The effect of cardiorespiratory fitness and habitual physical activity on cardiovascular responses to 2 h of uninterrupted sitting.

Prolonged uninterrupted sitting of >3 h has been shown to acutely cause central and peripheral cardiovascular dysfunction. However, individuals rarely sit uninterrupted for >2 h, and the cardiovascular response to this time is currently unknown. In addition, while increased cardiorespiratory fitness (CRF) and habitual physical activity (HPA) are independently associated with improvements in central and peripheral cardiovascular function, it remains unclear whether they influence the response to uninterrupted sitting. This study sought to 1) determine whether 2 h of uninterrupted sitting acutely impairs carotid-femoral pulse wave velocity (cfPWV), femoral ankle PWV (faPWV), and central and peripheral blood pressure and 2) investigate the associations between CRF and HPA versus PWV changes during uninterrupted sitting. Following 2 h of uninterrupted sitting, faPWV significantly increased [mean difference (MD) = 0.26 m·s-1, standard error (SE) = 0.10, P = 0.013] as did diastolic blood pressure (MD = 2.83 mmHg, SE = 1.08, P = 0.014), however, cfPWV did not significantly change. Although our study shows 2 h of uninterrupted sitting significantly impairs faPWV, neither CRF (r = 0.105, P = 0.595) nor HPA (r = -0.228, P = 0.253) was associated with the increases.NEW & NOTEWORTHY We demonstrate that neither cardiorespiratory fitness nor habitual physical activity influence central and peripheral cardiovascular responses to a 2-h bout of uninterrupted sitting in healthy young adults.

Estimating pulse wave velocity from the radial pressure wave using machine learning algorithms.

One of the European gold standard measurement of vascular ageing, a risk factor for cardiovascular disease, is the carotid-femoral pulse wave velocity (cfPWV), which requires an experienced operator to measure pulse waves at two sites. In this work, two machine learning pipelines were proposed to estimate cfPWV from the peripheral pulse wave measured at a single site, the radial pressure wave measured by applanation tonometry. The study populations were the Twins UK cohort containing 3,082 subjects aged from 18 to 110 years, and a database containing 4,374 virtual subjects aged from 25 to 75 years. The first pipeline uses Gaussian process regression to estimate cfPWV from features extracted from the radial pressure wave using pulse wave analysis. The mean difference and upper and lower limits of agreement (LOA) of the estimation on the 924 hold-out test subjects from the Twins UK cohort were 0.2 m/s, and 3.75 m/s & -3.34 m/s, respectively. The second pipeline uses a recurrent neural network (RNN) to estimate cfPWV from the entire radial pressure wave. The mean difference and upper and lower LOA of the estimation on the 924 hold-out test subjects from the Twins UK cohort were 0.05 m/s, and 3.21 m/s & -3.11m/s, respectively. The percentage error of the RNN estimates on the virtual subjects increased by less than 2% when adding 20% of random noise to the pressure waveform. These results show the possibility of assessing the vascular ageing using a single peripheral pulse wave (e.g. the radial pressure wave), instead of cfPWV. The proposed code for the machine learning pipelines is available from the following online depository (https://github.com/WeiweiJin/Estimate-Cardiovascular-Risk-from-Pulse-Wave-Signal).

Respiratory Variations in Peak Peripheral Artery Velocities and Waveforms for Rapid Assessment of Fluid Responsiveness in Traumatic Shock Patients.

BACKGROUND This study aimed to assess the correlation between the variability of the end-inspiratory and end-expiratory blood flow waveform and fluid responsiveness (FR) in traumatic shock patients who underwent mechanical ventilation by evaluating peripheral arterial blood flow parameters. MATERIAL AND METHODS A cohort of 60 patients with traumatic shock requiring mechanical ventilation-controlled breathing received ultrasound examinations to assess the velocity of carotid artery (CA), femoral artery (FA) and brachial artery (BA). A rehydration test was performed in which of 250 mL of 0.9% saline was administered within 30 min between the first and second measurement of cardiac output by echocardiography. Then, all patients were divided into 2 groups, a responsive group (FR+) and a non-responsive group (FR-). The velocity of end-inspiratory and end-expiratory peripheral arterial blood flow of all patients was ultrasonically measured, and the variability were measured between end-inspiratory and end-expiratory. RESULTS The changes in the end-inspiratory and end-expiratory carotid artery blood flow velocity waveforms of the FR+ groups were significantly different from those of the FR- group (P<0.001). A statistically significant difference in ΔVmax (CA), ΔVmax (BA), and ΔVmax (FA) between these 2 groups was found (all P<0.001). The ROC curve showed that DVmax (CA) and ΔVmax (BA) were more sensitive values to predict FR compared to ΔVmax (FA). The sensitivity of ΔVmax (CA), ΔVmax (FA), and ΔVmax (BA) was 70.0%, 86.7%, and 93.3%, respectively. CONCLUSIONS The study showed that periodic velocity waveform changes in the end-inspiratory and end-expiratory peripheral arterial blood flow can be used for quick assessment of fluid responsiveness.

Cardiovascular Responses to Muscle Stretching: A Systematic Review and Meta-analysis.

The aim of this study will be to review the current body of literature to understand the effects of stretching on the responses of the cardiovascular system. A literature search was performed using the following databases: Scopus, NLM Pubmed and ScienceDirect. Studies regarding the effects of stretching on responses of the cardiovascular system were investigated. Outcomes regarded heart rate(HR), blood pressure, pulse wave velocity (PWV of which baPWV for brachial-ankle and cfPWV for carotid-femoral waveforms), heart rate variability and endothelial vascular function. Subsequently, the effects of each outcome were quantitatively synthetized using meta-analytic synthesis with random-effect models. A total of 16 studies were considered eligible and included in the quantitative synthesis. Groups were also stratified according to cross-sectional or longitudinal stretching interventions. Quality assessment through the NHLBI tools observed a "fair-to-good" quality of the studies. The meta-analytic synthesis showed a significant effect of d=0.38 concerning HR, d=2.04 regarding baPWV and d=0.46 for cfPWV. Stretching significantly reduces arterial stiffness and HR. The qualitative description of the studies was also supported by the meta-analytic synthesis. No adverse effects were reported, after stretching, in patients affected by cardiovascular disease on blood pressure. There is a lack of studies regarding vascular adaptations to stretching.

Arterial elasticity, endothelial function and intracranial vascular health: A multimodal MRI study.

Vascular dysfunctions, including arterial stiffness and endothelial dysfunction, are prevalent in hypertensive subjects. We aimed to study their relations to subclinical intracranial vascular health in this study. A total of 200 older hypertensive males without overt cardiovascular or cerebrovascular diseases were recruited. Arterial elasticity was measured as carotid-femoral pulse wave velocity (cfPWV) and endothelial function was measured as digital reactive hyperemia index (RHI). Cerebrovascular health was evaluated using MRI in four aspects: intracranial atherosclerosis, brain perfusion as cerebral blood flow (CBF), vascular rarefaction analyzed as visible arterial branches on angiography using a custom-developed analysis technique and small vessel disease measured as white matter hyperintensity (WMH). There was a significant negative association between cfPWV and CBF, suggesting a link between arterial stiffness and CBF decline. Higher cfPWV was also associated with presence of intracranial stenotic plaque and greater WMH volume. RHI was positively related to CBF, indicating that endothelial dysfunction was associated with reduced CBF. All the associations remained significant after adjustment for confounding variables. Arterial stiffness and endothelial dysfunction are associated with reduced brain perfusion in older hypertensive males. Arterial stiffness is also associated with global cerebral vascular injury, affecting both small and medium-to-large arteries.

Arterial Stiffness and Left Ventricular Diastolic Function in Endurance Athletes.

The present study investigated the relationship between arterial stiffness and left ventricular diastolic function in endurance-trained athletes. Sixteen young male endurance-trained athletes and nine sedentary of similar age men participated in this study. Resting measures in carotid-femoral pulse wave velocity were obtained to assess arterial stiffness. Left ventricular diastolic function was assessed using 2-dimensional echocardiography. The athletes tended to have lower arterial stiffness than the controls (P=0.071). Transmitral A-waves in the athletes were significantly lower (P=0.018) than the controls, and left ventricular mass (P=0.034), transmitral E-wave/A-wave (P=0.005) and peak early diastolic mitral annular velocity at the septal site (P=0.005) in the athletes were significantly greater than the controls. A significant correlation was found between arterial stiffness and left ventricular diastolic function (E-wave: r=- 0.682, P=0.003, E-wave/A-wave: r=- 0.712, P=0.002, peak early diastolic mitral annular velocity at the septal site: r=- 0.557, P=0.025) in the athletes, whereas no correlation was found in controls. These results suggest that lower arterial stiffness is associated with higher left ventricular diastolic function in endurance-trained athletes.

Systolic Blood Pressure and Longitudinal Progression of Arterial Stiffness: A Quantitative Meta-Analysis.

Background Arterial stiffness predicts the risk of cardiovascular events and all-cause mortality and is associated with age and hypertension. However, the magnitude of the relationship between blood pressure (BP) and progression of arterial stiffness is unclear, limiting our understanding of how arterial stiffness mediates clinical effects of hypertension and planning of clinical trials. Methods and Results Medline and EMBASE were searched for prospective studies reporting linear models between baseline BP and progression of arterial stiffness, with and without adjustment for demographic characteristics and baseline stiffness. Standardized and unstandardized ß coefficients for pulse wave velocity were combined by fixed and random effects meta-analysis, weighted by the inverse variance. Of 566 fully reviewed articles from 30, 524 titles, 22 populations from 21 reports were included. In 9 cohorts, there were consistent, adjusted associations between baseline systolic BP and progression of arterial stiffness (11 781 patients; standardized ß=0.041; 95% CI, 0.026-0.055; P<0.001; P value for heterogeneity=0.70), equivalent to a 1.14-m/s increase in standard carotid-femoral pulse wave velocity per decade per 20-mm Hg systolic BP, independent of age. Unstandardized, adjusted associations were similar (1762 patients; ß=0.0047; 95% CI, 0.004-0.006; P<0.001; P value for heterogeneity=0.64), equivalent to a 0.94-m/s increase per decade per 20-mm Hg systolic BP. In limited studies, standardized associations between mean BP and arterial stiffness progression were not significant and heterogeneous (913 patients; ß=0.039; 95% CI, -0.008 to 0.086; P=0.11; P value for heterogeneity=0.03). Conclusions Baseline systolic BP was associated with a clinically important progression of arterial stiffness, independent of age, providing a reference for the potential effect of arterial stiffness in mediating changes in clinical outcomes associated with hypertension and providing a reference value to aid clinical trial design.

Adults With Type 2 Diabetes Mellitus Exhibit a Greater Exercise-Induced Increase in Arterial Stiffness and Vessel Hemodynamics.

Individuals with type 2 diabetes mellitus (T2DM) have a greater blood pressure (BP) response to acute maximal exercise compared to those without T2DM; however, whether they exhibit a different arterial stiffness response to maximal exercise has yet to be explored. Adults with (n=66) and without T2DM (n=61) underwent an arterial stress test: at rest and immediately postexercise, carotid-femoral pulse wave velocity, the gold standard measure of arterial stiffness, brachial BP, heart rate, and other hemodynamic measurements were assessed. Linear regression models were used to evaluate between-group differences at rest, and the response to exercise (postexercise value), adjusting for covariates including BP and heart rate when relevant, and the corresponding baseline value of each parameter. All participants (mean±SD: age 59.3±10.6 years; body mass index 31.2±3.9 kg/m2) had hypertension (mean BP 130±14/80±9 mm Hg). At rest, participants with T2DM had significantly higher carotid-femoral pulse wave velocity (10.3±2.7 versus 9.1±1.9 m/s), heart rate (69±11 versus 66±10 beats/min), and lower diastolic BP (79±9 versus 83±9 mm Hg), but systolic BP (129±15 versus 131±13 mm Hg) was similar. In response to exercise, participants with T2DM showed greater increases in carotid-femoral pulse wave velocity (1.6 [95% CI, 0.4-2.9 m/s]) and systolic BP (9 [95% CI, 1-17 mm Hg]) than participants without T2DM. A greater proportion of participants with T2DM had a hypertensive response to exercise compared to participants without T2DM (n=23, 35% versus n=11, 18%; P=0.033). By incorporating exercise as a vascular stressor, we provide evidence of a greater increase in arterial stiffness in individuals with T2DM, independently of resting arterial stiffness, and the BP postexercise.

Associations of Arterial Stiffness With Cognitive Performance, and the Role of Microvascular Dysfunction: The Maastricht Study.

The mechanisms underlying cognitive impairment are incompletely understood but may include arterial stiffness and microvascular dysfunction. In the population-based Maastricht Study, we investigated the association between arterial stiffness and cognitive performance, and whether any such association was mediated by microvascular dysfunction. We included cross-sectional data of 2544 participants (age, 59.7 years; 51.0% men; 26.0% type 2 diabetes mellitus). We used carotid-femoral pulse wave velocity and carotid distensibility coefficient as measures of aortic and carotid stiffness, respectively. We calculated a composite score of microvascular dysfunction based on magnetic resonance imaging features of cerebral small vessel disease, flicker light-induced retinal arteriolar and venular dilation response, albuminuria, and plasma biomarkers of microvascular dysfunction (sICAM-1 [soluble intercellular adhesion molecule-1], sVCAM-1 [soluble vascular adhesion molecule-1], sE-selectin [soluble E-selectin], and vWF [von Willebrand factor]). Cognitive domains assessed were memory, processing speed, and executive function. A cognitive function score was calculated as the average of these domains. Higher aortic stiffness (per m/s) was associated with lower cognitive function (ß, -0.018 SD [95% CI, -0.036 to -0.000]) independent of age, sex, education, and cardiovascular risk factors, but higher carotid stiffness was not. Higher aortic stiffness (per m/s) was associated with a higher microvascular dysfunction score (ß, 0.034 SD [95% CI, 0.014 to 0.053]), and a higher microvascular dysfunction score (per SD) was associated with lower cognitive function (ß, -0.089 SD [95% CI, -0.124 to -0.053]). Microvascular dysfunction significantly explained 16.2% of the total effect of aortic stiffness on cognitive function. The present study showed that aortic stiffness, but not carotid stiffness, is independently associated with worse cognitive performance, and that this association is in part explained by microvascular dysfunction.

Pulse wave velocity and short-term outcome in patients requiring intravascular volume expansion: a pilot study.

BACKGROUND: Fluid therapy has a pivotal role in the management of acutely ill patients. However, whether or not a patient can tolerate additional intravascular volume is controversial and optimal strategy is unknown. Carotid femoral pulse wave velocity (cfPWV) evaluates arterial stiffness. OBJECTIVE: To determine whether cfPWV can predict the ability of patients to tolerate clinically indicated acute fluid expansion. METHODS: 50 consecutive patients requiring intravascular volume expansion were prospectively recruited in intensive care units. All subjects underwent transthoracic echocardiography, pulmonary ultrasound assessment, and a cfPWV study (S. Giovanni Bosco Hospital in Turin, Italy, between 2015 and 2016) at baseline and after 24 hours. Acute outcomes were registered at 24 hours ("soft" end points) and 30 days ('hard' end points: death, acute myocardial infarction, stroke, occurrence of atrial fibrillation, need for dialysis) after initial fluid therapy. Multivariate logistic regression was used to assess association of the initial cfPWV with outcomes. RESULTS: cfPWV was significantly higher (10.6±3.6 vs 7.4±2.2 m/s, P<0.0001) in subjects who met the prespecified combined endpoints (hard or soft) than in those who did not. After adjustment for confounding factors, initial cfPWV was significantly and independently associated with the occurrence of hard events (OR=2.8 (95% CI 1.36 to 5.97), P=0.005; area under the receiver operating characteristic curve 84%). cfPWV of <9 m/s had a negative predictive value of 93%, excluding hard events associated with fluid expansion. CONCLUSION: cfPWV appears to reflect the ability of the patient to tolerate an intravascular fluid expansion when clinically indicated. Increased cfPWV could help to identify subjects at greater risk of developing signs and symptoms of fluid overload.

The association between salt intake and arterial stiffness is influenced by a sex-specific mediating effect through blood pressure in normotensive adults: The ELSA-Brasil study.

High salt intake is known to increase blood pressure (BP) and also to be associated with carotid-femoral pulse wave velocity (cf-PWV). However, recent data showed a sex-specific pattern in the salt-induced rise of BP. Thus, we aimed to investigate whether the association between salt intake and arterial stiffness also has a sex-specific pattern. A total of 7755 normotensive participants with a validated 12-h overnight urine collection in which daily salt intake was estimated were included. cf-PWV, as well as clinical and anthropometric parameters, was measured. Salt intake positively correlated with cf-PWV, in which the linear regression was steeper in women than in men (0.0199 ± 0.0045 vs 0.0326 ± 0.0052 m/s per gram of salt, P < .05). cf-PWV increases over the salt quartiles in men and women. However, after adjustment for confounders, the association remained significant only for men. In the path analysis, the direct path (men: 0.048 P < .001, women: 0.029 P = .028) was higher in men while that mediated by SBP (men: 0.020 P < .001, women: 0.034 P < .001) was higher in women. We clearly demonstrated that high salt intake has a direct and independent effect increasing arterial stiffness regardless of sex. Also, the association between salt intake and arterial stiffness is more dependent on BP in normotensive women than it is in normotensive men. These results highlight the need for a sex-specific approach in the evaluation of cardiovascular risk associated with dietary habits.

A novel methodology for rat aortic pulse wave velocity assessment by Doppler ultrasound: validation against invasive measurements.

There is still lack of a simple, accurate, and noninvasive method for rat aortic pulse wave velocity (PWV) measurement, especially the transit distance cannot be accurately measured. Thus, we aimed to derive an equation for aortic transit distance as a function of the nose-to-rump length (L) and to test the hypothesis that aortic PWV measured by new equation combined with Doppler ultrasound (the "equation method") may have stronger correlation with invasive measurements than traditional "body surface method." Two-hundred male Sprague-Dawley (SD) rats (age ranged 5-24 wk) were included in protocol 1, and the aortic transit distances were measured postmortem. In protocol 2, heart-femoral PWV and carotid-femoral PWV were measured by equation method (hfPWVE, cfPWVE) and also by traditional body surface method (hfPWVS, cfPWVS) in another 30 young and 28 old rats. These measurements were then validated against invasively measured hfPWVI and cfPWVI from the same animal. Protocol 1 showed that the heart-femoral transit distance could be calculated by 0.6086 × L - 1.6523, and the carotid-femoral transit distance by 0.4614 × L + 1.8335. In protocol 2, in young rats, the Pearson r between hfPWVE, cfPWVE, hfPWVS, and cfPWVS and their corresponding invasive measurement were 0.8962, 0.8509, 0.8387, and 0.7828, respectively (all P < 0.0001). In the old group, the results were 0.8718, 0.7999, 0.8330, and 0.7112, respectively (all P < 0.0001). The hfPWVE and cfPWVE showed better agreement with hfPWVI and cfPWVI and lower intra- and interobserver variability compared with hfPWVS and cfPWVS in both groups. These findings demonstrate that this novel methodology provides a simple and reliable method for rat noninvasive aortic PWV measurement.NEW & NOTEWORTHY First, when measuring aortic PWV in SD rat models, the heart-femoral transit distance can be estimated by 0.6086 × L - 1.6523, and the carotid-femoral distance transit distance can be estimated by 0.4614 × L + 1.8335, where L (in mm) is nose-to-rump length. Second, this novel methodology for aortic PWV measurement was validated with a closer correlation with the invasive measurements than traditional approach in young and old rats. Third, this study provides a simple and reliable method for rat noninvasive aortic PWV measurement.

Association of urinary sodium/potassium ratio with structural and functional vascular changes in non-diabetic hypertensive patients.

Studies aiming to associate the sodium/potassium (Na/K) ratio with hypertension use 24-hour urinary excretion as a daily marker of ingestion. The objective of this study was to evaluate the association between urinary Na/K ratio and structural and functional vascular alterations in non-diabetic hypertensive patients. In hypertensive patients (n = 72), aged between 40 and 70 years, both sexes (61% women), in use of hydrochlorothiazide, we measured blood pressure, 24-hour urine sample collection, assessment of carotid-femoral pulse wave velocity (cf-PWV, Complior), central hemodynamic parameters (SphygmoCor), and post-occlusive reactive hyperemia (PORH). The participants were divided according to the tertile of 24-hour urinary Na/K ratio. Each group contained 24 patients. Systolic blood pressure was higher in T2 (133 ± 9 vs 140 ± 9 mmHg, P = .029). C-reactive protein (CRP) presented higher values in T3 as compared to T1 [0.20(0.10-0.34) vs 1.19 (0.96-1.42) mg/dL, P < .001]. Higher values in T3 were also observed for aortic systolic pressure (aoSP) [119(114-130) vs 135(125-147) mmHg, P = .002] and cf-PWV (9.2 ± 1.6 vs 11.1 ± 1.5 m/s, P < .001). The urinary Na/K ratio presented significant correlations with proteinuria (r = .27, P = .023), CRP (r = .77, P < .001), cf-PWV (r = .41, P < .001), and post-occlusive reactive hyperemia on cutaneous vascular conductance (PORH CVC) (r = -.23, P = .047). By multivariate linear regression, it was detected an independent and significant association of cf-PWV with urinary Na/K ratio (R2  = 0.17, P < .001) and PORH CVC with CRP (R2  = 0.30, P = .010). Our data indicated that increased urinary Na/K ratio in non-diabetic hypertensive patients was associated with higher degree of inflammation, raised peripheral and central pressure levels, and changes suggestive of endothelial dysfunction and arterial stiffness.

Loss of the Normal Gradient in Arterial Compliance and Outcomes of Chronic Kidney Disease Patients.

BACKGROUND: In dialysis patients, loss of the normal gradient in arterial compliance, assessed by the pulse wave velocity (PWV) ratio, predicts all-cause mortality better than does carotid-femoral PWV (CF-PWV) alone. However, the prognostic significance of the PWV ratio for outcome in chronic kidney disease (CKD) patients remains unclear. METHODS: In this longitudinal cohort study, CKD patients who visited our CKD management clinic between April 27, 2006, and March 27, 2008, were included and followed up. To assess the gradient in arterial compliance, the PWV ratio was calculated using CF-PWV divided by carotid-radial PWV. RESULTS: A total of 209 patients in CKD stages 1-4 with a median follow-up of 3.74 years were included. Patients with higher PWV ratio were relatively older (p < 0.001) and had worse renal function (p < 0.001), more hypertension (p < 0.001), diabetes mellitus (p < 0.001), and cardiovascular or cerebrovascular disease (p < 0.001). The median time to patient outcome (death, renal replacement therapy, or double increase in serum creatinine from baseline) in the group with a PWV ratio above the median (89.8 months, 95% CI 84.2-95.5) was shorter than that in the group with a PWV ratio below the median (105.3 months, 95% CI 101.3-109.3, p = 0.001). Univariate Cox regression analysis showed that both PWV ratio and CF-PWV were significantly associated with patient outcome. In multivariate Cox regression analysis, both PWV ratio and CF-PWV were associated with patient outcome. However, the HR for CF-PWV (2.177, 95% CI 1.064-4.453, p = 0.033) was slightly higher than that for PWV ratio (2.091, 95% CI 1.049-4.167, p = 0.036). There was a significant interaction effect between PWV ratio and CKD stage. It was shown that patients with advanced CKD stages and higher PWV ratios had a significantly higher risk of adverse CKD outcome (p = 0.006). CONCLUSIONS: The PWV ratio, as a measure of loss of the normal gradient in arterial compliance, was associated with CKD patient outcome. Patients with advanced CKD and a higher PWV ratio had a significantly higher risk of adverse CKD outcome.

Serum osteoprotegerin is an independent marker of central arterial stiffness as assessed using carotid-femoral pulse wave velocity in hemodialysis patients: a cross sectional study.

BACKGROUND: Cardiovascular morbidity and mortality are highly prevalent in patients with end-stage renal disease, and osteoprotegerin (OPG) may be an important link between bone loss and vascular calcification. This study was conducted to evaluate the relationship between central arterial stiffness and serum OPG levels in hemodialysis (HD) patients. METHODS: Blood samples were collected from 120 HD patients, and the carotid-femoral pulse wave velocity (cfPWV) value was measured using a validated tonometry system. The cfPWV value of > 10 m/s was used to define the high artery stiffness group. Serum OPG levels were analyzed categorically into tertiles. RESULTS: Of the 120 HD patients, 53 (44.2%) were defined as the high arterial stiffness group, who had higher values of systolic blood pressure (p = 0.038), serum calcium (p = 0.007), and OPG (p <  0.001) levels and a higher prevalence of diabetes mellitus (DM, p = 0.001). Increasing tertiles of serum OPG levels were significantly associated with greater height (p = 0.011), male gender (p = 0.008), higher cfPWV values (p = 0.020), and lower intact parathyroid hormone (iPTH, p = 0.049) levels. Multivariable linear regression analysis showed that cfPWV value was independently associated with DM (ß = 1.83, p = 0.008) and increasing tertiles of serum OPG levels (ß = 0.89 and 1.63 for tertile 2 and tertile 3, respectively, p for trend = 0.035) in HD patients. Multivariable logistic regression analysis revealed that, in addition to age, DM, low iPTH levels, and high serum calcium levels, increasing tertiles of serum OPG levels (OR = 5.34 for tertile 2; OR = 7.06 for tertile 3; p for trend = 0.002) were an independent predictor of high arterial stiffness in HD patients. Serum calcium levels positively correlated with cfPWV value only in the highest OPG tertile group (r = 0.408, p = 0.009). CONCLUSION: A positive association was detected between serum OPG levels and central arterial stiffness in HD patients, and patients with high serum OPG levels may have greater influence of calcium load on central arterial stiffening.

Unreliable Estimation of Aortic Pulse Wave Velocity Provided by the Mobil-O-Graph Algorithm-Based System in Marfan Syndrome.

Background Several devices have been proposed to assess arterial stiffness in clinical daily use over the past few years, by estimating aortic pulse wave velocity (PWV) from a single measurement of brachial oscillometric blood pressure, using patented algorithms. It is uncertain if these systems are able to provide additional elements, beyond the contribution carried by age and blood pressure levels, in the definition of early vascular damage expressed by the stiffening of the arterial wall. Methods and Results The aim of our study was to compare the estimated algorithm-based PWV values, provided by the Mobil-O-Graph system, with the standard noninvasive assessment of aortic PWV in patients with Marfan syndrome (ie, in subjects characterized by premature aortic stiffening and low blood pressure values). Aortic stiffness was simultaneously evaluated by carotid-femoral PWV with a validated arterial tonometer and estimated with an arm cuff-based ambulatory blood pressure monitoring Mobil-O-Graph device on 103 patients with Marfan syndrome (50 men; mean± SD age, 38±15 years). Aortic PWV, estimated by the Mobil-O-Graph, was significantly ( P<0.0001) lower (mean± SD, 6.1±1.3 m/s) than carotid-femoral PWV provided by arterial tonometry (mean± SD , 8.8±3.1 m/s). The average of differences between PWV values provided by the 2 methods (±1.96×SD) was -2.7±5.7 m/s. Conclusions The Mobil-O-Graph provides PWV values related to an ideal subject for a given age and blood pressure, but it is not able to evaluate early vascular aging expressed by high PWV in the individual patient. This is well shown in patients with Marfan syndrome.