Increase In Arterial Stiffness Research Articles

From Rest to Stressed: Adults with Type 2 Diabetes Exhibit a Greater Exercise‐Induced Increase in Arterial Stiffness and Vessel Hemodynamics

ObjectiveIndividuals with type 2 diabetes mellitus (T2DM) are known to have a greater blood pressure (BP) response to acute maximal exercise. The nature of this exaggerated response is likely a function of vascular abnormalities; therefore, we aimed to examine the exercise‐induced response of carotid‐femoral pulse wave velocity (cfPWV), the gold‐standard measure of arterial stiffness, and other vessel hemodynamic parameters in adults with and without T2DM.MethodsAdults with T2DM (n=77) and without T2DM (n=105) underwent an exercise test to volitional exhaustion on a treadmill (following a modified Bruce protocol). Using applanation tonometry (SphygmoCor), cfPWV and augmentation index corrected for a heart rate (HR) of 75 beats/min (AIx75) were assessed at rest, and immediately following exercise termination. At the same time points, peripheral BP, and HR were measured with an automated oscillometric BP monitor (BPTru). Linear regression models were used to evaluate between‐group differences in parameters at rest, as well as the absolute change of each parameter in response to exercise, with adjustments for exercise time and the baseline value.ResultsMean age was 59.0±11.0 years and body mass index was 31.5±4.0 kg/m2 (non‐significantly different between groups). All subjects had hypertension and were taking anti‐hypertensive medication (mean BP 130±14/80±9 mmHg). At rest, subjects with T2DM had significantly higher cfPWV (10.2±2.5 vs. 9.3±1.8 m/s), HR (70±12 vs. 66±10 beats/min), and lower diastolic BP (80±9 vs. 83±9 mmHg), but no significant difference in systolic BP (118±14 vs. 121±12 mmHg) or AIx75 (23±9 vs. 23±10%). In response to exercise, subjects with T2DM had a significantly greater increase in cfPWV by 1.3 m/s (95% CI 0.1, 2.4), systolic BP by 11.2 mmHg (95% CI 2.9, 19.5) and pulse pressure (PP) by 5.63 mmHg (95%CI 0.19, 11.08). A greater number of subjects with T2DM had a hypertensive (systolic BP>210 mmHg in men, and >190 mmHg in women) response to exercise (n=31, 30%) compared to subjects without T2DM (n=14, 18%). The increase in AIx75 was significantly lower in subjects with T2DM by 2.6% (95% CI −4.9, −0.2).ConclusionBy incorporating exercise as a vascular stressor, we provide evidence of a greater increase in arterial stiffness, independently of exercise time and resting arterial stiffness. Despite no differences in systolic BP or PP at rest, we observed an exaggerated systolic BP response in subjects with T2DM, and importantly an altered arterial stiffness response to acute exercise. Therefore, evaluating the exercise‐induced response of arterial stiffness and hemodynamic parameters may serve as a useful model for evaluating vascular impairment and CVD risk in adults with T2DM.Support or Funding InformationThis work was funded by the Canadian Institutes of Health Research (CIHR). KD and SSD hold salary awards from the Fonds de recherche du Québec‐Santé. ABC holds a PhD award from CIHR.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Hookah Smoking Causes an Acute Adverse Effect on Arterial Stiffness and Wave Reflections in Young Adults

Hookah (waterpipe) smoking is a centuries‐old, revived yet understudied epidemic of tobacco use. Despite being heavily advertised and glamorized in the media as a healthier alternative to cigarettes, the toxicology of hookah smoke suggest otherwise. Cigarette smoking unequivocally causes an acute increase in arterial stiffness, but whether hookah does the same is unknown. In 48 young healthy habitual hookah but not cigarette smokers, we measured heart rate, peripheral and central blood pressure, carotid‐femoral pulse wave velocity (measure of arterial stiffness), aortic augmentation index (measure of wave reflection), plasma nicotine, and exhaled carbon monoxide (CO) before and after 30 minutes of ad lib hookah smoking. Hookah smoking increased heart rate by +16 ± 1 beats/min and mean brachial arterial pressure by +6 ± 1 mmHg (both p < 0.05, mean ± SE). Most importantly, it increased carotid‐femoral pulse wave velocity and aortic augmentation index by +0.66 ± 0.09 m/s−1and +8.76 ± 3.99%, respectively (p <0.05, mean ± SE), denoting increased acute arterial stiffness. These vascular effects were accompanied by increases in plasma nicotine concentration (+5.8 ± 1.2 ng/ml, p<0.05) and expired CO (+25.44 ± 1.68 ppm, p< 0.05). All these parameters were unchanged during time‐control studies (n=14). Thus, in contrast to effective media marketing of hookah as a safer alternative to cigarettes, the present study shows for the first time that in young adult hookah smokers, a single hookah smoking session causes an acute increase in arterial stiffness of comparable magnitude to what has been previously reported for cigarettes. Further research is warranted to determine whether habitual hookah smoking accelerates the age‐dependent development of hypertension and its cardiovascular complications.Support or Funding InformationThis study was funded by the Tobacco‐Related Disease Research Program to Dr. Mary Rezk‐ Hanna (#23DT‐0102) and Dr. Ronald Victor (#22XT‐0017).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Influence of Aging on Central Artery Stiffness and Cerebral Vascular Function Following an Acute Hypertensive Stimulus

Aging decreases cerebral blood flow and increases cerebral pulsatility. High‐intensity resistance exercise (RE) has been shown to acutely increase blood pressure (BP) and reduce cerebral blood velocity (CBv), resulting in greater flow pulsatility in the cerebral circulation, potentially injuring cerebral microvasculature. Understanding the relationship between aging and cerebral blood flow regulation in response to a hypertensive physiological stress (e.g. RE), is important due to its association with increased risk of cerebrovascular events in older adults.ObjectiveTo examine the effect of age on cerebral blood flow dynamics following acute RE in young and older adults.MethodsYoung (n=35, 26 yrs, BMI: 23.8 kg/m2) and older (n=26, 60 yrs, BMI: 30.1 kg/m2) adults performed maximal leg‐extension/flexion RE (3×10 rep), with hemodynamic measurements obtained pre and post‐RE (immediate, 5‐, 30‐min). CBv was measured via transcranial Doppler. Central pulse wave velocity (PWV) was acquired by an automated ambulatory BP cuff. Common carotid artery beta‐stiffness index (β) and blood flow pulsatility were measured by ultrasonography. Continuous beat‐to‐beat heart rate (HR), cardiac output (Q), blood pressure (SBP, DBP, MAP, PP) and end‐tidal CO2 were also measured.ResultsMean and diastolic CBv increased immediately post‐RE in the young (interaction, p<0.05) and decreased below baseline at 5‐min post‐RE (p<0.05) in both groups. Older adults had a greater increase in CBv pulsatility immediate post‐RE (interaction, p<0.05) compared to the young, but continued to rise at 5‐min post‐RE only in the young (interaction, p<0.05). MAP was higher and carotid pulsatility was lower in the older group and increased immediate post‐RE (p<0.05) in both groups. PWV increased immediate post‐RE (p<0.05), and remained elevated at 5‐min post‐RE in the young (interaction, p<0.05). There were no changes in β.ConclusionsImmediately following the cessation of the hypertensive stimulus, an increase in aortic arterial stiffness and BP occurred, accompanied by an increase in carotid and cerebral pulsatility. Despite obtaining higher BP during the stimulus in the older group, mean and diastolic CBv did not increase post‐RE, resulting in greater cerebral pulsatility in older adults. This differential age response indicates reduced cerebral hemodynamic responsiveness to an acute increase in BP with aging.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Effects of Sympathetic Activation on Aortic Stiffness in Young Healthy and Hypertensive Adults

Aortic stiffness is a major link between hypertension and cardiovascular risk. Anatomic features of the artery including the smooth muscle regulate aortic stiffness, in part. Importantly, vascular smooth muscle is under sympathetic nervous system control, and thus aortic stiffness may be influenced by the sympathetic nervous system. When exposed to physiological stress, older hypertensive adults demonstrate an exaggerated blood pressure response that may correspond with transient arterial stiffness increases, but this response in young hypertensive adults remains unknown.PURPOSEWe tested the hypothesis that sympathetic activation would increase aortic stiffness in young healthy adults (control, CTL), and that aortic stiffness increases during sympathetic activation would be greater in young hypertensive adults (HTN).METHODSSix healthy controls (males=4, females=2; 28.3±5.5 years; BMI: 23.5 ± 3.5 kg/m2) and three young hypertensive participants (males=2, females=1; 28.3±6.0 years; BMI: 30.3±8.2 kg/m2) were studied. Mean arterial pressure (MAP) and carotid‐femoral pulse wave velocity (PWV) were measured at rest and during 5 min of brachial circulatory occlusion (sympathetic activation condition) that followed isometric handgrip exercise.RESULTSResting MAP was higher in HTN (100±6 mmHg) than CTL (90±5 mmHg; P=.029). Occlusion MAP was also higher in HTN (116±6 mmHg) than CTL (102±7 mmHg; P=.016). Resting PWV was similar between CTL (8.6±1.6 m/s) and HTN (8.1±0.1 m/s; P=.47). The increase in PWV from rest to occlusion (1.2±1.4 m/s) in CTL was not significant (P=.09), whereas the increase in PWV from rest to occlusion (2.0±0.4 m/s) in HTN was significant (P=.01).CONCLUSIONSympathetic activation may significantly increase aortic stiffness in young hypertensive adults, but not young healthy adults.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Acute effects of repeated bouts of aerobic exercise on arterial stiffness after glucose ingestion

ABSTRACTThe aim of this study was to investigate the acute repeated bouts of aerobic exercise decrease leg arterial stiffness. However, the influence of repeated bouts of aerobic exercise on arterial stiffness after glucose ingestion is unknown. The present study investigates the acute effects of repeated bouts of aerobic exercise on arterial stiffness after the 75-g oral glucose tolerance test (OGTT). Ten healthy young men (age, 23.2 ± 0.9 years) performed repeated bouts of aerobic exercise trial (RE, 65% peak oxygen uptake; two 15 min bouts of cycling performed 20 min apart) and control trial (CON, seated and resting in a quiet room) at 80 min before the 75-g OGTT on separate days in a randomized, controlled crossover fashion. Carotid-femoral (aortic) and femoral-ankle (leg) pulse wave velocity, carotid augmentation index, brachial and ankle blood pressure, heart rate and blood glucose and insulin levels were measured before (baseline) and 30, 60 and 120 min after the 75-g OGTT. Leg pulse wave velocity, ankle systolic blood pressure and blood glucose levels increased from baseline after the 75-g OGTT in the CON trial, but not in the RE trial. The present findings indicate that acute repeated bouts of aerobic exercise before glucose ingestion suppress increases in leg arterial stiffness following glucose ingestion.Abbreviations: RE trial repeated bouts of aerobic exercise trial; CON trial control trial; BG blood glucose; VO2peak peak oxygen uptake; PWV Pulse wave velocity; AIx carotid augmentation index; BP blood pressure; HR heart rate; CVs coefficients of variation; RPE Ratings of perceived exertion; SE standard error

Assessment of Arterial Stiffness in Stable Heart Transplant Recipients

IntroductionArterial stiffness depends on both genetic and environmental factors. The aim of this study was to assess arterial stiffness in patients after heart transplant. MethodsThe study was conducted between May and June 2017. Fifty patients from the Transplantology Clinic of the Institute of Cardiology in Anin, Warsaw, Poland, were enrolled in the study. Pulse wave velocity (PWV), central systolic blood pressure (CSBP), and central diastolic blood pressure (CDBP) were measured and patients' medical records were also analyzed. ResultsIn the study, 50 patients aged 57.9 years on average were evaluated, of whom 88% were male patients, with average PWV of 8.94 m/s and an average time after transplant of 9.7 years. The study has shown that age (R = 0.77), total cholesterol concentration (R = 0.22, P = .017) and creatinine concentration (R = 0.34; P = .15) show positive correlation with PWV. ConclusionsOur data indicates that age has significant impact on arterial stiffness and the type of immunosuppressive drugs and transplant rejection episodes do not impact an increase in arterial stiffness.

Longitudinal Assessment of Vascular Function With Sunitinib in Patients With Metastatic Renal Cell Carcinoma.

Sunitinib, used widely in metastatic renal cell carcinoma, can result in hypertension, left ventricular dysfunction, and heart failure. However, the relationships between vascular function and cardiac dysfunction with sunitinib are poorly understood. In a multicenter prospective study of 84 metastatic renal cell carcinoma patients, echocardiography, arterial tonometry, and BNP (B-type natriuretic peptide) measures were performed at baseline and at 3.5, 15, and 33 weeks after sunitinib initiation, correlating with sunitinib cycles 1, 3, and 6. Mean change in vascular function parameters and 95% confidence intervals were calculated. Linear regression models were used to estimate associations between vascular function and left ventricular ejection fraction, longitudinal strain, diastolic function (E/e'), and BNP. After 3.5 weeks of sunitinib, mean systolic blood pressure increased by 9.5 mm Hg (95% confidence interval, 2.0-17.1; P=0.02) and diastolic blood pressure by 7.2 mm Hg (95% confidence interval, 4.3-10.0; P<0.001) across all participants. Sunitinib resulted in increases in large artery stiffness (carotid-femoral pulse wave velocity) and resistive load (total peripheral resistance and arterial elastance; all P<0.05) and changes in pulsatile load (total arterial compliance and wave reflection). There were no statistically significant associations between vascular function and systolic dysfunction (left ventricular ejection fraction and longitudinal strain). However, baseline total peripheral resistance, arterial elastance, and aortic impedance were associated with worsening diastolic function and filling pressures over time. In patients with metastatic renal cell carcinoma, sunitinib resulted in early, significant increases in blood pressure, arterial stiffness, and resistive and pulsatile load within 3.5 weeks of treatment. Baseline vascular function parameters were associated with worsening diastolic but not systolic function.

Influence of physical inactivity on arterial compliance during a glucose challenge.

What is the central question of this study? To understand better the effects of acute hyperglycaemia on arterial stiffness in healthy young individuals, we assessed arterial stiffness in physically active men before and after reduced ambulatory physical activity to decrease insulin sensitivity. What is the main finding and its importance? During an oral glucose tolerance test, we identified an increase in leg arterial stiffness (i.e. reduced femoral artery compliance) only when subjects were inactive for 5days (<5000stepsday-1 ) and not when they were engaging in regular physical activity (>10,000stepsday-1 ). These results demonstrate the deleterious consequence of acute reductions in daily physical activity on the response of the peripheral vasculature to acute hyperglycaemia. Acute hyperglycaemia has been shown to augment indices of arterial stiffness in patients with insulin resistance and other co-morbidities; however, conflicting results exist in healthy young individuals. We examined whether acute hyperglycaemia after an oral glucose tolerance test (OGTT) increases arterial stiffness in healthy active men before and after reduced ambulatory physical activity to decrease insulin sensitivity. High-resolution arterial diameter traces acquired from Doppler ultrasound allowed an arterial blood pressure (BP) waveform to be obtained from the diameter trace within a cardiac cycle. In 24 subjects, this method demonstrated sufficient agreement with the traditional approach for assessing arterial compliance using applanation tonometry. In 10men, continuous recordings of femoral and brachial artery diameter and beat-to-beat BP (Finometer) were acquired at rest, 60 and 120min of an OGTT before and after 5days of reduced activity (from >10,000 to<5000stepsday-1 ). Compliance and β-stiffness were quantified. Before the reduction in activity, the OGTT had no effect on arterial compliance or β-stiffness. However, after the reduction in activity, femoral compliance was decreased (rest, 0.10±0.03mm2 mmHg-1 versus 120min OGTT, 0.06±0.02mm2 mmHg-1 ; P<0.001) and femoral β-stiffness increased (rest, 8.7±2.7a.u. versus 120min OGTT, 15.3±6.5a.u.; P<0.001) during OGTT, whereas no changes occurred in brachial artery compliance (P=0.182) or stiffness (P=0.892). Insulin sensitivity (Matsuda index) was decreased after the reduction in activity (P=0.002). In summary, in young healthy men the femoral artery becomes susceptible to acute hyperglycaemia after 5days of reduced activity and the resultant decrease in insulin sensitivity, highlighting the strong influence of daily physical activity levels on vascular physiology.

The effect of creatine supplementation on the response of central and peripheral pulse wave velocity to high-intensity resistance exercise

Following a bout of high-intensity resistance exercise, a transient increase in arterial stiffness, as measured through central pulse wave velocity has been shown to occur. Preliminary creatine sup...

Role of β2- and β3-adrenoceptors in arterial stiffness in a state of hypertension

An increase in arterial stiffness is associated with a high risk for morbidity and mortality in a state of elevated systemic pressure. The sympathetic nervous system plays an important role in the regulation of vascular tone via activation of β-adrenoceptors. The aim of this investigation was to determine the involvement of β-adrenoceptors in the control of arterial stiffness in a state of hypertension versus normotension. Pulse wave velocity (PWV), an index of vascular stiffness, was assessed in isoflurane-anaesthetized 13–14-week-old male spontaneously hypertensive (SH) and Wistar-Kyoto (WKY) rats. At baseline, PWV was significantly higher in SH (9.2±0.9m/s) compared to WKY rats (6.7±0.4m/s). The stimulation of β2- but not β3-adrenoceptors significantly reduced PWV in SH rats despite comparable reductions in blood pressure. Stimulation of β2- or β3-adrenoceptors did not reduce PWV in WKY rats. The administration of sodium nitroprusside (SNP) also significantly reduced PWV in SH but not WKY rats. Immunofluorescence revealed the expression of β2- and β3-adrenoceptors in endothelial cells and vascular smooth muscle cells of the abdominal aorta. There were no significant differences in the distribution of the expression of β2- and β3-adrenoceptors in endothelial and/or smooth muscle cells in blood vessels of SH compared to WKY rats. The evidence suggests that β2-adrenoceptor stimulation and SNP infusion reduce PWV independently from reduction in blood pressure in a state of high systemic arterial pressure. A reduction in vascular tone of the central arteries may play a key role in decreasing PWV that is elevated due to stiffer arterial wall.

Abnormal pressure wave reflection accelerates the development of hypertension via the increase of arterial stiffness

ObjectivesIt is noted that not only arterial stiffness but also abnormal pressure wave reflection are risks for the development of hypertension. However, the association between arterial stiffness and pressure wave reflection in the development of hypertension has not been fully clarified. The present study was conducted to examine whether the abnormal pressure wave reflection accelerates the development of hypertension via the increase of arterial stiffness.MethodsIn 3102 middle-aged healthy Japanese men without hypertension at baseline, systolic/diastolic blood pressures, brachial-ankle pulse wave velocity (baPWV), and radial augmentation index (rAI) were annually measured during a 9-year study period.ResultsIn multivariate linear regression analysis and in mixed model linear regression analysis, baPWV was not longitudinally associated with rAI. Linear regression analysis demonstrated that the higher rAI at the baseline was associated with the larger longitudinal increase of baPWV (beta = 0.17, p < 0.01). At the end of study period, 404 subjects were developed to hypertension. The prevalence rate of the development of hypertension during the study period was higher in subjects with higher baPWV and higher rAI at the baseline (220 in 939 subjects: 23%) than that in other 3 groups classified by the status of baPWV and rAI at the baseline (e.g. 52 in 942 subjects with low baPWV combined with low rAI: 6%, p < 0.01).ConclusionThe abnormal pressure wave reflection, which may be derived from both arterial stiffness and peripheral vascular damages, may be an accelerator for the development of hypertension via the increase of arterial stiffness.

Effects of endothelin-related gene polymorphisms and aerobic exercise habit on age-related arterial stiffening: a 10-yr longitudinal study.

Increased arterial stiffness has emerged as a strong predictor of future cardiovascular events and all-cause mortality. The aim of this study was to elucidate influences of endothelin (ET)-related genetic polymorphisms and regular physical activity on age-related arterial stiffening through a 10-yr longitudinal study. A decadal change in brachial-ankle pulse wave velocity (baPWV), an index of arterial stiffness, was evaluated retrospectively among 92 volunteers (63 ± 14 yr, 51 men). The targeted single-nucleotide polymorphisms were ET-A receptor SNP rs5333 (ET-A) and ET-B receptor SNP rs5351 (ET-B). Subjects with either ET-A TC or CC genotypes exhibited significantly greater increases in baPWV (+15.3 ± 11.7 and +16.6 ± 15.7%/dec, respectively) than ET-A TT genotype holders (+9.2 ± 9.0%/dec), whereas subjects with the ET-B GG genotype showed a significantly greater increase in baPWV (+17.7 ± 14.1%/dec) than other ET-B genotype holders (AA: +9.5 ± 10.0%/dec; AG: +11.2 ± 9.6%/dec). The combination of these ET-related genetic risks was associated with a 2.4 times greater decadal increase in baPWV compared with no genetic risk (+8.1 ± 8.4 vs. 19.5 ± 16.0%/dec). In contrast, individuals engaging in >15 METs·h/wk of aerobic exercise showed substantially smaller increases in baPWV (+5.0 ± 9.7%/dec) compared with their physically inactive peers (approximately +13%/dec). These differences remained significant after adjusting for confounding factors, including baseline baPWV and ET-related genotype risk. Our current longitudinal study found that ET-related gene polymorphisms contribute to diverse age-related changes in arterial stiffness, and that regular sufficient aerobic exercise attenuates the age-related arterial stiffening independently of ET-related gene polymorphisms. NEW & NOTEWORTHY This 10-yr longitudinal study suggests that endothelin-related gene polymorphisms contribute to divergent increases in arterial stiffness with advancing age, whereas regular sufficient aerobic exercise attenuates age-related arterial stiffening independently of ET-related gene polymorphisms. This notion partly supports prevailing evidence that regular aerobic exercise contributes to a lower incidence of cardiovascular disease.

Gender-specific association of metabolic syndrome and its components with arterial stiffness in the general Chinese population.

ObjectivesMetabolic syndrome (MS) is considered to be a cluster of interrelated risk factors for metabolism, which may increase arterial stiffness and cardiovascular morbidity. The cardio-ankle vascular index (CAVI) is a reliable indicator of arterial stiffness and early arteriosclerosis. The main objective of this study is to evaluate the gender-specific relationship between MS and CAVI in the general Chinese population.MethodsA total of 1,301 subjects aged 20 to 60 years participated in this study. CAVI was measured noninvasively using a Vasera VS-1000 device. Blood samples and waist circumference were examined to identify metabolic syndrome according to the criteria set forth in the 2009 Joint Scientific Statement.ResultsThe prevalence of MS in the study subjects was 17.4% (30.7% in males and 7.0% in females, P < 0.001). CAVI values were significantly higher in MS subjects than in non-MS subjects and increased linearly as the number of MS components increased in females, but not in males. Using multiple regression analysis, we found that BMI was correlated with CAVI in the overall population and in both genders, and that high-density lipoprotein cholesterol (HDL-C) was associated with CAVI in males, while the number of MS components was related to CAVI in females. CAVI values increased linearly with age in both genders (P-trend < 0.001 for both), and this correlation was stronger in males than in females.ConclusionsThere are gender-specific differences in the association of MS and CAVI. First, the effects of the number of MS components on CAVI are stronger in females than in males. Second, the effect of each MS component on arterial stiffness may differ in relation to gender. In addition, aging affects arterial stiffness more severely in males, and the increase in arterial stiffness tends to occur at a younger age in males than in females. Larger samples and longitudinal studies are needed to further confirm our results in the future.

Carotid and Femoral Arterial Wall Distensibility During Long-Duration Spaceflight.

This study aimed to assess changes in common carotid (CA) and superficial femoral (FA) arterial stiffness during long-duration spaceflight. Ultrasound imaging was used to investigate the CA and FA of 10 astronauts preflight (PRE), on flight day 15 (FD15), after 4-5 mo (FD4-5m), and 4 d after return to Earth (R+4). Arterial wall properties were assessed through the calculation of strain, stiffness (β), pressure-strain elastic modulus (Ep), and distensibility (DI). Stiffness indices were assessed for potential correlations to measurements of intima-media thickness (IMT). Significant effects of spaceflight were found for all CA stiffness indices, indicating an increase in arterial stiffness. CA strain was reduced by 34 ± 31% on FD15 and 50 ± 16% on FD4-5m and remained reduced by 42 ± 14% on R+4 with respect to PRE values. On FD4-5m, with respect to PRE values, DI was reduced by 46 ± 25% and β and Ep were increased by 124 ± 95% and 118 ± 92%, respectively. FA arterial stiffness indices appeared to show similar changes; however, a main effect of spaceflight was only found for strain. Correlation analysis showed weak but significant relationships between measurements of CA IMT and arterial stiffness indices, but no relationships were found for FA measurements. The observed change in CA and FA stiffness indices suggest that spaceflight results in an increase in arterial stiffness. That these changes were not strongly related to measurements of IMT suggests the possibility of different mechanisms contributing to the observed results.Arbeille P, Provost R, Zuj K. Carotid and femoral arterial wall distensibility during long-duration spaceflight. Aerosp Med Hum Perform. 2017; 88(10):924-930.

Examination of Arterial Stiffness and Neurodynamics of Middle-Aged Individuals: A Pilot Study

Purpose: Increases in arterial stiffness can result in higher pulse wave velocity (PWV) of the arterial blood leading to arterial vascular disease. Studies have shown high PWV is correlated to poor trunk and hamstring flexibility. Poor trunk and hamstring flexibility has additionally been correlated to the presence of neuropathodynamics (NPD) within the peripheral nervous system. Although the coexistence of poor hamstring flexibility and NPD is clear, a paucity of data exists to suggest any relationship between NPD and increased arterial stiffness. We hypothesized a significant relationship would exist between NPD and increased arterial stiffness. Methods: This was a cross-sectional study. The PWV, blood pressure, range of motion, hamstring flexibility, and neurodynamic response to a straight leg raise was measured in 47 middle-aged adults. Correlation and regression analyses were performed to examine relationships among PWV, age, blood pressure, sex, fitness level, hamstring flexibility, and neurodynamic response. Results: The presence of NPD was found not to be a significant predictor of PWV. Only systolic blood pressure (SBP) (P = .003) and age (P = .012) was found to be significant predictor variables for PWV. Conclusions: The results of this study show no significant relationship between NPD and arterial stiffness. Our findings do, however, indicate that SBP and age should be considered valid predictor variables of underlying arterial vascular disease.

Vimentin knockout results in increased expression of sub-endothelial basement membrane components and carotid stiffness in mice

Intermediate filaments are involved in stress-related cell mechanical properties and in plasticity via the regulation of focal adhesions (FAs) and the actomyosin network. We investigated whether vimentin regulates endothelial cells (ECs) and vascular smooth muscle cells (SMCs) and thereby influences vasomotor tone and arterial stiffness. Vimentin knockout mice (Vim−/−) exhibited increased expression of laminin, fibronectin, perlecan, collagen IV and VE-cadherin as well as von Willebrand factor deposition in the subendothelial basement membrane. Smooth muscle (SM) myosin heavy chain, α-SM actin and smoothelin were decreased in Vim−/− mice. Electron microscopy revealed a denser endothelial basement membrane and increased SM cell-matrix interactions. Integrin αv, talin and vinculin present in FAs were increased in Vim−/− mice. Phosphorylated FA kinase and its targets Src and ERK1/2 were elevated in Vim−/− mice. Knockout of vimentin, but not of synemin, resulted in increased carotid stiffness and contractility and endothelial dysfunction, independently of blood pressure and the collagen/elastin ratio. The increase in arterial stiffness in Vim−/− mice likely involves vasomotor tone and endothelial basement membrane organization changes. At the tissue level, the results show the implication of FAs both in ECs and vascular SMCs in the role of vimentin in arterial stiffening.

Abstract P518: Abnormal Pressure Wave Reflection Accelerates the Development of Hypertension via the Increase of Arterial Stiffness

Objectives: Arterial stiffness (macrovascular damage) and peripheral vascular damage (microvascular damage) affect pressure wave reflection, and several prospective studies have demonstrated that not only arterial stiffness but also abnormal pressure wave reflection are risks for the development of hypertension. However, the association between arterial stiffness and pressure wave reflection in the development of hypertension has not been fully clarified. The present study was conducted to examine whether the abnormal pressure wave reflection accelerates the development of hypertension via the increase of arterial stiffness. Methods: In 3102 middle-aged healthy Japanese men without hypertension at baseline, systolic/diastolic blood pressures, brachial-ankle pulse wave velocity (baPWV), and radial augmentation index (rAI) were annually measured during a 9-year study period. Results: In multivariate linear regression analysis and in mixed model linear regression analysis, baPWV was not longitudinally associated with rAI. Linear regression analysis demonstrated that the higher rAI at the baseline was associated with the larger longitudinal increase of baPWV (beta = 0.17, p&lt;0.01). At the end of study period, 404 subjects were developed to hypertension. Binary logistic regression analysis demonstrated that baPWV (per SD increase = 1.43; 1.25 – 1.62, p&lt;0.01) and rAI (per SD increase = 1.56; 1.33 – 1.82, p&lt;0.01) at the baseline had significant odds ratio for the prediction of the development of hypertension. The prevalence rate of the development of hypertension during the study period was higher in subjects with higher baPWV and higher rAI at the baseline (220 in 939 subjects: 23 %) than that in other 3 groups classified by the status of baPWV and rAI at the baseline (e.g. 52 in 942 subjects with low baPWV combined with low rAI: 6%, p&lt;0.01). Conclusion: The abnormal pressure wave reflection, which may be derived from both arterial stiffness and peripheral vascular damages, may be an accelerator for the development of hypertension via the increase of arterial stiffness. In there, the combination of macro- and micro-vascular damages may accelerate the development of hypertension.

Abstract P516: Arterial Stiffness is a Mediator of Uric Acid-related Development of Hypertension

Objectives: Uric acid (UA) is a risk for the development of hypertension, but the underlying mechanisms of this development has not been fully clarified. On the other hand, arterial stiffness is also noted as a risk for the development of hypertension. Then, the present prospective observational study examined whether UA is associated with the development of hypertension mediated by the increase of arterial stiffness. Methods and Results: In 3274 middle-aged Japanese men (aged 42 ± 9 years old) without hypertension at the study baseline, the brachial-ankle pulse wave velocity (baPWV), radial augmentation index (rAI), systolic and diastolic blood pressure (SBP/DBP) and serum UA level were measured annually over a 9-year period. During this study period, 474 subjects (14.5%) developed hypertension. Binary logistic regression analysis demonstrated that serum UA levels has a significant odds ratio for the development of hypertension even after the adjustment [1.3 (1.1-1.5), p&lt;0.01]. Multivariate linear regression analysis also demonstrated that serum UA levels at the baseline of study period had a significant association with delta changes of SBP (beta=0.10 p&lt;0.01), DBP (beta = 0.13, p&lt;0.01) and baPWV (beta=1.12 p&lt;0.01), but not that of rAI, during the study period. Mixed model linear regression analysis in repeated measurement data revealed the following: 1) At each annual measurement, higher serum UA levels were associated with a higher annual increase of the SBP (estimate=0.63 p&lt;0.01), DBP (estimate=0.63 p&lt;0.01) and baPWV (estimate=6.70 p&lt;0.01). Mediation analysis demonstrated that baPWV had a significant indirect effect on the association of UA at the baseline with the delta change of SBP (indirect effect = 0.03 p&lt;0.01). Conclusion: UA is a risk for the development of hypertension. In there, UA may elevate blood pressure via increase in arterial stiffness, at least in parts.

Abstract P454: Does Intensive Pulse Pressure control results in lower rates of cardiovascular events? An Analysis of Systolic BP Intervention Trial (SPRINT) database

Introduction: A wide pulse pressure (PP) is a marker of increased artery stiffness and high cardiovascular risk. A high PP may reflect already diseased arterial walls, with several adverse cardiac implications of potential prognostic value. Previous studies show that arterial stiffness is itself an independent predictor of the risk of all-cause mortality, cardiovascular mortality, coronary events and stroke in hypertensive subjects. No guidelines exist regarding tight pulse pressure in chronic hypertension population. Method: For the purpose of our study, we examined SPRINT data collected between November 2010 and August 2015. The role of PP and DBP was studied as a qualitative parameter with separation according to the 4 quartiles defined in the studied population. We then combined the results of both PP and DBP in conjunction with preexistence intensive vs. control arm for further analysis. Results: Our secondary analysis of SPRINT data first confirmed NEJM article that intensive SBP control reduced rates of heart failure (HF), CVD death, Death from any cause, and SPRINT primary outcome or death. There was a significant difference in primary outcome in each PP quartile. Higher PP quartiles were more likely to have higher rate of MI, stroke, HF, CVD death, and SPRINT primary outcome or death. There also a significant increase in SPRINT primary outcome and Heart Failure when DBP &lt;70 in the intensive treatment arm. Finally, SPRINT data has confirmed that participants in PP 1 and PP 2 with DBP &gt; 70 have significant lower rate of SPRINT primary outcome and death compared to other group regardless of treatment arm. Conclusion: In the SPRINT database of 9347 participants, we found that higher PP conferred an increased risk for multiple adverse cardiovascular event. Our study is among the largest US studies of PP and adds further support to the prognostic utility of PP. In addition, the SPRINT database offers a contemporary analysis of the relationship between PP and DBP, which is important given that nature pathophysiology of blood pressure. Current study also strengthen the possibility that DBP &lt;70 mm Hg was associated with a higher rate of cardiac events.

Magnetic resonance imaging reveals elevated aortic pulse wave velocity in obese and overweight adolescents.

The aortic pulse wave velocity (PWV) measured via cardiac magnetic resonance (CMR) can be used to non-invasively assess changes in arterial stiffness and potential underlying vascular dysfunction. This technique could unmask early arterial dysfunction in overweight and obese youth at risk for cardiovascular disease. We sought to determine the association between vascular stiffness, percentage body fat, body mass index (BMI), and cardiac function in adolescents across the weight spectrum through both CMR and standard applanation tonometry (AT)-based PWV measurements. PWV and left-ventricular cardiac function were assessed using 3.0 T CMR in obese and overweight (OB/OW) participants (n = 12) and controls (n = 7). PWV was also estimated via carotid-femoral AT. OB/OW participants did not differ from healthy-weight controls regarding cardiometabolic risk factors or physical activity levels, but there was a trend towards higher levels of triglycerides in obese/overweight participants (P = 0.07). Mean PWV was higher in obese participants when corrected for age and sex (P = 0.01), and was positively associated with BMI (β = 0.51, P = 0.02). PWV estimated through AT was not significantly different between groups. Cardiac function measured by left-ventricular ejection fraction z-score was inversely associated with mean PWV (β = -0.57, P = 0.026). Increasing arterial stiffness and decreasing cardiac function were evident among our overweight and obese cohort. PWV estimated by CMR could detect early increases in arterial stiffness vs. traditional AT measurements of PWV.