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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.arteryresearch.com/?rss=yes"><title>Artery Research</title><description>Artery Research RSS feed: Current Issue.    
 ARTERY RESEARCH  is the official journal of the Association for Research into Arterial Structure and Physiology and promotes the 
advancement of knowledge and dissemination of information concerning the pathophysiology, epidemiology, detection, investigation and 
treatment of arterial structure and function. 
For further information on the Association, please go to    http://www.arterysociety.org .

 
 
The journal publishes original articles, review articles, case-studies, letters to the Editor and short communications. 
 
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material is subject to a strict peer-review process. 
 
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monthly via ScienceDirect between May 2010 and May 2011 
   </description><link>http://www.arteryresearch.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Artery Research</prism:publicationName><prism:issn>1872-9312</prism:issn><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:publicationDate>June 2012</prism:publicationDate><prism:copyright> © 2012 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS1872931212000294/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS1872931212000270/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS1872931212000269/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS1872931212000257/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS1872931212000245/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS187293121200021X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS187293121200004X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS1872931212000038/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arteryresearch.com/article/PIIS1872931212000026/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.arteryresearch.com/article/PIIS1872931212000294/abstract?rss=yes"><title>Editorial Board</title><link>http://www.arteryresearch.com/article/PIIS1872931212000294/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1872-9312(12)00029-4</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-06-01</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-06-01</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.arteryresearch.com/article/PIIS1872931212000270/abstract?rss=yes"><title>Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness</title><link>http://www.arteryresearch.com/article/PIIS1872931212000270/abstract?rss=yes</link><description>Abstract: Systemic inflammatory conditions are associated with an increased risk of cardiovascular disease (CVD). How exactly inflammation leads to this is not fully understood, but it has been suggested that arterial stiffening, could provide potential mechanisms to explain it. Chronic, systemic inflammatory conditions, as well as acute-models of inflammation are associated with arterial stiffening. Moreover, aortic stiffness can be reversed with successful immunomodulatory therapy. Although it seems evident that inflammation is involved in the process of aortic stiffening, the precise mechanism responsible for this remains unclear.There are number of possible mechanisms by which inflammation could lead to arterial stiffening. (1) Inflammation is associated with endothelial dysfunction and this can regulate arterial stiffness via changes in smooth muscle tone. (2) Inflammation leads to increased synthesis of matrix metalloproteinases, which can degrade elastin, resulting in stiffening. (3) Several mediators of inflammation may directly stimulate vascular calcification, whereas endogenous inhibitors of vascular calcification are downregulated during inflammation, both of which can lead to stiffening. (4) During inflammation arterial glycosaminoglycan (GAG) synthesis is upregulated. In animal models, an overproduction of certain GAGs in the aorta results in stiffening of the arterial wall by thinning of elastic lamellae. (5) Finally, direct vascular inflammation could lead to arterial stiffening by changing the composition of extracellular matrix. This review aims to discuss potential mechanisms by which inflammation could lead to aortic stiffening.</description><dc:title>Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness</dc:title><dc:creator>Kaisa M. Mäki-Petäjä, Ian B. Wilkinson</dc:creator><dc:identifier>10.1016/j.artres.2012.03.002</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-04-17</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-04-17</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section>Artery 11 Invited Speaker Extended Review Paper</prism:section><prism:startingPage>59</prism:startingPage><prism:endingPage>64</prism:endingPage></item><item rdf:about="http://www.arteryresearch.com/article/PIIS1872931212000269/abstract?rss=yes"><title>White blood cell count and endothelin-1 vasoconstrictor tone in middle-aged and older adults</title><link>http://www.arteryresearch.com/article/PIIS1872931212000269/abstract?rss=yes</link><description>Abstract: Background: Higher white blood cell (WBC) count is associated with impaired endothelium-dependent vasodilation. However, the influence of higher WBC count on endothelin (ET)-1 vasoconstrictor activity is currently unknown. We tested the hypothesis that adults with elevated WBC count demonstrate enhanced ET-1 system activity.Methods: Thirty-four healthy adults were studied: 17 with WBC count&lt;5.0×109cells/L (lower WBC; 9M/8F; age: 53±2 yr) and 17 with WBC count&gt;5.0×109cells/L (higher WBC; 10M/7F; 54±3 yr). Forearm blood flow (FBF) responses to intra-brachial infusion of ET-1 (5pmol/min for 20min) and selective ETA receptor blockade (BQ-123; 100nmol/min for 60min) were measured by venous occlusion plethysmography.Results: The vasoconstrictor response to ET-1 was significantly blunted (∼60%) in the higher WBC group versus the lower WBC group. The FBF responses to selective ETA receptor blockade were also significantly different (P&lt;0.05) between the groups. In the lower WBC group, resting FBF increased marginally (∼5%) to BQ-123, whereas the increase in FBF to BQ-123 was significantly greater (∼15%) in higher WBC group. Furthermore, there was a significant relation between WBC count and FBF response to ET-1 (r=−0.43) and BQ-123 (r=0.41).Conclusions: Relative elevations in WBC count in middle-aged and older adults, independent of adiposity and other cardiometabolic risk factors, are associated with enhanced ET-1-mediated vasoconstrictor tone. Elevated ET-1 system activity may be a mechanism linking higher WBC count with increased cardiovascular risk.</description><dc:title>White blood cell count and endothelin-1 vasoconstrictor tone in middle-aged and older adults</dc:title><dc:creator>Kyle J. Diehl, Brian R. Weil, Jared J. Greiner, Brian L. Stauffer, Christopher A. DeSouza</dc:creator><dc:identifier>10.1016/j.artres.2012.03.001</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>65</prism:startingPage><prism:endingPage>70</prism:endingPage></item><item rdf:about="http://www.arteryresearch.com/article/PIIS1872931212000257/abstract?rss=yes"><title>Vascular characteristics in patients with resistant hypertension and type-II-diabetes mellitus</title><link>http://www.arteryresearch.com/article/PIIS1872931212000257/abstract?rss=yes</link><description>Abstract: Background: Resistant hypertension is presumed to be common in patients with type-II-diabetes mellitus (type-II-DM) and arterial stiffness has been proposed to play a major role in the development hereof. Our objective with this study was to examine differences in vascular characteristics in patients with controlled (CH), uncontrolled (UH) and resistant hypertension (RH) and type-II-DM and to assess whether increased arterial stiffness could explain the prevalence of resistant hypertension.Methods and results: Vascular characteristics were examined using ambulatory blood pressure measurements, applanation tonometry and cardiac ultrasound. We estimated carotid-to-femoral pulse wave velocity using Sphygmocor. Characteristic impedance, arterial resistance, arterial compliance and augmentation index was estimated from analysis of pressure- and flow-curves. Finally ambulatory arterial stiffness index was estimated using ambulatory blood pressure measurements. We included 114 patients in the study of whom 39 had RH. When compared to patients with CH, patients with RH had increased pulse wave velocity (10.8 m/s [8.78; 12.23] versus 8.55 m/s [7.55; 10.6], P = 0.002) and reduced total arterial compliance (0.81 ml/mmHg [0.55; 0.95] versus 0.93 ml/mmHg [0.68; 1.36], P = 0.03) however differences were non-significant when adjusted for blood pressure (P = 0.2 and P = 0.2) Following statistical adjustment patients with UH had increased total arterial resistance though as compared to patients with CH (1.63 mmHg/ml*s−1 [1.37; 1.92] versus 1.38 mmHg/ml*s−1 [1.2; 1.71]) (P = 0.03).Conclusion: In the present study patients with RH and type-II-DM do not have increased intrinsic arterial stiffness when compared to patients with CH, thus we conclude that increased intrinsic arterial stiffness is not the cause of resistant hypertension in the present study.</description><dc:title>Vascular characteristics in patients with resistant hypertension and type-II-diabetes mellitus</dc:title><dc:creator>Trine Koustrup Soender, Jacob Eifer Møller, Brian Bridal Løgstrup, Jess Lambrechtsen, Jørgen Hangaard, Kenneth Egstrup</dc:creator><dc:identifier>10.1016/j.artres.2012.02.002</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-03-22</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-03-22</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>71</prism:startingPage><prism:endingPage>77</prism:endingPage></item><item rdf:about="http://www.arteryresearch.com/article/PIIS1872931212000245/abstract?rss=yes"><title>Reproducibility of cardiac output derived by impedance cardiography during postural changes and exercise</title><link>http://www.arteryresearch.com/article/PIIS1872931212000245/abstract?rss=yes</link><description>Abstract: Background: Evaluation of cardiac output (CO) and other haemodynamic parameters may aid in understanding factors involved in arterial blood pressure (BP) changes with exercise and postural stress. Impedance cardiography offers a rapid, non-invasive means to acquire this information, however there is limited data assessing the reproducibility of this technique during haemodynamic perturbation. This study aimed to assess reproducibility of CO and other haemodynamic parameters derived from impedance cardiography during exercise and in different postures.Methods: 51 participants (mean age 57 ± 9 years, 57% male) had CO and other haemodynamic variables (including end diastolic volume, left ventricular work, ejection fraction and systemic vascular resistance) measured via impedance cardiography (Physio Flow) at two visits separated by 12 ± 7 days. Measures were recorded at rest in three postures (supine, seated and standing), during upright cycle ergometry at a fixed workload (40 W), and also during steady state exercise at an intensity of 60% and 70% of age-predicted maximum heart rate (HRmax).Results: CO reproducibility was assessed over a wide range (5.27 ± 1.00–12.09 ± 2.02 l/min). There was good agreement between CO measured at each visit in all postures and exercise conditions (intra-class correlation coefficient [ICC] range 0.729–0.888, P &lt; 0.05 for all) with a small difference between visits (mean difference 0.06 ± 1.10 l/min). All other haemodynamic variables showed good agreement between visits (ICC range 0.714–0.970, P &lt; 0.05 for all).Conclusions: Non-invasive impedance cardiography provides an acceptably reproducible means to evaluate CO and other haemodynamic variables relevant to arterial BP regulation during different postures and light-to-moderate intensity exercise.</description><dc:title>Reproducibility of cardiac output derived by impedance cardiography during postural changes and exercise</dc:title><dc:creator>Martin G. Schultz, Rachel E.D. Climie, Sonja B. Nikolic, Kiran D. Ahuja, James E. Sharman</dc:creator><dc:identifier>10.1016/j.artres.2012.02.001</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-02-28</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-02-28</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>78</prism:startingPage><prism:endingPage>84</prism:endingPage></item><item rdf:about="http://www.arteryresearch.com/article/PIIS187293121200021X/abstract?rss=yes"><title>The addition of whole-body vibration to a lifestyle modification on arterial stiffness in overweight and obese women</title><link>http://www.arteryresearch.com/article/PIIS187293121200021X/abstract?rss=yes</link><description>Abstract: Background: Increased arterial stiffness is an independent risk factor for cardiovascular disease. Arterial stiffness increases in obese individuals as compared to normal weight. While weight loss by calorie-restriction alone decreases arterial stiffness in obesity, it decreases muscle mass. Resistance training is recommended treatment for this frailty, but it can also increase arterial stiffness. Whole-body vibration (WBV) has recently been indicated as an alternative for resistance training. The present study aimed to examine whether lifestyle modifications combined with WBV decrease arterial stiffness in overweight and obese women.Methods: Twelve overweight and obese women (age: 30–48 years) completed a 12-week lifestyle-modification program (1200kcal/day diet, brisk walking for 30min, 3 days/week) and WBV (30–35Hz, 30min, 3 days/week).Results: Before and after this program, we measured body weight and indices of arterial stiffness, i.e., carotid-femoral pulse wave velocity (cfPWV) and brachial-ankle PWV (baPWV). Body weight, cfPWV, and baPWV of the overweight and obese women significantly decreased after this intervention. The concentration of plasma pentraxin 3, which has a cardioprotective effect, significantly increased after the program.Conclusion: We recommend the addition of WBV to classical lifestyle modifications to decrease arterial stiffness, which would reduce the risk of cardiovascular disease and muscle weakness in obese individuals.</description><dc:title>The addition of whole-body vibration to a lifestyle modification on arterial stiffness in overweight and obese women</dc:title><dc:creator>Asako Miyaki, Seiji Maeda, Youngju Choi, Nobuhiko Akazawa, Yoko Tanabe, Rina So, Kiyoji Tanaka, Ryuichi Ajisaka</dc:creator><dc:identifier>10.1016/j.artres.2012.01.006</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-02-17</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-02-17</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>85</prism:startingPage><prism:endingPage>91</prism:endingPage></item><item rdf:about="http://www.arteryresearch.com/article/PIIS187293121200004X/abstract?rss=yes"><title>A comparison of SphygmoCor and Vicorder devices for measuring aortic pulse wave velocity in pregnancy</title><link>http://www.arteryresearch.com/article/PIIS187293121200004X/abstract?rss=yes</link><description>Abstract: Background: Aortic pulse wave velocity (aPWV) has been found to be increased in preeclampsia when compared to normal pregnancy. Preeclampsia is associated with increased risk of later cardiovascular disease and, as such, study of the aortic stiffness in pregnancy, and its hypertensive disorders, is important to the understanding the underlying vascular changes. We compared two different techniques to measure aPWV in the mid-trimester of pregnancy.Methods: 58 women were recruited from the obstetric ultrasound clinic, mean (±SD) age 33 (±6) years and gestation 27 (±1) weeks. Aortic PWV was measured using SphygmoCor and Vicorder devices.Results: We found that both devices provided similar aPWV values with no significant difference between devices: mean difference (±SD), 0.1 (±0.9)m/s, p = 0.4. We found good correlation between devices (r = 0.6, p &lt; 0.001). Good intra-observer variability was observed for both SphygmoCor and Vicorder devices, coefficients of variation 5.69% and 2.67%, respectively.Conclusions: The SphygmoCor and Vicorder devices produce similar readings for aPWV in the second trimester of pregnancy, with good intra-observer variability. Due to its simpler technique the Vicorder device may be more suited to the clinical setting, particularly in advanced pregnancy or obesity.</description><dc:title>A comparison of SphygmoCor and Vicorder devices for measuring aortic pulse wave velocity in pregnancy</dc:title><dc:creator>T.R. Everett, A. Mahendru, C.M. McEniery, C.C. Lees, I.B. Wilkinson</dc:creator><dc:identifier>10.1016/j.artres.2012.01.003</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-01-24</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-01-24</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>92</prism:startingPage><prism:endingPage>96</prism:endingPage></item><item rdf:about="http://www.arteryresearch.com/article/PIIS1872931212000038/abstract?rss=yes"><title>Increased aortic wave reflection and longitudinal regional diastolic dysfunction in patients with left ventricular hypertrophy</title><link>http://www.arteryresearch.com/article/PIIS1872931212000038/abstract?rss=yes</link><description>Abstract: Objectives: Increased arterial stiffness is associated with the progression of left ventricular hypertrophy (LVH); however, the endocardial layer (End) contracts more than the epicardial layer (Epi), and it is unclear whether increased arterial stiffness affects regional wall deformation in both the End and Epi in LVH.Methods: We performed echocardiography and measured the radial augmentation index (rAIx) in 41 patients with LVH. We evaluated the longitudinal strain, and early diastolic strain rate (SRdia) (measures of regional wall deformation) in both End and Epi in addition to measures of global diastolic function. The ratios of End strain to Epi strain (End/Epi strain) and End SRdia to Epi SRdia (End/Epi SRdia) were also calculated.Results: All of the patients had a decreased LV diastolic function (E/e′&gt;8) and preserved ejection fraction (&gt;45%). The rAIx was slightly related to the End/Epi SRdia (r=0.29, P=0.063); the relationship of rAIx to End/Epi SRdia (beta=0.52, P=0.034) was significant after adjustment for potential confounding factors. The rAIx at heart rate 75 beats per minute (rAIx@HR75) was significantly related to End/Epi SRdia (r=0.36, P=0.023); the relationship of rAIx@HR75 to End/Epi SRdia remained significant even after the adjustment (P=0.032). The relationships of rAIx@HR75 to End/Epi strain did not reach the level of statistical significance (r=0.30, P=0.06) in this study.Conclusion: Increased rAIx, a measure of aortic wave reflection, may be associated with a regional diastolic function in the ratio of endocardial to epicardial layer of the left ventricular wall in patients with left ventricular hypertrophy.</description><dc:title>Increased aortic wave reflection and longitudinal regional diastolic dysfunction in patients with left ventricular hypertrophy</dc:title><dc:creator>Joji Ishikawa, Yoshio Matsui, Cesare Russo, Eiichi Hyodo, Kotaro Arai, Marco R. DiTulio, Shunichi Homma, Kazuomi Kario</dc:creator><dc:identifier>10.1016/j.artres.2012.01.002</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-01-24</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-01-24</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>97</prism:startingPage><prism:endingPage>102</prism:endingPage></item><item rdf:about="http://www.arteryresearch.com/article/PIIS1872931212000026/abstract?rss=yes"><title>Relationship between 24 h ambulatory central blood pressure and left ventricular mass – Rationale and design of a prospective multicenter study</title><link>http://www.arteryresearch.com/article/PIIS1872931212000026/abstract?rss=yes</link><description>Abstract: The prognostic superiority of ambulatory over clinic blood pressure has been repeatedly proven. However, due to the mechanical properties of the arterial system, systolic and pulse pressures are higher in the brachial artery than in the ascending aorta. It seems logical that central pressures are more relevant to cardiovascular disease than peripheral (brachial) pressures, and indeed, using clinic blood pressures, it has been shown that central systolic and pulse pressures are more closely associated with hypertensive end-organ damage than their brachial counterparts. Moreover, antihypertensive drugs can have differential effects on central versus brachial blood pressures. All these effects have been described on the basis of clinic blood pressure measurements. Recent advances in technology allow the estimation of central systolic blood pressure from brachial pulse waves recorded with a regular brachial oscillometric blood-pressure cuff, using a transfer-function like algorithm (ARCSolver). This method has been invasively validated and allows the recording of 24 h ambulatory central blood pressure profiles. Our multicenter study now aims for the first time to investigate the relationship between central ambulatory blood pressure monitoring and hypertensive end-organ damage (left ventricular mass) in untreated adults.</description><dc:title>Relationship between 24 h ambulatory central blood pressure and left ventricular mass – Rationale and design of a prospective multicenter study</dc:title><dc:creator>Thomas Weber, Carmel McEniery, Ian Wilkinson, Giuseppe Schillaci, Maria Lorenza Muiesan, Robert Zweiker, Cristina Giannattasio, Kai Mortensen, Johannes Baulmann, Arno Schmidt-Trucksäss, Siegfried Wassertheurer</dc:creator><dc:identifier>10.1016/j.artres.2012.01.001</dc:identifier><dc:source>Artery Research 6, 2 (2012)</dc:source><dc:date>2012-01-24</dc:date><prism:publicationName>Artery Research</prism:publicationName><prism:publicationDate>2012-01-24</prism:publicationDate><prism:volume>6</prism:volume><prism:number>2</prism:number><prism:issueIdentifier>S1872-9312(12)X0003-6</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>103</prism:startingPage><prism:endingPage>108</prism:endingPage></item></rdf:RDF>
