Academic literature on the topic 'Large artery stiffness'
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Journal articles on the topic "Large artery stiffness"
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Benetos, Athanase, Stéphane Laurent, Roland G. Asmar, and Patrick Lacolley. "Large artery stiffness in hypertension." Journal of Hypertension 15 (1997): S89—S97. http://dx.doi.org/10.1097/00004872-199715022-00009.
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McEniery, C. M., and I. B. Wilkinson. "Large artery stiffness and inflammation." Journal of Human Hypertension 19, no. 7 (January 13, 2005): 507–9. http://dx.doi.org/10.1038/sj.jhh.1001814.
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Blacher, J., Athanase Protogerou, and M. Safar. "Large Artery Stiffness and Antihypertensive Agents." Current Pharmaceutical Design 11, no. 25 (October 1, 2005): 3317–26. http://dx.doi.org/10.2174/138161205774424654.
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Chirinos, Julio A. "Echocardiographic Assessment of Large Artery Stiffness." Journal of the American Society of Echocardiography 29, no. 11 (November 2016): 1117–21. http://dx.doi.org/10.1016/j.echo.2016.09.004.
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Chirinos, Julio A. "Large Artery Stiffness and New-Onset Diabetes." Circulation Research 127, no. 12 (December 4, 2020): 1499–501. http://dx.doi.org/10.1161/circresaha.120.318317.
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Kingwell, Bronwyn A., Tanya L. Medley, Tamara K. Waddell, Timothy J. Cole, Anthony M. Dart, and Garry L. Jennings. "Large Artery Stiffness: Structural And Genetic Aspects." Clinical and Experimental Pharmacology and Physiology 28, no. 12 (December 6, 2001): 1040–43. http://dx.doi.org/10.1046/j.1440-1681.2001.03580.x.
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Butlin, Mark, and Ahmad Qasem. "Large Artery Stiffness Assessment Using SphygmoCor Technology." Pulse 4, no. 4 (2016): 180–92. http://dx.doi.org/10.1159/000452448.
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Tan, Isabella, Bart Spronck, Hosen Kiat, Edward Barin, Koen D. Reesink, Tammo Delhaas, Alberto P. Avolio, and Mark Butlin. "Heart Rate Dependency of Large Artery Stiffness." Hypertension 68, no. 1 (July 2016): 236–42. http://dx.doi.org/10.1161/hypertensionaha.116.07462.
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Chirinos, Julio A., Patrick Segers, Timothy Hughes, and Raymond Townsend. "Large-Artery Stiffness in Health and Disease." Journal of the American College of Cardiology 74, no. 9 (September 2019): 1237–63. http://dx.doi.org/10.1016/j.jacc.2019.07.012.
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Wagenseil, Jessica E., and Robert P. Mecham. "Elastin in Large Artery Stiffness and Hypertension." Journal of Cardiovascular Translational Research 5, no. 3 (January 31, 2012): 264–73. http://dx.doi.org/10.1007/s12265-012-9349-8.
Full textDissertations / Theses on the topic "Large artery stiffness"
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Al, Maskari Raya. "Large artery stiffness : genes and pathways." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/277874.
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Aortic stiffness underlies systolic hypertension, promotes heart failure and is associated with increased cardiovascular morbidity and mortality. It is regarded as a primary driver of left ventricular hypertrophy and aortic aneurysms and is linked to the pathogenesis of cognitive impairment, stroke and renal failure. Like most cardiovascular traits, aortic stiffness is a complex trait and is moderately heritable, yet the precise molecular mechanisms that underpin the stiffening process remain poorly defined. This study aimed to employ multiple approaches to further identify the genetic basis of aortic stiffness in a large repository of human donor aortas that had undergone ex vivo pulse wave velocity (PWV) phenotyping. The first part of this work sought to investigate the molecular basis of Loeys-Dietz type 4 syndrome in a pedigree with multiple cases of aortic aneurysms and dissections. A missense variant p.(Arg320Cys) was identified in a highly evolutionary conserved region of TGFB2. There was striking upregulation of TGFB1, TGFB2 and pSMAD2/3 on imunocytochemical straining and western blotting of the aortic tissue from the index case confirming the functional importance of the variant. This case highlighted the striking paradox of predicted loss-of-function mutations in TGFB2 causing enhanced TGFβ signalling in this emerging familial aortopathy and underscored the significance of TGFβ signalling in aortic extracellular matrix biology. The second part of this work attempted to characterise the biological basis for the susceptibility locus identified in the most recent genome wide analysis of carotid-femoral PWV. While the locus lies within the 14q32.2 gene desert, it contains regulatory elements, with the transcriptional regulator B-cell CLL/lymphoma 11B (BCL11B) and non-coding RNA DB129663 representing potential targets for these enhancers. The association of five lead SNPs from the genome-wide association studies (GWAS) meta-analysis was examined for ex vivo aortic stiffness and BCL11B and DB129663 aortic mRNA expression. Three of the five SNPs associated significantly with PWV and showed allele-specific differences in BCL11B mRNA. The risk alleles associated with lower BCL11B suggesting a protective role for BCL11B. Despite the strong association, BCL11B protein was not detected in the human aorta; however, qPCR for CD markers showed that BCL11B transcript correlated strongly with markers for activated lymphocytes. In contrast, DB129663 transcripts were detected in 55% of the samples, and of the five SNPs only one showed allele-specific differences in aortic DB129663 transcripts. No significant differences were observed in PWV between samples expressing or lack- ing DB129663, and therefore the implication of this lncRNA in aortic stiffness remains elusive. The BCL11B transcript detected in the human aorta may reflect lymphocyte infiltration, suggesting that immune mechanisms contribute to the observed association with PWV. For the final part of this work genetic associations with aortic stiffness were explored in a candidate gene-based study utilising tagging SNPs to effectively capture the genetic information from linkage disequilibrium blocks. Association analyses were performed in young, healthy ENIGMA study par- ticipants selected for high and low PWV values then validated in the remaining ENIGMA cohorts. The association of four lead SNPs was then examined for ex vivo aortic stiffness in human donor aortas. The tissue expression of these SNPs and their encoded proteins was also explored. Neither the aggrecan nor the fibulin-1 SNPs showed significant associations with ex vivo PWV in the donor aortas. The exonic aggrecan tagSNP rs2882676 displayed differential transcript abundance between homozygous allele carriers but this did not translate at the protein level. Both aggrecan and fibulin-1 were found in the aortic wall, but with marked differences in the distribution and glycosylation of aggrecan, reflecting loss of chondroitin-sulphate binding domains. These differences were age-dependent but the striking finding was the acceleration of this process in stiff versus elastic young aortas. These findings suggest that aggrecan and fibulin-1 have critical roles in determining the biomechanics of the aorta and their modification with age could underpin age-related aortic stiffening.
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Brodjeski, Alexander Lee. "Reduced SIRT3 contributes to large elastic artery stiffness with aging." Thesis, University of Iowa, 2017. https://ir.uiowa.edu/etd/5426.
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Age-related increases in arterial stiffness are mediated in part by mitochondrial dysfunction. Sirtuin 3 (SIRT3) is a mitochondrial NAD+-dependent deacetylase that regulates mitochondrial function. SIRT3 deficiency contributes to physiological dysfunction in a variety of pathological conditions. Here, we tested the hypothesis that age-associated arterial stiffness, assessed by aortic pulse wave velocity (PWV), would be accompanied with decreased renal and aortic SIRT3 expression and activity due to decreased NAD+ levels. We further tested whether boosting NAD+ concentration with nicotinamide riboside (NR), a NAD+ precursor, for 6 months would reverse the effects of aging. Old (~26 mo, n = 9) C57BL/6 male mice had higher PWV vs. young (6 mo, n = 10) (448 ± 14 vs 382 ± 13, p < 0.005), which was associated with reduced arterial SIRT3 protein (0.365 ± 0.088 AU’s vs 1.000 ± 0.000); p < 0.05). Furthermore, SIRT3 deficient male mice demonstrated higher PWV compared to age-matched control mice (480 ± 21 n = 6 vs. 391 ±12 n = 7, p < 0.005). Aortic SIRT3 protein was negatively correlated with PWV (r=-0.7798, p < 0.005). Old mice also exhibited reduced kidney SIRT3 protein (0.73 ± 0.10 AU’s) compared to young controls (1.00 ± 0.00; p = 0.0192) and reduced NAD+ (918.6 ± 50.5 pmol/mg vs. young 1302.0 ± 56.6 pmol/mg, p = 0.0036). Old mice supplemented with NR had increased NAD+ concentration in kidney tissue (1303.0 ± 90.2 pmol/mg) however, had no effect on normalizing age-associated arterial stiffness (402 ± 18 old with NR vs 418 ± 15 old; p = 0.78). Here we show for that SIRT3 protein correlates with aortic stiffness and may be required for the maintenance of healthy arteries and for the first time that supplementation with NR, a commercially available supplement, ameliorates age-associated decreases in renal NAD+ demonstrating therapeutic potential in kidney disease.
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Wallace, Sharon Mary Louise. "Nitric oxide and large artery stiffness : investigation of mechanisms and clinical implications." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612222.
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Westerbacka, Jukka. "Insulin action on large artery stiffness in normal and insulin resistant subjects." Helsinki : University of Helsinki, 2001. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/westerbacka/.
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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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Werner, Timothy Jason. "Effect of Nebivolol and Lifestyle Modification on Large Artery Stiffness in Middle-Aged and Older Hypertensive Adults." Diss., Virginia Tech, 2013. http://hdl.handle.net/10919/23316.
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For more than half a century cardiovascular disease has been the leading cause of death in the United States. Aging, hypertension, and obesity are major risk factors for cardiovascular disease and clearly associated with arterial stiffness. Arterial stiffness generates higher afterloads and diminishes coronary perfusion thereby causing ventricular hypertrophy and ischemia. Importantly, arterial stiffness is an independent predictor of cardiovascular disease risk and all-cause mortality. Current strategies such as inhibition of angiotensin II or angiotensin converting enzyme, reduction of smooth muscle tone, blood volume, or inflammatory mediators, and improving glucose homeostasis are effective destiffening options. Nebivolol, a third generation beta-blocker, has unique vasodilatory characteristics and may be particularly efficacious as a destiffening agent. Only a few studies have addressed this issue while relying on indirect, blood pressure-dependent stiffness indices precluding clear understanding of study outcomes. There remains a need to determine the potential utility of nebivolol therapy as an arterial destiffening strategy. Thus, we hypothesized that the combination of nebivolol and lifestyle modification would reduce central arterial stiffness in middle-aged and older hypertensive adults more than either intervention alone. To test this hypothesis, we randomized 45 hypertensive adults to receive lifestyle modification, nebivolol, or combination for 12 weeks. Î"-stiffness index, pulse wave analysis, and arterial compliance were measured at baseline and following the intervention. No baseline differences in variables of
interest were observed between groups. In contrast to our hypothesis, lifestyle modification, nebivolol, and combination groups had similar (P>0.05) reductions in beta-stiffness index (-1.87±0.83; -2.03±0.60; and -2.51±0.90 U), respectively, while carotid-femoral pulse wave velocity declined only in the nebivolol and combination groups. Our findings suggest combination of nebivolol and lifestyle modification reduces arterial stiffness to a similar degree as either intervention alone in middle-aged and older hypertensive adults. Further studies are needed to determine if the changes in arterial stiffness continue to occur or remain clinically significant over longer durations.Ph. D.
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DuBose, Lyndsey Elisabeth. "Role of aging and aerobic fitness on large elastic artery stiffness, brain structure and cognitive performance in humans." Thesis, University of Iowa, 2015. https://ir.uiowa.edu/etd/1590.
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Older age is a primary risk factor for the development of cardiovascular disease in part through the stiffening of the large cardiothoracic elastic arteries (e.g., aorta, carotid arteries). Aging is also associated with reduced cognitive function, cerebrovascular reactivity and brain white matter integrity, but whether these changes in brain structure and function are associated with age-related large artery stiffness remains unclear. In contrast, older adults who have high aerobic fitness demonstrate attenuated large artery stiffness and better cognitive performance compared to their sedentary counterparts, but the effects of aerobic fitness on white matter integrity and cerebrovascular reactivity with aging are conflicting and limited. Moreover, whether high aerobic fitness-associated lower large artery stiffness in older adults is associated with, and perhaps mediates, the beneficial changes in cognitive function and white matter structure remains unknown. The purpose of this study was to investigate the extent to which high aerobic fitness is associated with preserved white matter structure, cerebrovascular reactivity, and cognitive performance in aged individuals, and if these changes in brain structure and function are associated with attenuated large artery stiffness. In young (n=19, 23.6 ± 2.5 years) and old (n=22, 64.4 ± 4.2 years) healthy adults, large elastic artery stiffness was measured by carotid-femoral pulse wave velocity (cfPWV, aortic stiffness) via non-invasive applanation tonometry of carotid and femoral pulse waveforms and carotid artery beta-stiffness index (β-stiffness index) and compliance using high-resolution ultrasound and carotid blood pressure via applanation tonometry. Aerobic fitness was measured as maximal exercise oxygen uptake (VO2max) using respiratory gas analysis on an upright cycle ergometer. Older subjects were stratified as high or low fit based on gender and age VO2max classification. Letter, pattern and N-Back cognitive tests were used to assess processing speed and working memory respectively. Fractional anisotropy (FA) from diffusion tensor images and Blood Oxygenation Level Dependent (BOLD) imaging was used to assess cerebrovascular reactivity (CVR) response to a breath hold and brain activation during a working memory task. The association between large artery stiffness and FA was then assessed using a voxel-wise general linear model approach and a region-of-interest analysis.
Our results confirmed age-related increases in cfPWV, carotid β-stiffness index and central (carotid) but not brachial systolic blood pressure, and expected reductions in carotid compliance, VO2max, working memory and processing speed, and in white matter integrity in select brain regions (bilateral cingulate, frontal, occipital, temporal). In contrast, we found no age-associated differences in CVR to breath hold stimulus or change in BOLD response to the N-Back. In our cohort of health adults, we found that the age-related changes in large artery stiffness were not attenuated by high compared with low VO2max. Among older adults, large elastic artery stiffness was not associated with regional white matter integrity or cerebrovascular reactivity in any regions-of-interest. Greater carotid artery compliance and lower β-stiffness index was associated with higher processing speed, while compliance was related to higher d'Prime scores and lower reaction time on the 2-Back task among the older adults. CVR to a breath hold stimulus was not related to any measure of cognitive performance. VO2max was not associated with any measures of vascular function, brain structure, function or cognition, indicating relations between large artery stiffness and cognition were independent of aerobic fitness capacity. Taken together, these data suggest that select measures of cognitive performance, but not white matter structure or CVR, may be susceptible to age-related changes in carotid stiffness/compliance and that are unaffected by aerobic fitness. More work is needed to understand the mechanisms by which age-related declines in carotid artery compliance and increased carotid stiffness are associated with reductions in cognitive function in older adults.
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Ajibewa, Tiwaloluwa Adedamola. "Role of anxiety on vascular dysfunction." Thesis, University of Iowa, 2016. https://ir.uiowa.edu/etd/3035.
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High anxiety is associated with an increased risk of developing cardiovascular disease (CVD), in particular, atherosclerotic coronary artery disease. However, the mechanisms by which anxiety contributes to the development of CVD are unclear. Unlike other common psychiatric disorders such as depression, anxiety and its effects on CVD risk has not been studied extensively. Moreover, whether elevated anxiety is associated with arterial stiffness and vascular endothelial dysfunction, biomarkers of CVD risk, in healthy adults and whether a psychological intervention designed to lower anxiety levels in healthy adults with moderate to high baseline anxiety levels ameliorates vascular dysfunction remains unclear. The purpose of this study was twofold; first to determine the extent to which moderate to high anxiety levels are associated with vascular dysfunction including aortic stiffness as measured by carotid-femoral pulse wave velocity (cf-PWV), carotid artery stiffness via ultrasound-based β-stiffness index, and forearm resistance artery function measured as peak forearm blood flow using venous occlusion plethysmograph (VOP). Secondly, to determine whether the empirically validated Acceptance and Commitment Training (ACT) anxiety intervention improved vascular function after 12 weeks and if this was associated with reductions in anxiety in adults with moderate to high baseline anxiety levels.
Our results indicated that there was no association between increased anxiety levels and any of the three vascular outcomes of interest. Conversely, there was an association between the ACT intervention participation and improvement in forearm resistance artery function independent of age, sex, education, race/ethnicity, BMI and STAI Trait anxiety. Taken together, these data suggest that although higher State and Trait anxiety was not associated with aortic stiffness, carotid stiffness or forearm resistance artery function, and the ACT intervention was associated with improved peripheral resistance artery function. Additional studies are needed to determine whether this effect occurs earlier than 12 weeks and sustained longer that 12 weeks, and whether it occurs in adults with CVD risk factors (i.e. atherosclerosis), non-white racial/ethnic backgrounds and in resistance vessel function in response to intra-arterial vasoactive agonists such as acetylcholine.
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OCHOA, MUNERA JUAN EUGENIO. "Effects of insulin resistance on systemic haemodynamics and autonomic cardiovascular regulation in normotensive healthy adults." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2013. http://hdl.handle.net/10281/46090.
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Hemodynamic effects of insulin resistance (IR) are thought to be largely dependent on its relationship with body mass index (BMI) and blood pressure (BP) levels. The first part of the present thesis was aimed at exploring whether IR is associated with hemodynamic indices of cardiovascular function in a large sample of non-diabetic individuals from the general population (n=731) and if so, to explore if such relationship is continuous across different categories of BMI (lean, overweight and obese), and BP (normal BP, high-normal BP and hypertension). IR was assessed with the homeostasis model assessment of IR (HOMA-IR). Based on a value of HOMA-IR of 2.09 (75th percentile of distribution curve), subjects were classified as insulin-sensitive (IS, HOMA<2.09) or insulin-resistant (IR, HOMA≥2.09). Synchronized beat-to-beat recordings of stroke volume (impedance cardiography) and R-R interval (ECG), along with repeated BP measurements were performed over 5 minutes. Stroke index (SI), cardiac index (CI), systemic vascular resistance index (SVRI), left cardiac work index (LCWI), pre-ejection period (PEP) and left ventricular ejection time (LVET) were computed and averaged. In analysis of co-variance allowing for confounders, IR subjects showed significantly higher BP levels and SVRI, and reduced R-R interval, SI, CI, LCWI, PEP and LVET. These differences remained significant when analyses were performed within each BMI and BP category. Overall, these results indicate that effects of IR on hemodynamic indices of cardiovascular function are continuous across different BMI and BP categories, reinforcing the importance of IR in the pathogenesis of cardiovascular alterations beyond its association with obesity and hypertension. The finding of a significant association between IR and hemodynamic alterations even in lean and normotensive subjects was the rationale to explore potential mechanisms for these alterations in this selected group of subjects. Specific objectives of this second part of the thesis were: 1) To explore the relationship between insulin resistance and systemic hemodynamics, cardiac baroreflex sensitivity and indices of autonomic CV modulation. 2) To explore the relationship of insulin resistance with 24h heart rate, average blood pressure levels and blood pressure variability over the 24h; and 3) To explore the relationship of insulin resistance with central blood pressure levels and with measures of large artery stiffness and wave reflections.
The study population for these analyses was constituted by subjects who were below the 30th percentile of diastolic blood pressure (DBP) distribution curve (DBP ≤72 mmHg) and who had no elevation in systolic BP levels. In addition, subjects were excluded in case of diabetes mellitus (fasting blood glucose ≥126 mg/dL or use of medications for previously diagnosed type 2 diabetes) obesity (BMI≥30) or taking medications with effects on BP. A total of 90 subjects fulfilling inclusion criteria were considered for the present analysis and underwent further assessments. Insulin resistance was assessed with HOMA-index and subjects classified into IR tertiles, based on the distribution of HOMA-index values. 24h Ambulatory BP monitoring was performed. Mean SBP and DBP were averaged for the day, night and 24h, and the respective day-to-night dipping was calculated. BPV was assessed for SBP and DBP as 24h standard deviation (SD), weighted 24h SD (wSD), daytime and night-time SD. Recordings of pulse waveform were obtained by means of a previously validated oscillometric device for ambulatory BP monitoring with in-built transfer-function like method. Aortic pulse wave velocity (PWV, m/s) and other measures derived from pulse wave analysis such as augmentation index (AIx, %), central SBP (cSBP), central DBP (cDBP) and central pulse pressure (cPP) were computed. Peripheral SBP and DBP, and heart rate (HR) were recorded and pulse pressure (PP) calculated as the difference between SBP and DBP. Non-invasive assessment of beat-to-beat BP, R-R interval (ECG) and stroke volume (by means of impedance cardiography) were performed during 10 min in supine position and specific hemodynamic indices associated with their measurement were computed and averaged: RRI (msec), heart rate (HR, bpm), stroke volume index (SI, mL/beat/m2), cardiac index (CI, L/min/m2), SBP (mmHg) and DBP (mmHg), systemic vascular resistance index (SVRI, dyn/sec/cm-5/m2), left cardiac work index (LCWI, Kg/m/m2), pre-ejection period (PEP, msec), left ventricular ejection time (LVET, msec) and PEP/LVET ratio were calculated. Cardiac autonomic modulation was assessed by computer analysis of 10 min beat-to-beat BP and ECG recordings in resting supine position. Cardiac baroreflex sensitivity (BRS) was estimated by sequence method. Total variance, low-frequency (LF) and high-frequency (HF) spectral components of HR variability (HRV) were assessed by autoregressive analysis. LF/HF ratio was calculated. After multiple regression analysis, adjusting for common confounders such as age, sex, HR and BMI, increasing values of HOMA-IR were associated with reduced RRI, SI, CI, and with increased SVRI, SBP and DBP. IR was also associated with reduced BRS (up, down, and total slopes), decreased parasympathetic indices of autonomic CV modulation (SDRRI, HF-power, total power) and a predominance of sympathetic component of HRV (increased LF/HF ratio). Increasing values of HOMA-IR were also associated with increased HR and average SBP levels (during day, night and 24-h period), with augmented BP variability (Day SBP SD, and SBP wSD) and with a reduced dipping of HR. Finally, insulin resistance was shown to be associated with increasing values of aortic PWV, and with higher central and peripheral SBP and DBP levels. Overall, these results support significant associations between insulin resistance and changes in hemodynamic and autonomic indices of cardiovascular function, even after accounting for common confounders. These findings suggest that in normotensive healthy adults, increases in insulin resistance may promote alterations in autonomic cardiovascular modulation, in systemic hemodynamics and in arterial stiffness, all of which are known contributors to the pathogenesis of hypertension.
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Maritz, Melissa. "Vascular and metabolic profile of 5-year sustained hypertensive versus normotensive black South Africans / Melissa Maritz." Thesis, 2014. http://hdl.handle.net/10394/15399.
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Motivation
A close association exists between hypertension and arterial stiffness. Whether the increased arterial stiffness seen in hypertensives are due to structural or functional adaptations in the vasculature is uncertain. Hypertension is more common in blacks and they have an increased arterial stiffness and higer stroke prevalence than white populations. Arterial stiffening, or a loss of arterial distensibility, increases the risk for cardiovascular events, including stroke and heart failure, as it increases the afterload on the heart, as well as creating a higher pulsatile load on the microcirculation. The stiffness of the carotid artery is associated with cardiovascular events, like stroke, and all-cause mortality. Furthermore, carotid stiffness is independently associated with stroke, probably because stiffening of the carotid artery may lead to a higher pressure load on the brain. Inflammation, endothelial activation, dyslipidemia, hyperglycemia and health behaviours may also influence hypertension and arterial stiffness. Limited information is availiable on these associations in black South Africans. The high prevalence of hypertension and cardiovascular disease in blacks creates the need for effective prevention and intervention programs in South Africa.
Aim
We aimed to compare the characteristics of the carotid artery between 5-year sustained hypertensive and normotensive black participants. Furthermore, we aimed to determine whether blood pressure, conventional cardio-metabolic risk factors, markers of inflammation, endothelial activation and measures of health behaviours are related to these carotid characteristics.
Methodology
This sub-study forms part of the South African leg of the multi-national Prospective Urban and Rural Epidemiology (PURE) study. The participants of the PURE-SA study were from the North West Province of South Africa, and baseline data collection took place in 2005 (N=2010), while follow-up data was collected five years later, in 2010 (N=1288). HIV-free participants who were either hypertensive or normotensive (N=592) for the 5-year period, and who had complete datasets, were included in this sub-study. The study population thus consists of a group of 5-year sustained normotensive (n=241) and hypertensive (n=351) black participants.
Anthropometric measurements included height, weight, waist circumference and the calculation of body mass index (BMI). We included several cardiovascular measurements, namely brachial systolic- and diastolic blood pressure, heart rate, central systolic blood pressure, central pulse pressure and the carotid dorsalis-pedis pulse wave velocity. Carotid characteristics included distensibility, intima media thickness, cross sectional wall area, maximum and minimum lumen diameter. Biochemical
variables that were determined included HIV status, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, triglycerides, fasting glucose, glycated haemoglobin (HbA1c), creatinine clearance, interleukin-6, C-reactive protein, intracellular adhesion-molecule-1 and vascular adhesion molecule-1. Health behaviours were quantified by measuring γ-glutamyltransferase and by self-reported alcohol, tobacco and anti-hypertensive, anti-inflammatory and lipid-lowering medication use.
We compared the normotensive and hypertensive groups by using independent t-tests and chi-square tests. The carotid characteristics were plotted according to quartiles of central systolic blood pressure by making use of standard analyses of variance (ANOVA) and the analyses of co-variance (ANCOVA). Pearson correlations done in the normotensive and hypertensive Africans helped to determine covariates for the multiple regression models. We used forward stepwise multiple regression analyses with the carotid characteristics as dependent variables to determine independent associations between variables.
Results and Conclusion
The cardiovascular measures, including pulse wave velocity, were significantly higher in the hypertensive group (all p≤0.024). The lipid profile, markers of inflammation, endothelial activation and glycaemia, as well as health behaviours, did not differ between the hypertensives and normotensives after adjustments for age, sex, waist circumference, γ-glutamyltransferase, tobacco use and anti-hypertensive medication use. After similar adjustments, all carotid characteristics, except IMT, were significantly different between the groups (all p≤0.008). However, upon additional adjustment for cSBP, significance was lost.
The stiffness and functional adaptation seen in this study are not explained by the classic cardio-metabolic risk factors, markers of endothelial activation or health behaviours of the participants. The differences that exist in terms of arterial stiffness between the normotensive and hypertensive groups may be explained by the increased distending pressure in the hypertensive group. Despite their hypertensive status, it seems that there are no structural adaptations in these hypertensive Africans.MSc (Physiology), North-West University, Potchefstroom Campus, 2015
Book chapters on the topic "Large artery stiffness"
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Climie, Rachel E. D. "Endothelial Dysfunction and Large Artery Stiffness." In Blood Pressure Disorders in Diabetes Mellitus, 181–93. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-13009-0_12.
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Gielen, Stephan, M. Harold Laughlin, and Dirk J. Duncker. "Vascular remodelling." In The ESC Textbook of Sports Cardiology, edited by Antonio Pelliccia, Hein Heidbuchel, Domenico Corrado, Mats Börjesson, and Sanjay Sharma, 41–48. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198779742.003.0005.
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Vascular remodelling plays an important role in the adaptation of the athlete to increased exercise duration and intensity. Endurance exercise improves endothelium-dependent flow-mediated vasodilation and leads to increases in conduit artery lumen diameter after regular exercise, typically in the trained limb. These changes result in a reduced vascular stiffnes. On the contrary strength training (e.g. for weight-lifting) produces increased vascular stiffness and enlarged central vessels (e.g. aortic root diameters), while the diameters of peripheral vessels are unchanged. In the skeletal muscle, endurance training increases capillary density and improves oxygen exchange, thus adding further functional reserves to the aerobic exercise capacity. Aerobic exercise leads to a large increase in cardiac functional reserves, hence myocardial perfusion is increased in line with metabolic demands. In addition to improved endothelium-dependent vasodilation, coronary arterioles also exhibit an increased myogenic tone.
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Capric, Violeta, Harshith Priyan Chandrakumar, Jessica Celenza-Salvatore, and Amgad N. Makaryus. "The Role of the Renin-Angiotensin-Aldosterone System in Cardiovascular Disease: Pathogenetic Insights and Clinical Implications." In Renin-Angiotensin Aldosterone System [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96415.
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Increased attention has been placed on the activation of the renin-angiotensin-aldosterone system (RAAS) and pathogenetic mechanisms in cardiovascular disease. Multiple studies have presented data to suggest that cardiac and arterial stiffness leading to adverse remodeling of both the heart and vasculature leads to the various pathological changes seen in coronary artery disease, heart failure (with preserved and reduced ejection fractions), hypertension and renal disease. Over-activation of the RAAS is felt to contribute to these structural and endocrinological changes through its control of the Na+/K+ balance, fluid volume, and hemodynamic stability. Subsequently, along these lines, multiple large investigations have shown that RAAS blockade contributes to prevention of both cardiovascular and renal disease. We aim to highlight the known role of the activated RAAS and provide an updated description of the mechanisms by which activation of RAAS promotes and leads to the pathogenesis of cardiovascular disease.
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K. Day, Thomas. "Role of Arterial Pressure, Wall Stiffness, Pulse Pressure and Waveform in Arterial Wall Stress/Strain and Its Clinical Implications." In Risk Factors for Cardiovascular Disease. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.100048.
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Biomechanical stress applied to the intima of arteries has long been suspected as a factor in the initiation and localisation of atherosclerotic plaque, and it is implicated in the separation of plaque from the underlying arterial wall giving rise to the acute clinical consequences of thrombosis, dissection and embolism. The factors underlying transmural stress were investigated in-vitro using fresh porcine abdominal aortas on an experimental rig in which pulse pressure, pulse waveform, fluid viscosity, pulse rate, vessel wall compliance and systolic and diastolic blood pressure could be varied at will. Vessel wall compliance was progressively reduced by exposure of the artery to formaldehyde vapour for increased periods of time, a saline-treated artery being used as control. Centripetal transmural stress (CTS) and strain were studied by direct observation of the displacement of a compliant false intima (FI) using real-time B and M mode ultrasound, and by measuring the differential pressure between the space beneath the FI and the adjacent vessel lumen. CTS was found to be directly related to pulse pressure (r = 0.907, p < 0.001) and inversely related to vessel wall compliance. It was independently affected by ranked peak pressure waveform (R = 0.93, p < 0.01) being higher with sharp peak pressure and lower when the waveform was rounded, and it peaked in early diastole in untreated vessels, and both in diastole and peak systole in ones stiffened by formaldehyde vapour. Mean arterial pressure exerted a profound effect via its effect on vessel wall stiffness, which was found to rise 7-fold across the mean arterial pressure range 50-130 mmHg and continued to increase in a logarithmic fashion as the upper physiological range of mean arterial pressure was exceeded. There are two potential clinical implications: in mitigating the postulated biomechanical aspects atherogenesis and atherosclerotic plaque detachment, maintaining large vessel wall compliance is important, and the main factor determining this in a healthy artery is mean arterial pressure; if the arterial wall has already become stiffened as a result of disease, and in the absence of critical stenosis, the findings suggest that the appropriate therapeutic targets are modification of pulse pressure and pulse waveform profile. Simply reducing the diastolic pressure in elderly patients may be unwise if the result is a widened pulse pressure and increased transmural strain. The distribution of atheroma at points of focal mechanical strain in the vessel wall may be explicable if the stress induced by an excessive pulse pressure provokes the inflammatory changes seen in repetitive strain injury. Investigation of inflammatory signalling in the vessel wall provoked by repeated mechanical stress may represent a productive area for future research.
Conference papers on the topic "Large artery stiffness"
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Ooi, Chen Yen, and Naomi C. Chesler. "The Role of Collagen in Pulmonary Hypertension-Induced Large Artery Stiffening." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192951.
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Hypoxic pulmonary hypertension (HPH) leads to stiffening of large pulmonary arteries, which affects right ventricular afterload. We hypothesized that vascular collagen accumulation is the major cause of large pulmonary artery (PA) stiffening in HPH. We tested this hypothesis with transgenic mice that produce collagen type I resistant to degradation (Col1a1R/R) and wild type littermate controls (Col1a1+/+) exposed to hypoxia and allowed to recover. Pressure-diameter testing on left PAs demonstrated that stiffness in control mice increased with hypoxia and decreased with recovery (p < 0.05). Preliminary tests in degradation-resistant mice suggest that PA stiffness decreases less with recovery than in controls. Quantitative measurements of vascular collagen content in right PAs are planned to develop statistical correlations between structure and function.
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Demoux, AL, K. Aissi, B. Chaudier, S. Carijn, P.-Y. Chouc, H. De Baillou, and P. Rossi. "FRI0696 Impact of adalimumab therapy on brachial endothelial function and large artery stiffness in patients with rheumatoid arthritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6128.
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Dodson, Reuben Blair, Paul J. Rozance, Kendall S. Hunter, and Virginia L. Ferguson. "Increased Stiffness of the Abdominal Aorta With Intrauterine Growth Restriction in the Near-Term Fetal Sheep." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80634.
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Fetal intrauterine growth restriction (IUGR) results in increased placental resistance to blood flow, fetal hypertension and increased pulsatility [1]. These hemodynamic changes have been shown to lead to vascular remodeling in adolescents and adults [2, 3] but have received little study of its effect during this critical period of vascular formation. Epidemiological studies link IUGR to cardiovascular disease in adulthood [4], but the reason for this is not clearly understood. Here, we examine a large elastic artery for developmental alterations under hypertensive conditions. We hypothesize that fetal hypertension induces abdominal aorta (AA) stiffening in the fetal ovine model of IUGR and that the increased systemic artery stiffness is due to altered extracellular matrix (ECM) composition and structural changes.
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Wang, Zhijie, Roderic S. Lakes, and Naomi C. Chesler. "Changes in Conduit Pulmonary Arterial Static and Dynamic Mechanical Properties During Severe Hypoxic Pulmonary Hypertension." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80382.
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Pulmonary hypertension (PH) is a complex disorder that manifests as abnormally high blood pressure in the vasculature of the lungs. The chronic structural and mechanical changes in the proximal pulmonary artery (PA) associated with PH include smooth muscle cell hypertrophy and proliferation, accumulation of extracellular matrix (ECM) protein and increased stiffness1–4. Recent evidence has shown that conduit PA stiffness is a strong predictor of mortality in pulmonary arterial hypertension5,6. This suggests a potential association between large PA biomechanics and right ventricle failure.
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Liu, Aiping, Lian Tian, Diana M. Tabima, and Naomi C. Chesler. "Sex Differences in Right Ventricular-Vascular Coupling and Pulmonary Artery Impedance in Response to Chronic Hypoxia and Recovery." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80835.
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Pulmonary artery hypertension (PAH) is a female dominant disease (the female-to-male ratio is 4:1), characterized by small distal pulmonary arterial narrowing and large proximal arterial stiffening, which increase right ventricle (RV) afterload and ultimately lead to RV failure [1,2]. Our recent studies have shown that collagen accumulation induced by chronic hypoxia increases the stiffness of the large extralobar pulmonary arteries (PAs) [3], and affects pulmonary vascular impedance (PVZ) [4]. The role of collagen in the female predominance in developing PAH has not been explored to date.
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Gourisankaran, Vijay. "Effects of Stenosis Severity and Balloon Characteristics on Stresses in Balloon Angioplasty — A FEM Study." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0465.
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Abstract Studies of stresses in an artery under normal physiological pressure loads have been made to gain insight into the possible causes of plaque rupture and progression of atherosclerosis. This study addresses the effects of stenosis severity, and balloon stiffness on the peak stresses experienced in the system during angioplasty. It is proposed that the effectiveness and therefore success of an angioplasty procedure can be measured by the non-propensity for restenosis to occur, and the absence of high stresses in the diseased artery at peak balloon dilation pressures. The models used in this study use nonlinear material properties of the arterial wall and the balloon, large deformations during the angioplasty procedure and contact between the arterial wall and the balloon.
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Hansen, Laura, Manu Platt, Roy L. Sutliff, and Rudolph L. Gleason. "The Mechanical and Structural Effects of HIV Proteins on Murine Carotid Arteries." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53693.
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Acquired immunodeficiency syndrome (AIDS) is considered a global epidemic with over 65 million people worldwide infected with the HIV-1 virus, the causative agent [1]. The development of highly active antiretroviral therapy (HAART) has significantly increased the life expectancy of people infected with the virus by slowing the progression to the development of AIDS. However, the treatment has also led to the emergence of early onset cardiovascular complications including myocardial infarction [2] and atherosclerotic lesions [3], as well as subclinical markers of atherosclerosis including increased carotid artery intima-media thickness [4], increased arterial stiffness [5–6], and endothelial dysfunction [6]. It appears that HAART and HIV-1-infection are independent risk factors for the development of atherosclerosis in adults [7]; however, the mechanism of disease progression remains unclear. There is a pressing need to identify mechanisms of early on-set cardiovascular disease associated with HIV-1 infection and HAART and to identify therapeutic strategies to reduce cardiovascular disease in HIV patients. The overall goal of this study is to test the hypothesis that over-expression of HIV proteins will lead to alterations in the biomechanical properties of large arteries.
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Delgado, Ana, Pengfei Dong, Mahyar Sameti, Vladislav N. Zimin, Juhwan Lee, Yazan Gharaibeh, Hiram G. Bezerra, David Wilson, Christopher Bashur, and Linxia Gu. "Mechanical Characterization of Calcificaiton in Diseased Coronary Artery with Atomic Force Microscope." In 2022 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/dmd2022-1055.
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Abstract In this work, the mechanical propertied of calcification in diseased coronary artery was evaluated with atomic force microscope (AFM). The heavily calcified coronary artery was harvest from a cadaver’s heart. The artery slices with thickness of 10 um were prepared with cryosectioning. Staining with Alizarin Red has been performed to highlight the calcification region. Results have shown that the calcified areas have a significant larger stiffness compared with the surrounding plaque and the media layer of a healthy artery. The calcification showed a heterogeneous property with larger deviation in stiffness distribution. The staining process affected the mechanical properties. Results will enhance the mechanical property database in the literature.