness and plaque burden and composition. CINE MRI was used to measure vessel wall stiffness; whereas a multi-contrast MRI protocol was applied to characterize vessel wall morphology and composition.
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Yu, Mei, and Ian Grosse. "Prediction of Mechanical Behavior of Balloon-Expandable Stents." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-59455.

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Coronary heart disease is a major health threat for people in the developed countries. Narrowing of the coronary arteries is one of the most common types of coronary heart diseases and is often treated by percutaneous transluminal coronary angioplasty (PTCA) and recently by stenting. A stenting procedure involves inserting a slotted metal tube or coil into the artery and expanding it to help achieve a sufficient luminal size. To optimize the design of stents, we have developed a finite element model of the stenting procedure. The results showed the distal ends of the stent could damage arteries due to non-uniform expansion of the stent. Our model also showed that inclusion of the plaque and artery is important for predicting the final stent shape and diameter. A response surface of the stent hoop stiffness is proposed to help designers quickly decide the stiffness of the stent for a given design. Results show that contact stresses are inversely proportional to stent stiffness and a minimum stent hoop stiffness is needed to prevent stent collapse after balloon removal.
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