How to Measure Arterial Stiffness in Humans.
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ABSTRACT:
SUBMITTER: Segers P
PROVIDER: S-EPMC7180118 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Epidemiological studies reveal a J-shaped association between alcohol consumption and arterial stiffness, with arterial stiffening lower among mild-to-moderate drinkers than heavy drinkers or nondrinkers. This study aimed to examine the effects of ingesting a small amount of beer, corresponding to the amount consumed per day by a mild drinker, on arterial stiffness. Eleven men (20-22 years) participated, in random order and on different days, in four separate trials. The participants each drank 200 or 350 mL of alcohol-free beer (AFB200 and AFB350) or beer (B200 and B350), and were monitored for 90 min postingestion. There were no significant changes in arterial stiffness among trials that ingested AF200 or AF350. However, among trials ingesting B200 and B350, breath alcohol concentrations increased significantly, while indexes of arterial stiffness decreased significantly for approximately 60 min: carotid-femoral pulse wave velocity (B200: -0.6 ± 0.2 m/sec; B350: -0.6 ± 0.2 m/sec); brachial-ankle pulse wave velocity (B200: -53 ± 18 cm/sec; B350: -57 ± 19 cm/sec); and cardio-ankle vascular index (B200: -0.4 ± 0.1 unit; B350: -0.3 ± 0.1 unit). Furthermore, AFB showed no effect on arterial stiffness, regardless of whether or not it contained sugar, and no significant difference in antioxidant capacity was found between AFB and B. This is the first study to demonstrate that acute ingestion of relatively small amounts of beer reduces arterial stiffness (for approximately 60 min). Our data also suggest that the reduction in arterial stiffness induced by ingestion of beer is largely attributable to the effects of alcohol.
| S-EPMC5555901 | biostudies-other
Project description:ObjectiveWe have reported that renal hyperfiltration is associated with endothelial dysfunction in early type 1 diabetes. However, the relationship between renal hyperfiltration and arterial stiffness is unknown. Accordingly, we measured arterial stiffness in type 1 diabetic subjects with hyperfiltering (n = 20) or normofiltering (n = 18).Research design and methodsAugmentation index (AIx), aortic pulse wave velocity (PWV), renal hemodynamic function (inulin and paraaminohippurate clearances), and urinary and circulating plasma cGMP were measured in normoalbuminuric subjects with type 1 diabetes during clamped euglycemia (glucose 4-6 mmol/l) and hyperglycemia (glucose 9-11 mmol/l).ResultsDuring clamped euglycemia, hyperfiltering subjects (glomerular filtration rate >or=135 ml/min/1.73 m(2)) exhibited lower AIx values (-6.1 +/- 2.9 vs. 13.9 +/- 2.7%, P = 0.001) and higher cGMP levels in urine and plasma compared with normofiltering subjects. These differences were maintained during clamped hyperglycemia. As expected, renal hemodynamic responses to clamped hyperglycemia were exaggerated in normofilterers, but values for AIx remained unchanged.ConclusionsRenal hyperfiltration is associated with reduced arterial stiffness in subjects with uncomplicated type 1 diabetes.
| S-EPMC2928365 | biostudies-literature
Project description:The primary objective of this study was to elucidate mechanisms underlying the link between vitamin D status and cardiovascular disease by exploring the relationship between 25-hydroxyvitamin D (25-OH D), an established marker of vitamin D status, and vascular function in healthy adults.Mechanisms underlying vitamin D deficiency-mediated increased risk of cardiovascular disease remain unknown. Vitamin D influences endothelial and smooth muscle cell function, mediates inflammation, and modulates the renin-angiotensin-aldosterone axis. We investigated the relationship between vitamin D status and vascular function in humans, with the hypothesis that vitamin D insufficiency will be associated with increased arterial stiffness and abnormal vascular function.We measured serum 25-OH D in 554 subjects. Endothelial function was assessed as brachial artery flow-mediated dilation, and microvascular function was assessed as digital reactive hyperemia index. Carotid-femoral pulse wave velocity and radial tonometry-derived central augmentation index and subendocardial viability ratio were measured to assess arterial stiffness.Mean 25-OH D was 31.8 ± 14 ng/ml. After adjustment for age, sex, race, body mass index, total cholesterol, low-density lipoprotein, triglycerides, C-reactive protein, and medication use, 25-OH D remained independently associated with flow-mediated vasodilation (? = 0.1, p = 0.03), reactive hyperemia index (? = 0.23, p < 0.001), pulse wave velocity (? = -0.09, p = 0.04), augmentation index (? = -0.11, p = 0.03), and subendocardial viability ratio (? = 0.18, p = 0.001). In 42 subjects with vitamin D insufficiency, normalization of 25-OH D at 6 months was associated with increases in reactive hyperemia index (0.38 ± 0.14, p = 0.009) and subendocardial viability ratio (7.7 ± 3.1, p = 0.04), and a decrease in mean arterial pressure (4.6 ± 2.3 mm Hg, p = 0.02).Vitamin D insufficiency is associated with increased arterial stiffness and endothelial dysfunction in the conductance and resistance blood vessels in humans, irrespective of traditional risk burden. Our findings provide impetus for larger trials to assess the effects of vitamin D therapy in cardiovascular disease.
| S-EPMC3896949 | biostudies-literature
Project description:Emissions from biomass combustion are a major source of indoor and outdoor air pollution, and are estimated to cause millions of premature deaths worldwide annually. Whilst adverse respiratory health effects of biomass exposure are well established, less is known about its effects on the cardiovascular system. In this study we assessed the effect of exposure to wood smoke on heart rate, blood pressure, central arterial stiffness and heart rate variability in otherwise healthy persons.Fourteen healthy non-smoking subjects participated in a randomized, double-blind crossover study. Subjects were exposed to dilute wood smoke (mean particle concentration of 314±38 ?g/m3) or filtered air for three hours during intermittent exercise. Heart rate, blood pressure, central arterial stiffness and heart rate variability were measured at baseline and for one hour post-exposure.Central arterial stiffness, measured as augmentation index, augmentation pressure and pulse wave velocity, was higher after wood smoke exposure as compared to filtered air (p < 0.01 for all), and heart rate was increased (p < 0.01) although there was no effect on blood pressure. Heart rate variability (SDNN, RMSSD and pNN50; p = 0.003, p < 0.001 and p < 0.001 respectively) was decreased one hour following exposure to wood smoke compared to filtered air.Acute exposure to wood smoke as a model of exposure to biomass combustion is associated with an immediate increase in central arterial stiffness and a simultaneous reduction in heart rate variability. As biomass is used for cooking and heating by a large fraction of the global population and is currently advocated as a sustainable alternative energy source, further studies are required to establish its likely impact on cardiovascular disease.ClinicalTrials.gov, NCT01488500.
| S-EPMC3685524 | biostudies-literature
Project description:Physical stiffening of the large arteries is the central paradigm of vascular aging. Indeed, stiffening in the larger central arterial system, such as the aortic tree, significantly contributes to cardiovascular diseases in older individuals and is positively associated with systolic hypertension, coronary artery disease, stroke, heart failure and atrial fibrillation, which are the leading causes of mortality in the developed countries and also in the developing world as estimated in 2010 by World Health Organizations. Thus, better, less invasive and more accurate measures of arterial stiffness have been developed, which prove useful as diagnostic indices, pathophysiological markers and predictive indicators of disease. This article presents a review of the structural determinants of vascular stiffening, its pathophysiologic determinants and its implications for vascular research and medicine. A critical discussion of new techniques for assessing vascular stiffness is also presented.
| S-EPMC3078647 | biostudies-other
Project description:This study sought to assess sex differences in ventricular-arterial interactions.Heart failure with preserved ejection fraction is more prevalent in women than in men, but the basis for this difference remains unclear.Echocardiography and arterial tonometry were performed to quantify arterial and ventricular stiffening and interaction in 461 participants without heart failure (189 men, age 67 ± 9 years; 272 women, age 65 ± 10 years). Aortic characteristic impedance (Z(c)), total arterial compliance (pulsatile load), and systemic vascular resistance index (steady load) were compared between men and women, and sex-specific multivariable regression analyses were performed to assess associations of these arterial parameters with diastolic dysfunction and ventricular-arterial coupling (effective arterial elastance/left ventricular end-systolic elastance [Ea/Ees]) after adjustment for potential confounders.Z(c) was higher and total arterial compliance was lower in women, whereas systemic vascular resistance index was similar between sexes. In women but not men, higher log Z(c) was associated with mitral inflow E/A ratio (? ± SE: -0.17 ± 0.07), diastolic dysfunction (odds ratio: 7.8; 95% confidence interval: 2.0 to 30.2) and Ea/Ees (? ± SE: 0.13 ± 0.04) (p ? 0.01 for all). Similarly, total arterial compliance was associated with E/A ratio (? ± SE: 0.12 ± 0.04), diastolic dysfunction (odds ratio: 0.33; 95% confidence interval: 0.12 to 0.89), and Ea/Ees (? ± SE: -0.09 ± 0.03) in women only (p ? 0.03 for all). Systemic vascular resistance index was not associated with diastolic dysfunction or Ea/Ees.Proximal aortic stiffness (Z(c)) is greater in women than men, and women may be more susceptible to the deleterious effects of greater pulsatile and early arterial load on diastolic function and ventricular-arterial interaction. This may contribute to the greater risk of heart failure with preserved ejection fraction in women.
| S-EPMC3773521 | biostudies-literature
Project description:Cardiovascular morbidity and mortality is high in patients with chronic obstructive pulmonary disease (COPD) and arterial stiffness is a potentially modifiable risk factor with added predictive value beyond that obtained from traditional risk factors. Arterial stiffness has been the target of pharmacologic and exercise interventions in patients with COPD, but the effects appear limited to those patients with more significant elevations in arterial stiffness. We aimed to identify predictors of increased arterial stiffness in a cohort with moderate to severe COPD.Aortic pulse wave velocity (aPWV) was measured in subjects with moderate to severe COPD enrolled in a multicenter randomized controlled trial. Subjects were categorized into quartiles based on aPWV values and factors affecting high arterial stiffness were assessed. Multivariate models were created to identify independent predictors of high aPWV, and cardiovascular disease (CVD).153 patients were included. Mean age was 63.2 (SD 8.2) years and mean FEV1 was 55.4 (SD 15.2) % predicted. Compared to the quartile with the lowest aPWV, subjects in the highest quartile were older, had higher systolic blood pressure (SBP), were more likely to be current smokers, and had greater burden of thoracic aortic calcification. On multivariate analyses, age (adjusted OR 1.14, 95%CI 1.05 to 1.25, p = 0.003) and SBP (adjusted OR 1.06, 95% CI 1.02 to 1.09, p = 0.001) were independent predictors of elevated aPWV. Body mass index, therapy with cholesterol lowering medications and coronary calcification were independent predictors of CVD.Elevated arterial stiffness in patients with COPD can be predicted using age, blood pressure and thoracic aortic calcification. This will help identify subjects for enrollment in clinical trials using aPWV for assessing the impact of COPD therapies on CV outcomes.
| S-EPMC3890490 | biostudies-literature
Project description:Chronic kidney disease is characterized by stiffening, thinning, dilatation, and increased circumferential wall stress of large arteries, associated with increased cardiovascular risk. Kidney transplantation (KT) reverses many pathological features of chronic kidney disease and improves life expectancy; however, longitudinal studies exploring the impact of KT on recipient large arteries are scarce.This study was designed to appraise arterial changes following KT. Carotid-femoral pulse wave velocity, carotid remodeling (circumferential wall stress and carotid internal diameter), and stiffness were measured in 161 consecutive recipients receiving either a living (n=49) or a deceased (n=112) donor allograft, at 3 and 12 months after transplantation. Mean pulse wave velocity decreased from 10.8 m/s (95% confidence interval, 10.5-11.2 m/s) (at month 3) to 10.1 m/s (95% confidence interval, 9.8-10.5 m/s) (at month 12) (P<0.001). After multivariate adjustment, pulse wave velocity reduction from month 3 to month 12 was significantly larger in the living donor allograft KT (P<0.001). Circumferential wall stress decreased, 70 kPa (95% confidence interval, 68-72 kPa) to 64 kPa (95% confidence interval, 62-67 kPa), as well as carotid internal diameter and carotid stiffness (P<0.001 for all). Reductions in circumferential wall stress, diameter, and stiffness were significantly larger in the living donor allograft KT (P<0.001). When deceased donor allograft patients were classified into standard and expanded criteria donors, changes in both pulse wave velocity and circumferential wall stress were blunted in expanded criteria donors. Changes were independent of graft function and blood pressure changes.Large-artery stiffness and maladaptive carotid artery remodeling of chronic kidney disease is partially reversed within 12 months of KT and appears unrelated to renal function. Improvements were independently associated with live organ donation. Our data suggest that expanded criteria donors may hamper vascular recovery.
| S-EPMC5634273 | biostudies-other
Project description:In patients with phenylketonuria (PKU) compliant to diet greater tendency to overweight and higher inflammatory biomarkers levels than controls were reported. Although this could lead to atherogenesis, the elastic properties of large arteries in PKU patients have never been assessed. The aim of this study was to assess arterial stiffness measured by applanation tonometry in PKU patients compared to healthy controls.We carried out a cross-sectional study in 41 PKU patients (range age: 6-50 years old) and 41 age- and gender-matched healthy controls. Evaluated data included pharmacological treatment with sapropterin, clinical, and biochemical parameters. Aortic stiffness was assessed noninvasively by applanation tonometry measuring central blood pressure, aortic augmentation index (Aix@HR75), augmentation pressure (AP), and pulse wave velocity (PWV).We found higher PWV in classic PKU patients (6.60?m/second vs 5.26?m/second; P: .044). Percentage of PKU patients with PWV above 90 percentile was higher than controls (14.63% vs 2.32%; P: .048). A positive relationship was observed between the annual Phe median and PWV (r: 0.496; P: .012). PKU subjects with lower Phe tolerance showed more body weight (67.6?kg vs 56.8?kg; P: .012) and more PWV than those with higher Phe tolerance (6.55?m/second vs 5.42?m/second; P: .044).Our data show increased aortic stiffness in PKU patients, measured by applanation tonometry, when compared to healthy controls. Higher Phe levels are associated with a bigger PWV increase, which is not present in those subjects compliant to diet or under sapropterin treatment. These results could have marked effects in both research and clinical daily practice for a proper evaluation of cardiovascular risk in PKU subjects.
| S-EPMC5758209 | biostudies-literature
Project description:Arterial stiffness is an important predictor of cardiovascular risk besides classic cardiovascular risk factors. Previous studies showed that arterial stiffness is increased in patients with COPD compared to healthy controls and exercise training may reduce arterial stiffness. Since physical inactivity is frequently observed in patients with COPD and exercise training may improve arterial stiffness, we hypothesized that low daily physical activity may be associated with increased arterial stiffness.In 123 patients with COPD (72% men; mean [standard deviation] age: 62 [7.5] years; median [quartile] forced expiratory volume in 1 second 35 [27/65] %predicted), arterial stiffness was assessed by augmentation index (AI). Daily physical activity level (PAL) was measured by an activity monitor (SenseWear Pro™) >1 week. The association between AI and PAL was investigated by univariate and multivariate regression analysis, taking into account disease-specific characteristics and comorbidities.Patients suffered from moderate (35%), severe (32%), and very severe (33%) COPD, and 22% were active smokers. Median (quartile) PAL was 1.4 (1.3/1.5) and mean (standard deviation) AI 26% (9.2%). PAL showed a negative association with AI (B=-9.32, P=0.017) independent of age, sex, blood pressure, and airflow limitation.In COPD patients, a higher PAL seems to favorably influence arterial stiffness and therefore may reduce cardiovascular risk.http://www.ClinicalTrials.gov, NCT01527773.
| S-EPMC4573078 | biostudies-literature