Increase In Pulse Wave Velocity Research Articles

SUBCLINICAL TARGET ORGAN DAMAGE IN A SAMPLE OF CHILDREN WITH SOLITARY FUNCTIONING KIDNEY. A PRELIMINARY OBSERVATIONAL STUDY

Objective: Solitary Functioning Kidney (SFK) is a condition characterized by a single-functioning kidney. Children bearing this condition are exposed to an increased risk of subclinical organ damage (SOD) due to the compensatory hyperfiltration in the remaining kidney and increased peripheral blood pressure (pBP) values. The aim of the present study was to assess the impact of traditional (pBP) and novel (central systolic blood pressure, cSBP) cardiovascular risk factors on SOD in children and adolescents with solitary functional kidney. Design and method: Carotid ultrasonography was performed to measure carotid Intima-Media Thickness (cIMT), an index of subclinical atherosclerosis. Arterial stiffness was assessed by measuring carotid Distensibility Coefficient (cDC) and carotid-femoral Pulse Wave Velocity (PWV). Cardiac mass and remodeling were analyzed using transthoracic echocardiography. Central and peripheral (both office and ambulatory) BP measurements, as well as biochemical data from blood and urine samples were collected. Results: Forty-eight SFK children and adolescents were included, of whom 45.5% were hypertensive at the Ambulatory Blood Pressure Monitoring. Twenty-four patients had increased cIMT and RWT while 8.4% and 8.9% demonstrated a reduction of cDC and an increase of PWV. Two patients had a left ventricular mass index (LVMi) above the 95th percentile. cSBP correlated with all vascular indices measured (cIMT r = 0.43; cDC r = -0.33; PWV r = 0.42, p < 0.05) and with LVMi (r = 0.41; p = 0.005). Office pSBP correlated with cDC (r = -0.31; p = 0.03), PWV (r = 0.42 and p = 0.004) and LVMi (r = 0.33; p = 0.02). Regarding ABPM measurements, daytime systolic BP correlated with all vascular indices (cIMT r = 0.34, cDC r = -0.31, PWV r = 0.39 p < 0.005) but not with echocardiographic ones. No correlation was found between cardiovascular parameters and the estimated glomerular filtration rate or the urinary albumin to creatinine ratio. Conclusions: Our data show a high prevalence of subclinical atherosclerosis and cardiac remodeling in children and adolescents with SFK. A lesser proportion of patients presented an increased arterial stiffening. cSBP more than pBP (office or ambulatory) associates with SOD. Children with SFK could bear a greater cardiovascular risk pointing out the importance of early preventive efforts.

ARTERIAL WALL CONDITION IN WOMEN WITH HYPERTENSION AND POSTMENOPAUSAL OSTEOPOROSIS

Objective: The aim of the study was to investigate the indices of arterial stiffness and central aortic pressure in women with hypertension in combination with osteoporosis. Design and method: The study included 68 females (mean age 62.7±3.8 years) with hypertension, grade 2 in postmenopause including 35 females with osteoporosis (group 1) and 33 females without signs of osteoporosis (group 2) according to osteodensitometry investigation. The control group consisted of 20 healthy females (mean age 61.3±3.5 years). Before the study, the patients did not receive regular antihypertensive drugs and hormone replacement therapy. In addition to conventional studies the levels of calcium, phosphorus, alkaline phosphatase, deoxypyridinoline, parathyroid hormone, 25(OH) vitamin D, osteocalcin, C-terminal telopeptide of type I collagen in blood were determined. Fracture risk assessment (FRAX), daily blood pressure monitoring, applanation tonometry and dual-energy X-ray absorptiometry were performed. Results: It was found that in group 1 the levels of office systolic blood pressure (SBP) and diastolic blood pressure (DBP) were 3.7% and 4.9% (p<0.05) higher than in group 2. According to the data of daily BP monitoring a more pronounced increase of mean daily SBP and DBP by 4.1% and 6.6% (p<0.05) was observed in group 1 in comparison to group 2. Indicators of pressure load according to the time index of hypertension by SBP and DBP were significantly higher by 21.7% and 25.4% during the day and 22% and 18.2% at night (all p<0.05). In patients of group 1 an increase in the aortic augmentation index of wave reflection (Aix) and the augmentation index of wave reflection, adjusted for heart rate (AIx @ HR 75) by 26.6% and 29.8% compared to patients of group 2 respectively, was revealed. It was found that in group 1, compared with the control group and group 2, an increase in pulse wave velocity by 37.2% and 26.4% respectively was detected. Conclusions: It was found that in patients with hypertension in combination with postmenopausal osteoporosis, according to office, daily monitoring and applanation tonometry, blood pressure levels and arterial stiffness parameters were significantly higher than in patients with hypertension without osteoporosis.

PULSE WAVE VELOCITY AND BLOOD PRESSURE VARIABILITY AS PROGNOSTIC INDICATORS IN VERY ELDERLY PATIENTS WITH DECOMPENSATED CHRONIC CONDITIONS

Objective: There is scarce evidence of the prognostic importance of hemodynamic measures, such as blood pressure (BP), BP variability and arterial stiffness in the very elderly population with advanced chronic conditions. We aimed to evaluate the prognostic importance of 24-hour BP, BP variability and arterial stiffness in a cohort of very elderly patients admitted to the hospital due to a decompensated chronic disease. Design and method: We studied 249 patients older than 80 (66% women), admitted due to a chronic disease decompensation (60% congestive heart failure). During admission, 24-hour brachial and central BP, BP and heart rate variabilities, aortic pulse wave velocity and BP variability ratio were determined through non-invasive 24-hour monitoring. The primary outcome was 1-year mortality. Secondary outcome was the composite of 1-year mortality or readmission. Results: Increased arterial stiffness (aortic pulse wave velocity and BP variability ratio) was associated with 1-year mortality. For each standard deviation (SD) increase in aortic pulse wave velocity and BP variability ratio, mortality increased 3.3 times and 31%, respectively, after adjustments for clinical confounders and BP. Increased BP variability (38% increase for each SD change) and reduced heart rate variability (32% increase for each SD change) also predicted 1-year mortality in fully adjusted models. No association was found between 24-hour BP (either brachial or aortic) and 1-year mortality. Conclusions: Increased aortic stiffness and BP and heart rate variabilities predict 1-year mortality in very elderly patients with decompensated chronic conditions. Measurements of such estimates could be useful in the prognostic evaluation of this specific population.

Association of Arterial Stiffness and Atherosclerotic Burden With Brain Structural Changes Among Japanese Men.

Background Little is known regarding whether arterial stiffness and atherosclerotic burden are each independently associated with brain structural changes. Simultaneous assessments of both arterial stiffness and atherosclerotic burden in associations with brain could provide insights into the mechanisms of brain structural changes. Methods and Results Using data from the SESSA (Shiga Epidemiological Study of Subclinical Atherosclerosis), we analyzed data among 686 Japanese men (mean [SD] age, 67.9 [8.4] years; range, 46-83 years) free from history of stroke and myocardial infarction. Brachial-ankle pulse wave velocity and coronary artery calcification on computed tomography scans were measured between March 2010 and August 2014. Brain volumes (total brain volume, gray matter, Alzheimer disease signature and prefrontal) and brain vascular damage (white matter hyperintensities) were quantified using brain magnetic resonance imaging from January 2012 through February 2015. In multivariable adjustment models including mean arterial pressure, when brachial-ankle pulse wave velocity and coronary artery calcification were entered into the same models, the β (95% CI) for Alzheimer disease signature volume for each 1-SD increase in brachial-ankle pulse wave velocity was -0.33 (-0.64 to -0.02), and the unstandardized β (95% CI) for white matter hyperintensities for each 1-unit increase in coronary artery calcification was 0.68 (0.05-1.32). Brachial-ankle pulse wave velocity and coronary artery calcification were not statistically significantly associated with total brain and gray matter volumes. Conclusions Among Japanese men, higher arterial stiffness was associated with lower Alzheimer disease signature volumes, whereas higher atherosclerotic burden was associated with brain vascular damage. Arterial stiffness and atherosclerotic burden may be independently associated with brain structural changes via different pathways.

Gastrodin attenuates angiotensin II-induced vascular contraction and MLCK/p-MLC2 pathway activation

Context Gastrodin has been used as antihypertension therapy in China; however, the mechanisms underlying the effects of gastrodin have yet to be fully elucidated. Objective To explore the therapeutic efficiency of gastrodin as an antihypertensive and determine the mechanisms underlying this effect. Materials and methods C57BL/6 mice were continuously administered angiotensin II (Ang II) (500 ng/kg/min) to induce hypertension. Mice were randomly divided into control, Ang II and Ang II + gastrodin groups. Mice received intragastric administration of gastrodin (5 mg/kg) or double distilled water once a day for 4 weeks. Blood pressure, pulse wave velocity (PWV), thickness of the abdominal aorta, pathological morphology and differential expression transcripts (DETs) were assessed. Abdominal aorta rings and primary isolated vascular smooth muscle cells were subjected to Ang II stimulation to induce hypertension as ex vivo and in vitro models, respectively. Vascular ring tension, release of Ca2+ and levels of proteins involved in the myosin light chain kinase (MLCK)/phospho-myosin light chain 2 (p-MLC2) pathway were determined. Results Gastrodin treatment attenuated increases in blood pressure, PWV and thickness of the abdominal aorta. Treatment with gastrodin resulted in 2785 DETs and the enrichment of vascular contraction and calcium signalling pathways. Gastrodin treatment attenuated Ang II-induced vasoconstriction, produced a norepinephrine-precontracted vasodilation effect (attenuated by verapamil), and reduced intracellular Ca2+ release. Furthermore, gastrodin suppressed activation of the MLCK/p-MLC2 pathway in vivo and in vitro. Conclusions Gastrodin treatment lowers blood pressure, suppresses Ang II-induced vascular contraction and MLCK/p-MLC2 pathway activation, thereby demonstrating the mechanisms underlying the therapeutic efficacy of gastrodin as an antihypertensive.

Biomechanical and transcriptional evidence that smooth muscle cell death drives an osteochondrogenic phenotype and severe proximal vascular disease in progeria.

Hutchinson-Gilford Progeria Syndrome results in rapid aging and severe cardiovascular sequelae that accelerate near end-of-life. We found a progressive disease process in proximal elastic arteries that was less evident in distal muscular arteries. Changes in aortic structure and function were then associated with changes in transcriptomics assessed via both bulk and single cell RNA sequencing, which suggested a novel sequence of progressive aortic disease: adverse extracellular matrix remodeling followed by mechanical stress-induced smooth muscle cell death, leading a subset of remnant smooth muscle cells to an osteochondrogenic phenotype that results in an accumulation of proteoglycans that thickens the aortic wall and increases pulse wave velocity, with late calcification exacerbating these effects. Increased central artery pulse wave velocity is known to drive left ventricular diastolic dysfunction, the primary diagnosis in progeria children. It appears that mechanical stresses above ~ 80kPa initiate this progressive aortic disease process, explaining why elastic lamellar structures that are organized early in development under low wall stresses appear to be nearly normal whereas other medial constituents worsen progressively in adulthood. Mitigating early mechanical stress-driven smooth muscle cell loss/phenotypic modulation promises to have important cardiovascular implications in progeria patients.

Aortic Stiffness and Cardiac Modification After Open Or Endovascular Aortic Treatment: Preliminary Results of a Single Centre Prospective Cohort Study

Objective: Increased arterial stiffness, particularly aortic stiffness (AoS), is considered an independent marker of cardiovascular mortality and morbidity. According to the literature, aortic endovascular treatment correlates to a worsening of AoS in the medium term, indirectly evaluated as an increase in pulse wave velocity (PWV). This appears to lead to changes in cardiac geometry and efficiency. The arterial elastance (Ea) represents the total workload opposite to the left ventricle; it is a poorly researched parameter in this field but it could estimate the total arterial compliance. The aim of this study is to evaluate possible changes in AoS with consequent alterations in cardiac function after endovascular repair (ER) or open surgery (OS), also by comparing these two different techniques.

Time Restricted Feeding Reverses Western Diet-Induced Disruptions in Diurnal Blood Pressure Rhythms and Aortic Media Thickening

Cardiovascular disease is one of the primary contributors to the global burden of disease. A poor diet commonly observed in the western world consisting of elevated fat, salt, and sugar is estimated to contribute to 14% of disability-associated life years and increased mortality. High fat fed animals have altered circadian rhythms and increased aortic and renal damage. As the timing of food intake is critical for establishing and maintaining proper circadian rhythms, and disruption of these rhythms is detrimental to cardiovascular health, we hypothesize that time restricted feeding, similar to intermittent fasting, will rescue western diet-induced cardiovascular disease. In this study, alongside normal diet (ND 10% kcal fat, 0.25% by weight salt. 0.7% kcal sucrose) controls, C57Bl/6J male mice were switched to a high fat (45% kcal), high salt (4% by weight), and high sugar (17% kcal) diet for 20 weeks. At 18 weeks, a portion of the western-diet (WD) mice were subjected to time-restricted feeding (TRF) where access to food was restricted to the active period, 6pm to 6am. A subset of mice were implanted with radiotelemeters 14 weeks into the study to measure 24hr conscious blood pressure. Body weight was measured throughout the study confirming increased weight gain in WD mice compared to ND mice and that TRF did not induce weight loss. By 10 weeks, WD fed animals showed increased pulse wave velocity indicative of vascular remodeling (p<0.05). Remarkably, WD mice exhibited a non-dipping phenotype of their blood pressure. Active blood pressures were similar across groups 137 to 142mmHg; however, WD mice exhibited an elevation in inactive blood pressure (124mmHg) compared to ND mice (108mmHg). TRF returned inactive blood pressure (110mmHg) to ND levels despite being on a WD. The mesor of a cosiner analysis of the diurnal pattern of blood pressure is elevated in WD mice which is rescued by TRF. WD and WD-TRF mice exhibited increased perirenal fat accumulation, serum insulin, renal mass, and albuminuria compared to ND mice. There was no difference between WD and WD-TRF mice in these endpoints. We also observed increased renal inflammation in WD and WD-TRF mice measured by flow cytometric analysis of immune infiltrates, yet no effect of TRF itself. Histological analysis of aortic sections by Masson’s trichrome revealed a significant thickening of the tunica media in WD mice (52.91±1.70μm, n=15) compared to ND mice (47.12±1.88μm, n=14, p<0.05) which was reversed by TRF treatment (44.97±1.22μm, n=14, p<0.01). These results demonstrate that western diet contributes to chronic renal inflammation and aortic remodeling. We present novel findings that TRF rescues WD-induced non-dipping blood pressure and tunica media thickening. AHA-DF837441, NIH-1T32AI138932-01A1, 1R01HL161212-01A1, 19EIA34480023, 19IPLOI34760558, NIH-5T32GM 8111-35, AHA-MRT827566 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The acute effects of resistance training on arterial stiffness: A systematic review

Objectives: The effects of resistance training (RT) and the potential role of isolated training variables on arterial stiffness (AS) remain inconclusive. This review summarises the current literature examining the acute effects of RT on AS from a distinct perspective, considering ‘intensity of effort’ as an independent loading variable, potentially affecting AS responses to RT. Design: Systematic review Methods: SPORTDiscus, PubMed/MEDLINE, CHINAHL and Google Scholar electronic databases were searched between 2000 and 2022. Randomised control trials, non-randomised or repeated measures comparative studies assessing arterial responses to acute RT protocols measured by pulse wave velocity (PWV) were included. Results: From the 645 articles identified, 16 articles were included. Ten studies reported a significant increase in carotidfemoral PWV (cfPWV) post-exercise (p < 0.05), with increases between 2% and 20.8% reported. Five studies found no significant differences in cfPWV while in one study femoral-dorsalis pedis PWV decreased by 14%. Loading intensities ranging from 30% to 95% of 1RM had an ambiguous effect on AS, although there was a trend towards increased AS following acute RT. Higher intensities of effort and slower repetition velocities appeared to further increase AS. Conclusions: Available evidence shows a trend for increased AS following acute RT. Nonetheless, it remains to be deter mined whether additional RT variables (e.g., intensity of effort, repetition duration) could attenuate or limit increases in AS. Further research, having more RT variables controlled, is needed to draw definite conclusions.

Qingda granule ameliorates vascular remodeling and phenotypic transformation of adventitial fibroblasts via suppressing the TGF-β1/Smad2/3 pathway

Ethnopharmacological relevanceQingda granule (QDG) exhibits significant therapeutic effects on high blood pressure, vascular dysfunction, and elevated proliferation of vascular smooth muscle cells by inhibiting multiple pathways. However, the effects and underlying mechanisms of QDG treatment on hypertensive vascular remodeling are unclear. Aim of the studyThe aim of this study was to determine the role of QDG treatment in hypertensive vascular remodeling in vivo and in vitro. Materials and methodsAn ACQUITY UPLC I-Class system coupled with a Xevo XS quadrupole time of flight mass spectrometer was used to characterize the chemical components of QDG. Twenty-five spontaneously hypertensive rats (SHR) were randomly divided into five groups, including SHR (equal volume of double distilled water, ddH2O), SHR + QDG-L (0.45 g/kg/day), SHR + QDG-M (0.9 g/kg/day), SHR + QDG-H (1.8 g/kg/day), and SHR + Valsartan (7.2 mg/kg/day) groups. QDG, Valsartan, and ddH2O were administered intragastrically once a day for 10 weeks. For the control group, ddH2O was intragastrically administered to five Wistar Kyoto rats (WKY group). Vascular function, pathological changes, and collagen deposition in the abdominal aorta were evaluated using animal ultrasound, hematoxylin and eosin and Masson staining, and immunohistochemistry. Isobaric tags for relative and absolute quantification (iTRAQ) was performed to identify differentially expressed proteins (DEPs) in the abdominal aorta, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed. Cell Counting Kit-8 assays, phalloidin staining, transwell assays, and western-blotting were performed to explore the underlying mechanisms in primary isolated adventitial fibroblasts (AFs) stimulated with transforming growth factor-β 1 (TGF-β1) with or without QDG treatment. ResultsTwelve compounds were identified from the total ion chromatogram fingerprint of QDG. In the SHR group, QDG treatment significantly attenuated the increased pulse wave velocity, aortic wall thickening, and abdominal aorta pathological changes and decreased Collagen I, Collagen III, and Fibronectin expression. The iTRAQ analysis identified 306 DEPs between SHR and WKY and 147 DEPs between QDG and SHR. GO and KEGG pathway analyses of the DEPs identified multiple pathways and functional processes involving vascular remodeling, including the TGF-β receptor signaling pathway. QDG treatment significantly attenuated the increased cell migration, actin cytoskeleton remodeling, and Collagen I, Collagen III, and Fibronectin expression in AFs stimulated with TGF-β1. QDG treatment significantly decreased TGF-β1 protein expression in abdominal aortic tissues in the SHR group and p-Smad2 and p-Smad3 protein expression in TGF-β1-stimulated AFs. ConclusionsQDG treatment attenuated hypertension-induced vascular remodeling of the abdominal aorta and phenotypic transformation of adventitial fibroblasts, at least partly by suppressing TGF-β1/Smad2/3 signaling.

Echinatin maintains glutathione homeostasis in vascular smooth muscle cells to protect against matrix remodeling and arterial stiffening

Decreased vascular compliance of the large arteries as indicated by increased pulse wave velocity is shown to be associated with atherosclerosis and the related cardiovascular events. The positive correlation between arterial stiffening and disease progression derives a hypothesis that softening the arterial wall may protect against atherosclerosis, despite that the mechanisms controlling the cellular pathological changes in disease progression remain unknown. Here, we established a mechanical-property-based screening to look for compounds alleviating the arterial wall stiffness through their actions on the interaction between vascular smooth muscle cells (VSMCs) and the wall extracellular matrix (ECM). We found that echinatin, a chalcone preferentially accumulated in roots and rhizomes of licorice (Glycyrrhiza inflata), reduced the stiffness of ECM surrounding cultured VSMCs. We examined the potential beneficial effects of echinatin on mitigating arterial stiffening and atherosclerosis, and explored the mechanistic basis by which the compound exert the effects. Administration of echinatin in mice fed on an adenine diet and in hyperlipidemia mice subjected to 5/6 nephrectomy mitigated arterial stiffening and atherosclerosis. Mechanistic insights were gained from the RNA-sequencing results showing that echinatin upregulated the expression of glutamate cysteine ligases (GCLs), both the catalytic (GCLC) and modulatory (GCLM) subunits. Further study indicated that upregulation of GCLC/GCLM in VSMCs by echinatin maintains the homeostasis of glutathione (GSH) metabolism; adequate availability of GSH is critical for counteracting arterial stiffening. As a consequence of regulating the GSH synthesis, echinatin inhibits ferroptosis and matrix remodeling that being considered two contributors of arterial stiffening and atherosclerosis. These data demonstrate a pivotal role of GSH dysregulation in damaging the proper VSMC-ECM interaction and uncover a beneficial activity of echinatin in preventing vascular diseases.

Arterial stiffness for the early prediction of pre-eclampsia compared with blood pressure, uterine artery Doppler and angiogenic biomarkers: a prospective cohort study.

Our aim was to evaluate the ability of arterial stiffness parameters to predict pre-eclampsia early compared with peripheral blood pressure, uterine artery Doppler and established angiogenic biomarkers. Prospective cohort study. Tertiary care antenatal clinics in Montreal, Canada. Women with singleton high-risk pregnancies. In the first trimester, arterial stiffness was measured by applanation tonometry, along with peripheral blood pressure and serum/plasma angiogenic biomarkers; uterine artery Doppler was measured in the second trimester. The predictive ability of different metrics was assessed through multivariate logistic regression. Arterial stiffness (carotid-femoral pulse wave velocity, carotid-radial pulse wave velocity) and wave reflection (augmentation index, reflected wave start time), peripheral blood pressure, ultrasound indices of velocimetry and circulating angiogenic biomarker concentrations. In this prospective study, among 191 high-risk pregnant women, 14 (7.3%) developed pre-eclampsia. A first-trimester 1m/s increase in carotid-femoral pulse wave velocity was associated with 64% increased odds (P < 0.05), and a 1-millisecond increase in time to wave reflection with 11% decreased odds for pre-eclampsia (P < 0.01). The area under the curve of arterial stiffness, blood pressure, ultrasound indices and angiogenic biomarkers was 0.83 (95% confidence interval [CI] 0.74-0.92), 0.71 (95% CI 0.57-0.86), 0.58 (95% CI 0.39-0.77), and 0.64 (95% CI 0.44-0.83), respectively. With a 5% false-positive rate, blood pressure had a sensitivity of 14% for pre-eclampsia and arterial stiffness a sensitivity of 36%. Arterial stiffness predicted pre-eclampsia earlier and with greater ability than blood pressure, ultrasound indices or angiogenic biomarkers.

Arterial hypertension and pulse wave velocity

Abstract Aim. The purpose of the study is to identify the connection between high blood pressure and PWV in patients with AH and determine if AH is a risk factor that accelerates the development of atherosclerosis. Material and methods. With quantitative research method we investigated, explained, and defi ned the eff ects of arterial hypertension with the PWV increase‐rate observed across diff erent age groups of patients who already have AH. Data from patients’ medical records from the At Cor Sphygmocor operating system were extracted. Results. The sample included 191 patients with AH. PWV values were normal in 72% of patients with optimal blood pressure (BP), 60% of patients with normal BP had increased PWV in high normal BP and grade 1 AH were 53% of increased PWV, 53% of normal PWV in grade 2 AH, increased in 94% in grade 3 AH, and 50% of patients had increased PWV values in isolated systolic AH. Conclusions. The research results undoubtedly show the importance of arterial hypertension for the increase in pulse wave velocity, with the clearest correlation at grade 3 AH and in the age groups between 30 and 49 years. On average, the PWV value in hypertensive patients rose by 8%, which represents an increased risk of cardiovascular complications.

SAGE Score in Normotensive and Pre-Hypertensive Patients: A Proof of Concept.

The SAGE score was developed to detect individuals at risk for increased pulse wave velocity (PWV). So far, studies have been focused on hypertensive patients. To assess the ability of the score to detect non-hypertensive and pre-hypertensive patients at risk for increased PWV. Retrospective cross-sectional study of analysis of central blood pressure data and calculation of the SAGE score of non-hypertensive and pre-hypertensive patients. Each score point was analyzed for sensitivity, specificity, positive and negative predictive values, using the cut-off point for positive diagnosis a PVW ≥ 10m/s, ≥9.08 m/s (75thpercentile) and ≥7.30 m/s (50thpercentile). A p<0.05 was considered statistically significant. The sample was composed of 100 normotensive and pre-hypertensive individuals, with mean age of 52.64 ± 14.94 years and median PWV of 7.30 m/s (6.03 - 9.08). The SAGE score was correlated with age (r=0.938, p<0.001), glycemia (r=0.366, p<0.001) and glomerular filtration rate (r=-0.658, p<0.001). The area under the ROC curve was 0.968 (p<0.001) for PWV ≥ 10 m/s, 0.977 (p<0.001) for PWV ≥ 9.08 m/s and 0.967 (p<0.001) for PWV ≥ 7.30 m/s. The score 7 showed a specificity of 95.40% and sensitivity of 100% for PWV≥10 m/s. The cut-off point would be of five for a PWV≥9.08 m/s (sensitivity =96.00%, specificity = 94.70%), and two for a PWV ≥ 7.30 m/s. The SAGE score could identify individuals at higher risk of arterial stiffness, using different PWV cutoff points. However, the development of a specific score for normotensive and pre-hypertensive subjects is needed.

The Prolonged Effect of Shift Work and the Impact of Reducing the Number of Nightshifts on Arterial Stiffness-A 4-Year Follow-Up Study.

To assess changes in blood pressure (BP) and arterial stiffness among 84 rotating shift and 25 dayworkers (control subjects) at two industrial plants during a 4-year follow-up, and to assess changes in outcome variables among shift workers at the two plants after a reduction in the number of night shifts during the last year of follow-up in one of the plants. We collected demographic data using a questionnaire, examined systolic and diastolic blood pressure (sBP, dBP), central systolic and diastolic aorta pressure (cSP, cDP), augmentation pressure (AP), central pulse pressure (cPP), and pulse wave velocity (PWV). We registered sleep quality. The last 4-14 months of follow-up one plant implemented a 12-week shift plan reducing the total number of night shifts and consecutive night shifts from 16.8 to 14 and from 7.2 to 4. To assess differences in change of outcomes between study groups we applied linear mixed models. The dayworkers were older, more hypertensive, reported less sleep disturbance, and smoked/snuffed less than the shift workers did. The adjusted annual increase in PWV was 0.34 m/s (95%CI, 0.22, 0.46) among shift workers and 0.09 m/s (95%CI, -0.05, 0.23) in dayworkers, yielding a significant difference of change of 0.25 m/s (95%CI, 0.06, 0.43). No significant differences were found between the two groups of shift workers in any cardiovascular disease (CVD) outcome during the last year of follow-up. Shift work in industry is associated with arterial stiffness, reflecting an increased risk of future CVD. No significant changes in arterial stiffness were identified as a consequence of a small reduction in the number of night shifts and consecutive night shifts.

S-11-2: AORTIC PULSE WAVE VELOCITY AND CARDIOVASCULAR RISK

Aortic pulse wave velocity (PWV), which can be non-invasively approached by measuring carotid-femoral (cf) PWV, but also to a certain degree by measuring brachial-ankle (ba) PWV, is currently thought to be the gold standard assessment of aortic / large artery stiffness, an important physical property of the arterial system. The assessment of cfPWV/baPWV can be recommended at several stages in the cardiovascular continuum: + Primordial and primary prevention: cfPWV/baPWV increase the risk of incident hypertension and diabetes mellitus (thus, cardiovascular (CV) risk) in apparently healthy adolescents and young and middle aged adults. + Patients with arterial hypertension: Increased PWV is associated with masked hypertension and is the most prevalent measure of hypertension-mediated organ damage (which is, in turn, an important marker of increased CV risk in patients with hypertension) + Patients with diabetes mellitus: PWV is associated with CV and renal complications in patients with type 1 and type 2 diabetes (and, thus, with very high CV risk in these patients). + Young and middle-aged patients up to their 60ies with intermediate CV risk: Increased cfPWV/baPWV can reclassify CV risk in many of these patients, which was confirmed in a metaanalysis including individual participant data of 17.635 patients of 16 observational studies. Associations stratified by sex, diabetes and hypertension were similar, but decreased with age. Adding cfPWV to the traditional CV risk estimation method resulted in net reclassification indices of 25%, 10%, 13% and 11% for 10-year CV mortality, CHD events, CVD events, and stroke events, respectively. In a large meta-analysis including individual participant data of 14.673 Japanese participants (mean age 59–66 years) from 8 cohort studies without a history of CV disease, similar findings were reported for baPWV. Addition of baPWV to a model incorporating the Framingham risk score (FRS) significantly improved the category-free net reclassification (0.247). Finally, improvement in PWV over a few years is associated with improved prognosis. Although no randomised study so far has proven a reduction of CV events, based on a PWV driven strategy (as compared to a strategy based on traditional CV risk factors), prevention of the normal age-related increase in PWV has been shown recently in the SPARTE study. Furthermore, it is reasonable to treat high and very-high risk patients, detected by measurement of PWV, according to the respective risk category in current prevention guidelines.

Comparison of Two Generations of Thoracic Aortic Stent Grafts and Their Impact on Aortic Stiffness in an Ex Vivo Porcine Model

Little is known about the cardiovascular changes after TEVAR and regarding the impact on aortic stiffness for different stent graft generations specifically, following changes in device design. The present study evaluated the stent graft induced aortic stiffening of two generations of the Valiant thoracic aortic stent graft. This was an exvivo porcine investigation using an experimental mock circulatory loop. Thoracic aortas of young healthy pigs were harvested and connected to the mock circulatory loop. At a 60 bpm heart rate and stable mean arterial pressure, baseline aortic characteristics were obtained. Pulse wave velocity (PWV) was calculated before and after stent graft deployment. Paired and independent sample t tests or their non-parametric alternatives were performed to test for differences where appropriate. Twenty porcine thoracic aortas were divided into two equal subgroups, in which a Valiant Captivia or a Valiant Navion stent graft was deployed. Both stent grafts were similar in diameter and length. Baseline aortic characteristics did not differ between the subgroups. Mean arterial pressure values did not change after either stent graft, while pulse pressures increased statistically significantly after Captivia (mean 44±10mmHg to 51±13mmHg, p=.002) but not after Navion. Mean baseline PWV increased after both Captivia (4.4±0.6 m/s to 4.8±0.7 m/s, p=.007) and Navion (4.6±0.7 m/s to 4.9±0.7m/s, p=.002). There was no statistically significant difference in the mean percentage increase in PWV for either subgroup (8±4% vs. 6±4%, p=.25). These experimental findings showed no statistically significant difference in the percentage increase of aortic PWV after either stent graft generation and confirm that TEVAR increases aortic PWV. As a surrogate for aortic stiffness, this calls for further improvements in future thoracic aortic stent graft designs regarding device compliance.

THE EFFECT OF PARICALCITOL AND CALCITRIOL WITH OR WITHOUT CALCIMIMETICS ON PULSE WAVE VELOCITY AND SERUM LEVELS FOR PARATHYROID HORMONE, CALCIUM AND PHOSPHORUS IN MAINTENANCE HEMODIALYSIS PATIENTS.

Different vitamin D analogs might have advantages over calcitriol. To evaluate the effects of paricalcitol vs. calcitriol based vitamin D receptor activators on calcium-phosphate metabolism and pulse wave velocity in hemodialysis patients. Observational, cross-sectional and 1 year follow-up study. 181 hemodialysis patients were enrolled in this study as divided in to 5 groups based on vitamin D therapy. Baseline and 12th month data on blood biochemistry, pulse wave velocity and cumulative dose of treatments were compared in each study group as well as in overall paricalcitol vs. calcitriol-based treatment groups. From baseline to 12th month, significant improvement in pulse wave velocity and parathyroid hormone was shown in paricalcitol-based treatment group without a significant change in calcium, phosphate, alkaline phosphatase. A significant increase in pulse wave velocity, serum phosphate levels, calcium x phosphate product and serum alkaline phosphatase levels were noted in calcitriol-based treatment group with no significant change in serum calcium and parathyroid hormone levels. Our findings revealed superiority of paricalcitol than calcitriol based vitamin D receptor activator therapy in terms of serum phosphate levels, CaxP product, dose requirement for vitamin D and the control of pulse wave velocity.

Serum levels of Nitric Oxide metabolites in relation to Body Mass Index and Arterial stiffness in young individuals

Introduction: Obesity is a multi-factorial disorder defined as abnormally high levels of body fat accumulation. It is a major emerging pandemic of this century which can be attributed to alterations in eating habits, lifestyle choices and rise in sedentary behaviour. The activation of pro-inflammatory signalling pathways linked to obesity can result in vascular endothelial dysfunction and changed levels of Nitric oxide (NO). Hyperlipidaemia may exacerbate arterial stiffness which is a precursor to atherosclerosis. In this study, we tried to evaluate the changes in levels of nitric oxide in obese individuals and its association with arterial stiffness. Objectives: To identify the association of serum levels of Nitric oxide metabolites with Body Mass Index (BMI) in apparently healthy subjects. To evaluate any correlation between serum nitric oxide metabolites, BMI and arterial stiffness in obese individuals. Result: The results showed a significant increase in systolic blood pressure (p&lt;0.001) and no change in diastolic blood pressure and significant increase in pulse pressure(p&lt;0.001) with increase in visceral adiposity (Waist Circumference) more than BMI. Results of Pearson correlation indicated that there is a significant small negative relationship between BMI and Serum NO levels, (r =- 0.534, p &lt;.001). There was significant increase in Brachial ankle Pulse Wave Velocity (Ba PWV) (p=0.001) and Carotid Femoral Pulse Wave Velocity (CF PWV) (p=0.01) in obese subjects when compared to controls. Conclusion: Our study results showed that abdominal obesity more than overall obesity is more strongly associated with decreased serum NO levels and increased arterial stiffness. In obese individuals, increased arterial stiffness as reflected by increased pulse wave velocity may contribute to predicting cardiovascular disease in both genders in addition to development of hypertension.

PS-BPB01-8: IMPACT OF DIFFERENT DIURETIC TYPES ON ARTERIAL STIFFNESS AND CALCIFICATION IN A RAT MODEL OF CHRONIC KIDNEY DISEASE

Introduction: We reported that antihypertensive therapy with a hydrochlorothiazide (HCTZ)-based regimen aggravates arterial stiffness and vascular calcification in a rat model of chronic kidney disease (CKD) with mineral and bone disorder (MBD). In this study, we investigated whether the aggravation of arterial stiffness and vascular calcification in CKD-MBD rats is induced by HCTZ and whether these abnormalities could also occur with other types of diuretic currently used in clinic. Methods: In rats with renal mass ablation-induced CKD, MBD was generated by a Ca/P-rich diet and calcitriol supplementation. The animals were divided into 4 groups; 1) CKD-MBD control; 2) CKD-MBD + HCTZ (thiazide diuretic, 5 mg/kg/d); 3) CKD-MBD + Chlorthalidone (thiazide-like diuretic, 5 mg/kg/d), and; 4) CKD-MBD + Furosemide (loop diuretics, 10 mg/kg/d). At week 6, hemodynamic parameters including systolic and mean blood pressure (SBP and MBP), pulse pressure (PP) and pulse wave velocity (PWV) were determined. The thoracic aorta was harvested to assess vascular calcification. Results: SBP was reduced by all types of diuretic in CKD-MBD rats. Contrary to chlortalidone nor furosemide, HCTZ treatment led to a reduction of MBP, but an increase in PP and PWV in CKD-MBD rats (p &lt; 0.05). As expected from these hemodynamic changes, medial calcification in the thoracic aorta was significantly greater in CKD-MBD rats treated with HCTZ as compared to all the other groups of rats (p &lt; 0.05). Conclusion: In rats with CKD-MBD, antihypertensive therapy with the thiazide diuretic HCTZ, but not other types of diuretic, exacerbated arterial stiffness and vascular calcification despite a reduction in SBP. The deleterious effect of HCTZ in CKD-MBD rats may have major clinical impact as this diuretic is widely use in patients with CKD that often develop MBD.