Arterial stiffness decreases with weight loss in overweight/obese young adults. We aimed to determine the mechanisms by which this occurs.
We evaluated carotid-femoral pulse wave velocity (cfPWV) and brachial-ankle pulse wave velocity (baPWV) in 344 young adults (23% male, BMI 25–40 kg/m2) at baseline, 6, and 12 months in a behavioral weight loss intervention. Linear mixed models were used to evaluate associations between weight loss and arterial stiffness and to examine whether improvements in obesity-related factors explained these associations.
At 6 months (7% mean weight loss), there was a significant median decrease of 47.5 cm/s in cfPWV (p<0.0001) and a mean decrease of 11.7 cm/s in baPWV (p=0.049). At 12 months (6% mean weight loss), only cfPWV remained reduced. In models adjusting for changes in mean arterial pressure and obesity-related factors, changes in BMI (p=0.01) and common carotid artery diameter (p=0.003) were positively associated with change in cfPWV. Reductions in heart rate (p<0.0001) and C-reactive protein (p=0.02) were associated with reduced baPWV and accounted for the association between weight loss and reduced baPWV.
Weight loss is associated with reduced cfPWV independently of changes in established hemodynamic and cardiometabolic risk factors, but its association with reduced baPWV is explained by concurrent reductions in heart rate and inflammation.
arterial stiffness; obesity; lifestyle modification
Physical activity (PA) is associated with decreased levels of arterial stiffness in adults, but the relationship between PA and multiple measures of arterial stiffness in adolescents and young adults is not clear. The objective of this study was to test the hypothesis that PA is an independent predictor of multiple measures of arterial stiffness in adolescents and young adults. A total of 548 participants were enrolled in a study of the cardiovascular effects of obesity and type 2 diabetes mellitus (T2DM) (lean, 201; obese, 191; T2DM, 156). Anthropometrics, blood pressure, central and peripheral measures of arterial stiffness (pulse wave velocity, brachial distensibility, and augmentation index), blood (lipids and metabolic tests), and accelerometry data were collected. General linear modeling was performed to test for the independent relationship of PA on arterial stiffness. The mean age of the participants was 17.9 years (standard deviation, 3.5 years). After adjusting for other cardiovascular disease risk factors such as age, sex, body size, mean arterial pressure, and the presence of obesity or T2DM, PA was an independent predictor of augmentation index and brachial distensibility (P < .001). A greater effect of PA on pulse wave velocity was found in participants with T2DM (P = .009) compared with participants in the lean or obese groups. Physical activity is significantly and independently associated with multiple measures of arterial stiffness in adolescents and young adults. The role of PA in the prevention of cardiovascular disease target organ damage in youth, independent of energy balance, merits further exploration.
Background and purpose
Aerobic exercise has been reported to be associated with reduced arterial stiffness. However, the intensity, duration, and frequency of aerobic exercise required to improve arterial stiffness have not been established. In addition, most reports base their conclusions on changes in pulse wave velocity, which is an indirect index of arterial stiffness. We studied the effects of short-term, intermittent, moderate-intensity exercise training on arterial stiffness based on measurements of the stiffness parameter (β) and pressure–strain elastic modulus (Ep), which are direct indices of regional arterial stiffness.
A total of 25 young healthy volunteers (18 men) were recruited. By use of ultrasonic diagnostic equipment we measured β and Ep of the carotid artery before and after 8 weeks of exercise training.
After exercise training, systolic pressure (Ps), diastolic pressure (Pd), pulse pressure, systolic arterial diameter (Ds), and diastolic arterial diameter (Dd) did not change significantly. However, the pulsatile change in diameter ((Ds − Dd)/Dd) increased significantly, and β and Ep decreased significantly.
For healthy young subjects, β and Ep were reduced by intermittent, moderate-intensity exercise training for only 8 weeks.
Arterial stiffness; Exercise; Echo tracking
Increased arterial stiffness is a risk factor for adverse cardiovascular events in adults with obesity-related insulin resistance (IR) or type 2 diabetes mellitus. Adolescents with type 2 diabetes have stiffer vessels. Whether stiffness is increased in obesity/IR in youth is not known. We sought to determine if IR was a determinant of arterial stiffness in youth, independent of obesity and cardiovascular risk factors.
We measured cardiovascular risk factors, IR, adipocytokines and arterial stiffness (brachial artery distensibility [BrachD], pulse wave velocity [PWV]) and wave reflection (augmentation index [AIx]) in 343 adolescents and young adults without type 2 diabetes (15–28 years old, 47% male, 48% non-white). Individuals <85th percentile of BMI were classified as lean (n=232). Obese individuals were grouped by HOMA index as not insulin resistant (n=46) or insulin resistant (n=65) by the 90th percentile for HOMA for lean. Mean differences were evaluated by ANOVA. Multivariate models evaluated whether HOMA was an independent determinant of arterial stiffness.
Risk factors deteriorated from lean to obese to obese/insulin resistant (all p≤ 0.017). Higher AIx, lower BrachD and higher PWV indicated increased arterial stiffness in obese and obese/insulin resistant. HOMA was not an independent determinant. Age, sex, BMI and BP were the most consistent determinants, with HDL-cholesterol playing a role for BrachD and leptin for PWV (AIx R2 = 0.34; BrachD R2 = 0.37; PWV R2 = 0.40; all p≤0.02).
Although IR is associated with increased arterial stiffness, traditional cardiovascular risk factors, especially obesity and BP, are the major determinants of arterial stiffness in healthy young people.
Adolescents; Arterial stiffness; Cardiovascular risk factors; Insulin resistance; Obesity
Arterial stiffness is an important clinical marker of cardiovascular diseases. Although many studies have been conducted on different racial groups, less is known about arterial stiffness in Asian Americans. Korean Americans constitute the fifth largest subgroup in the Asian American population and reportedly have a noticeably high prevalence of hypertension. The aims of this study were to assess arterial stiffness and blood pressure and to examine the effect of age and gender on arterial stiffness and blood pressure in 102 Korean American men and women aged 21 to 60 years. The values of arterial stiffness for Korean Americans in this study were compared to published reference values for other racial and ethnic groups. Arterial stiffness was measured by carotid-femoral pulse wave velocity, which is the gold standard for determining arterial stiffness. Findings indicated that aging was an important determinant of arterial stiffness, which increased linearly with age. Although there was no gender difference observed in arterial stiffness, the effect of age on arterial stiffness was greater in women than in men. After adjusting for covariates including age, body mass index, and smoking, multiple regression models showed that arterial stiffness and gender were significant predictors of systolic and diastolic blood pressure. The comparisons of these findings to those from several other studies that used the same method to measure arterial stiffness showed that Korean Americans may have levels of arterial stiffness that are similar to or slightly higher than those of other racial groups. Considering that arterial stiffness is an independent predictor of future development of hypertension, more studies are required to examine cardiovascular risk of this understudied group.
arterial stiffness; hypertension; Korean Americans
We tested the hypothesis that weight loss via a hypocaloric diet would reduce arterial stiffness in overweight and obese middle-aged and older adults. Thirty-six individuals were randomly assigned to a weight loss (n=25; age: 61.2±0.8 years; body mass index: 30.0±0.6 kg/m2) or a control (n=11; age: 66.1±1.9 years; body mass index: 31.8±1.4 kg/m2) group. Arterial stiffness was measured via carotid artery ultrasonography combined with applanation tonometry and carotid-femoral pulse wave velocity via applanation tonometry at baseline and after the 12-week intervention. Body weight, body fat, abdominal adiposity, blood pressure, β-stiffness index, and carotid-femoral pulse wave velocity were similar in the 2 groups at baseline (all P>0.05). Body weight (−7.1±0.7 versus −0.7±1.1 kg), body fat, and abdominal adiposity decreased in the weight loss group but not in the control group (all P<0.05). Brachial systolic and diastolic blood pressures declined (P<0.05) only in the weight loss group. Central systolic and pulse pressures did not change significantly in either group. β-Stiffness index (−1.24±0.22 versus 0.52±0.37 U) and carotid-femoral pulse wave velocity (−187±29 versus 15±42 cm/s) decreased in the weight loss group but not in the control group (all P<0.05). The reductions in carotid-femoral pulse wave velocity were correlated with reductions in total body and abdominal adiposity (r=0.357– 0.602; all P<0.05). However, neither total body nor abdominal adiposity independently predicted reductions in arterial stiffness indices. In summary, our findings indicate that weight loss reduces arterial stiffness in overweight/obese middle-aged and older adults, and the magnitudes of these improvements are related to the loss of total and abdominal adiposity.
arterial structure; arterial compliance; aging; pulse wave velocity; caloric restriction
Arterial stiffness plays a key role in the pathophysiology of the cardiovascular system. Some indices of arterial stiffness (pulse wave velocity, augmentation index, characteristics of central blood pressure waveform) may be presently calculated and evaluated in the clinical setting. Age and blood pressure are the two major clinical determinants of increased arterial stiffness, while molecular determinants of arterial stiffness are related to fibrotic components of the extracellular matrix, mainly elastin, collagen and fibronectin. Increased arterial stiffness has been consistently observed in conditions such as hypertension, dyslipidemia and diabetes. Arterial stiffness evaluated by means of carotid-femoral pulse wave velocity yielded prognostic significance beyond and above traditional risk factors. A more favorable effect of calcium channel blockers, diuretics and ACE inhibitors compared with β-blockers on indices of arterial stiffness was observed in several studies. It is conceivable that newer β-blockers with additional vasodilating properties, such as nebivolol, which has favorable effects on carbohydrate and lipid metabolism, as well as on endothelial function and on oxidative stress, may have favorable effects on arterial stiffness, compared with atenolol. In fact, in recent studies, nebivolol was demonstrated to improve artery stiffness to a greater extent than older β-blockers. Because endothelial dysfunction and increased arterial stiffness play an important role in the early atherosclerotic processes and are associated with poor outcomes and increased mortality, independently of blood pressure, the ability of nebivolol to enhance release of endothelium-derived nitric oxide, and consequently improve endothelial function and arterial stiffness, may have significant clinical implications for the use of this agent in the treatment of hypertension and cardiovascular diseases.
arterial stiffness; hypertension; nebivolol
Arterial stiffness is the major determinant of isolated systolic hypertension and increased pulse pressure. Aortic stiffness is also associated with increased cardiovascular morbidity and mortality in patients with chronic kidney disease, hypertension, and general population. Hemodynamically, arterial stiffness results in earlier aortic pulse wave reflection leading to increased cardiac workload and decreased myocardial perfusion. Although the clinical consequence of aortic stiffness has been clearly established, its pathophysiology in various clinical conditions still remains poorly understood. The aim of the present paper is to review the studies that have looked at the impact of dialysis calcium concentration on arterial stiffness. Overall, the results of small short-term studies suggest that higher dialysis calcium is associated with a transient but significant increase in arterial stiffness. This calcium dependant increase in arterial stiffness is potentially explained by increased vascular smooth muscle tone of the conduit arteries and is not solely explained by changes in mean blood pressure. However, the optimal DCa remains to be determined, and long term studies are required to evaluate its impact on the progression of arterial stiffness.
Individuals with bipolar disorder face a nearly two-fold increased risk of cardiovascular mortality relative to the general population. Endothelial dysfunction precedes cardiovascular disease and serves as a quantifiable phenotype for vasculopathy. We investigated whether individuals with bipolar disorder had poorer vascular function than controls using a case-control design.
The sample of 54 participants included 27 individuals with bipolar disorder and 27 age- and gender-matched controls. Participants underwent an assessment of metabolic (weight, lipids, and insulin resistance) and vascular parameters (endothelial function using flow-mediated dilation; arterial stiffness using pulse wave velocity and estimated aortic pressure).
Participants had a mean age of 32 years and 41% were female. No significant differences were found between groups in endothelial function or arterial stiffness. Individuals with bipolar disorder demonstrated 100% greater insulin resistance.
The lack of clinically significant differences in vascular function in this young sample suggests any increased risk either occurs later in the course of illness or is largely due to behavioral risk factors, such as smoking, which was balanced between groups. Substantial insulin resistance is identifiable early in course of illness, perhaps secondary to treatment.
Bipolar disorder; cardiovascular disease; cardiovascular mortality; endothelial dysfunction; insulin resistance; pulse wave analysis
Increased arterial stiffness and wave reflection have been reported in heart failure with normal ejection fraction (HFNEF) and in asymptomatic left ventricular (LV) diastolic dysfunction, a precursor of HFNEF. It is unclear whether women, who have higher frequency of HFNEF, are more vulnerable than men to the deleterious effects of arterial stiffness on LV diastolic function. We investigated in a large community-based cohort, whether sex differences exist in the relationship between arterial stiffness, wave reflection and LV diastolic function. Arterial stiffness and wave reflection were assessed in 983 participants from the Cardiovascular Abnormalities and Brain Lesions (CABL) study using applanation tonometry. Central pulse pressure/stroke volume index (cPP/SVi), total arterial compliance, pulse pressure amplification and augmentation index were used as parameters of arterial stiffness and wave reflection. LV diastolic function was evaluated by two-dimensional echocardiography and tissue-Doppler imaging. Arterial stiffness and wave reflection were greater in women compared to men, independent of body size and heart rate (all p<0.01), and showed inverse relationships with parameters of diastolic function in both sexes. Further adjustment for cardiovascular risk factors attenuated these relationships; however, higher cPP/SVi predicted LV diastolic dysfunction in women [odds ratio (OR) 1.54, 95% confidence intervals (CI) 1.03–2.30] and men (OR: 2.09, 95% CI 1.30–3.39) independent of other risk factors. In conclusion, in our community-based cohort study, higher arterial stiffness was associated with worse LV diastolic function in men and women. Women’s higher arterial stiffness, independent of body size, may contribute to their greater susceptibility to develop HFNEF.
Arterial stiffness; Wave reflection; Diastole; Sex; Echocardiography
Background and Objectives
Several studies have shown that angiotensin II receptor blockers (ARBs) improve endothelial function and arterial stiffness. Telmisartan is a highly selective ARB that activates peroxisome proliferator-activated receptor γ (PPARγ). The purpose of this study was to evaluate the effects of telmisartan, such as endothelial function, arterial stiffness, and insulin sensitivity, in patients with essential hypertension.
Subjects and Methods
Thirty-nine patients with essential hypertension were administered telmisartan (80 mg once daily) using an open-labeled and prospective protocol. The patients were examined before and 8 weeks after treatment to assess changes in flow mediated-vasodilation (FMD), pulse wave velocity (PWV), quantitative insulin-sensitivity check index (QUICKI), homeostasis model assessment (HOMA), and adiponection.
The systolic and diastolic blood pressure (BP) decreased from 153±15 mmHg and 90±13 mmHg to 137±16 mmHg and 84±10 mmHg after telmisartan treatment, respectively (p<0.01). Telmisartan therapy increased the FMD from 7.6±3.5 to 9.0±2.8% (p<0.01). The following parameters of arterial stiffness were significantly improved after telmisartan therapy: brachial-ankle pulse wave velocity (baPWV), from 17.2±3.1 to 15.9±2.6 m/sec; heart-carotid PWV (hcPWV), from 9.7±1.8 to 9.0±1.9 m/sec; and heart-femoral PWV (hfPWV), from 11.3±1.9 to 10.7±1.9 m/sec (p<0.01). There were no changes in QUICKI, the HOMA level, and plasma adiponectin (p=NS).
These results suggest that telmisartan is effective in improving endothelial function and arterial stiffness in patients with essential hypertension.
Angiotensin II type 1 receptor blockers; Endothelium, vascular; Arteriosclerosis
The degree of arterial stiffness is correlated with the risk of cardiovascular diseases and it is a powerful predictor for morbidity and mortality. Studies have shown that arterial stiffness reduction is associated with an improvement in survival. Reduction of arterial stiffness by pharmacological drugs varies according to the drugs and doses used and duration of treatment. This effect on the arteries differs among the various classes of drugs and among individual drugs in the same class. Quantification of the stiffness and other properties of the arterial wall can be used to monitor the responses to therapy in individuals with hypertension and other cardiovascular diseases. These measures can then be used as surrogate markers for the risk of clinical events. Inhibition of the renin-angiotensin system (RAS) is associated with an important decrease in cardiovascular risk. Findings from clinical trials support the hypothesis that the protective effects of RAS inhibition are partly independent from blood pressure reduction and related to several mechanisms including vascular protective effects. The aim of the TRanscend Arterial stiffNess Substudy (TRANS) is to assess the effect of an angiotensin II receptor blocker (ARB), telmisartan, on the arterial stiffness in a subgroup of patients from the Telmisartan Randomized Assessment Study in aCE iNtolerant subjects with cardiovascular Disease (TRANSCEND) trial. The TRANSCEND trial is an international, multicenter, randomized double blind placebo controlled trial of telmisartan that enrolled patients at high risk for cardiovascular events. Some clinical baseline data of the TRANS substudy are reported. When completed, the results of the TRANS substudy will show whether the beneficial effects of treatment with telmisartan on cardiovascular outcome may be related to an improvement in arterial stiffness.
arterial stiffness; cardiovascular prevention; ARBs; telmisartan; pulse wave velocity; antihypertensive
In hypertension, the blood pressure curve may be divided into two sets of components. The first set is mean arterial pressure, steady flow, and vascular resistance, thus acting on small arteries; the second set refers to large arteries, hence to pulse pressure, arterial stiffness, and wave reflections. The angiotensin-converting enzyme (ACE) inhibitor perindopril not only reduces mean arterial pressure but also acts specifically on pulse pressure. The effect on pulse pressure predominates on central rather than peripheral (brachial) large arteries, reducing aortic stiffness and most wave reflections. Such hemodynamic changes are not observed with standard β-blockade, which reduces aortic stiffness and brachial systolic and pulse pressure but not central pulse pressure and wave reflections. In hypertensive subjects, perindopril and other ACE inhibitors seem to predict more consistently the reduction of cardiovascular events, mainly of cardiac origin, than standard β-blockers alone. This effect is associated with the important biochemical finding that mechanotransductions of angiotensin and β-blockade are markedly different, acting in the former specifically on the α5β1 integrin complex and on the fibronectin ligand of arterial vessels.
antihypertensive therapy; arterial stiffness; renal function
This study sought to evaluate whether pulse wave velocity (PWV), a noninvasive index of arterial stiffness, is a predictor of the longitudinal changes in systolic blood pressure (SBP) and of incident hypertension.
Although arterial stiffness is believed to underlie, in part, the age-associated changes in SBP, particularly at older ages, few longitudinal studies in humans have examined the relationship between arterial stiffness and blood pressure.
Pulse wave velocity was measured at baseline in 449 normotensive or untreated hypertensive volunteers (age 53 ± 17 years). Repeated measurements of blood pressure were performed during an average follow-up of 4.9 ± 2.5 years.
After adjusting for covariates including age, body mass index, and mean arterial pressure, linear mixed effects regression models showed that PWV was an independent determinant of the longitudinal increase in SBP (p = 0.003 for the interaction term with time). In a subset of 306 subjects who were normotensive at baseline, hypertension developed in 105 (34%) during a median follow-up of 4.3 years (range 2 to 12 years). By stepwise Cox proportional hazards models, PWV was an independent predictor of incident hypertension (hazard ratio 1.10 per 1 m/s increase in PWV, 95% confidence interval 1.00 to 1.30, p = 0.03) in individuals with a follow-up duration greater than the median.
Pulse wave velocity is an independent predictor of the longitudinal increase in SBP and of incident hypertension. This suggests that PWV could help identify normotensive individuals who should be targeted for the implementation of interventions aimed at preventing or delaying the progression of subclinical arterial stiffening and the onset of hypertension.
Arterial stiffness occurs early in the atherosclerotic process; however, few data are available concerning risk factors for arterial stiffness in youth with diabetes. We identified factors associated with arterial stiffness in youth with diabetes and assessed the effects of these factors on the relationship between arterial stiffness and diabetes type (type 1 vs. type 2).
RESEARCH DESIGN AND METHODS
A subset of patients from the SEARCH for Diabetes in Youth study with type 1 (n = 535) and type 2 diabetes (n = 60), aged 10–23 years (52% male; 82% non-Hispanic white; diabetes duration 65 ± 49 months) had arterial stiffness, anthropometrics, blood pressure, fasting lipids, and A1C measured. Arterial stiffness was measured by brachial distensibility (brachD), pulse wave velocity (PWV), and augmentation index adjusted to heart rate of 75 beats/min (AI75).
Youth with type 2 diabetes had worse brachD (5.2 ± 0.9 vs. 6.1 ± 1.2%/mmHg), PWV (6.4 ± 1.3 vs. 5.3 ± 0.8 m/s), and AI75 (6.4 ± 9.9 vs. 2.2 ± 10.2%) than those with type 1 diabetes (P < 0.01 for each). These differences were largely mediated through increased central adiposity and higher blood pressure in youth with type 2 diabetes. We also found a pattern of association of arterial stiffness measures with waist circumference and blood pressure, independent of diabetes type.
Youth with type 2 diabetes have worse arterial stiffness than similar youth with type 1 diabetes. Increased central adiposity and blood pressure are associated with measures of arterial stiffness, independent of diabetes type. Whether these findings indicate that youth with type 2 diabetes will be at higher risk for future complications requires longitudinal studies.
Arterial stiffness increases with age and contributes to the pathogenesis of systolic hypertension and cardiovascular disease in the elderly. Knowledge about pathophysiological processes that determine arterial stiffness may help guide therapeutic approaches.
Methods and Results
We related seven circulating biomarkers, representing distinct biological pathways (C-reactive protein [CRP], aldosterone-to-renin ratio [ARR], N-terminal pro–atrial natriuretic peptide and B-type natriuretic peptide, plasminogen activator inhibitor [PAI]-1, fibrinogen, homocysteine) to 5 vascular function measures (central pulse pressure, carotid-femoral pulse wave velocity, mean arterial pressure, forward pressure wave amplitude [all measures of conduit artery stiffness], and augmented pressure, an indicator of wave reflection) in 2,000 Framingham Offspring Study participants (mean age 61 years, 55% women). Tonometry measures were obtained on average three years after biomarkers were measured. In multivariable linear regression models adjusting for covariates, the biomarker panel was significantly associated with all 5 vascular measures (p<0.003 for all). Upon backwards elimination, the ARR was positively associated with each stiffness measure (p≤0.002 for all). In addition, CRP was positively related to augmented pressure (p=0.0003), whereas PAI-1 was positively associated with mean arterial pressure (p=0.003), central pulse pressure (p=0.001) and forward pressure wave (p=0.01).
Our cross-sectional data on a community-based sample suggest a distinctive pattern of positive associations of biomarkers of renin-angiotensin-aldosterone system activation with pan-arterial vascular stiffness, PAI-1 with central vascular stiffness indices, and of CRP with wave reflection. These observations support the notion of differential influences of biological pathways on vascular stiffness measures.
arterial stiffness; renin-angiontensin-aldosterone system; C-reactive protein; plasminogen activator inhibitor; biomarker
Increased central arterial stiffness, involving accelerated vascular ageing of the aorta, is a powerful and independent risk factor for early mortality and provides prognostic information above and beyond traditional risk factors for cardiovascular disease (CVD). Central arterial stiffness is an important determinant of pulse pressure; therefore, any pathological increase may result in left ventricular hypertrophy and impaired coronary perfusion. Central artery stiffness can be assessed noninvasively by measurement of aortic pulse wave velocity, which is the gold standard for measurement of arterial stiffness. Earlier, it was believed that changes in arterial stiffness, which are primarily influenced by long-term pressure-dependent structural changes, may be slowed but not reversed by pharmacotherapy. Recent studies with drugs that inhibit the renin–angiotensin–aldosterone system, advanced glycation end products crosslink breakers, and endothelin antagonists suggest that blood pressure (BP)-independent reduction and reversal of arterial stiffness are feasible. We review the recent literature on the differential effect of antihypertensive agents either as monotherapy or combination therapy on arterial stiffness. Arterial stiffness is an emerging therapeutic target for CVD risk reduction; however, further clinical trials are required to confirm whether BP-independent changes in arterial stiffness directly translate to a reduction in CVD events.
aortic pulse wave velocity; augmentation index; blood pressure; renin–angiotensin–aldosterone system
Patients on peritoneal and hemodialysis have accelerated atherosclerosis associated with an increase in cardiovascular morbidity and mortality. The atherosclerosis is associated with increased arterial stiffness, endothelial dysfunction and elevated oxidative stress and inflammation. The aims of this study are to investigate the effects of peritoneal and hemodialysis on arterial stiffness, vascular function, myocardial structure and function, oxidative stress and inflammation in incident patients with end stage kidney disease.
This is an observational study. Eighty stage five CKD patients will be enrolled and followed for one-year. Primary outcome measures will be changes in 1) arterial stiffness measured by aortic pulse wave velocity, 2) oxidative stress assessed by plasma F2 isoprostanes and 3) inflammation measured by plasma pentraxin-3. Secondary outcomes will include additional measures of oxidative stress and inflammation, changes in vascular function assessed using the brachial artery reactivity technique, carotid artery intimal medial thickness, augmentation index and trans thoracic echocardiography to assess left ventricular geometry, and systolic and diastolic function. Patients will undergo these measures at baseline (6–8 weeks prior to starting dialysis therapy), then at six and 12 months after starting dialysis.
The results of this study may guide the choice of dialysis modality in the first year of treatment. It may also lead to a larger study prospectively assessing the effect of dialysis modality on cardiovascular morbidity and mortality.
Brachial-ankle pulse wave velocity (baPWV) is simple, noninvasive method which correlates well with arterial stiffness. Herein, we assessed the determinants of baPWV in normotensive young adults with type 2 diabetes. We retrospectively enrolled 103 consecutive type 2 diabetic patients aged between 30 and 39 yr who measured baPWV with noninvasive pulse wave analyzer. The anthropometric parameters, blood pressure, pulse rate, fasting plasma glucose, fasting insulin, fasting C-peptide, HbA1c, lipid profile, hs-CRP, albuminuria status, AST/ALT, γ-GTP were checked concurrently. Also, we investigated history of smoking, alcohol drinking and medications by questionnaire. We found that maximal baPWV was positively correlated with mean blood pressure (r = 0.404, P < 0.001), heart rate (r = 0.285, P = 0.004), AST (r = 0.409, P < 0.001), ALT (r = 0.329, P = 0.001), γ-GTP (r = 0.273, P = 0.006), Urine albumin/creatinine ratio (r = 0.321, P = 0.003). By multiple linear regression, mean blood pressure and heart rate were significantly associated with maximal baPWV in male and total group. In female group, mean blood pressure was the only variable associated with maximal baPWV. These factors can be surrogate markers of arterial stiffness in this population.
Pulse Wave Velocity; Type 2 Diabetes; Normotension
Arterial stiffness has been identified as an independent predictor of prognostic outcomes for patients with cardiovascular disease. Although measurement of pulse wave velocity has been a widely accepted noninvasive approach to the assessment of arterial stiffness, its accuracy is hampered by changes in blood pressure. Taking the exponential relation between intravascular pressure and arterial diameter into consideration, a stiffness parameter can be obtained by plotting the natural logarithm of systolic–diastolic pressure ratio against the arterial wall extensibility. Cardio-ankle vascular index (CAVI), which is calculated based on the stiffness parameter thus obtained, is theoretically independent of changes in blood pressure. With this distinct advantage, CAVI has been widely applied clinically to assess arterial stiffness in subjects with known cardiovascular diseases including those with diagnosed atherosclerosis, coronary heart disease, and stroke as well as those at risk, including those with hypertension, diabetes, the elderly, and the obese. Because of its enhanced sensitivity, not only has the index been used to discern subtle changes in the disease process, it has also been utilized in studying normal individuals to assess their potential risks of developing cardiovascular diseases. The primary aims of assessing arterial stiffness using CAVI are not only to aid in early detection of arteriosclerosis to allow timely treatment and change in lifestyle, but also to quantitatively evaluate the progression of disease and the effectiveness of treatment. Despite its merit of being unaffected by blood pressure, discretion in data interpretation is suggested because an elevated CAVI represents not just vascular stiffness caused by pathological changes in the arterial wall, but can also be attributed to an increased vascular tone brought about by smooth muscle contraction. Moreover, certain patient populations, such as those with an ankle-brachial index < 0.9, may give falsely low CAVI and are suggested to be excluded from study.
cardio-ankle vascular index; stiffness parameter; cardiovascular disease; atherosclerosis; arteriosclerosis; pulse wave velocity
Stiffness of the central arteries in aging may contribute to cerebral microvascular disease independent of hypertension and other vascular risk factors. Few studies of older adults have evaluated the association of central arterial stiffness with longitudinal cognitive decline.
We evaluated associations of aortic pulse wave velocity (centimeters per second), a measure of central arterial stiffness, with cognitive function and decline in 552 participants in the Health, Aging, and Body Composition (Health ABC) study Cognitive Vitality Substudy (mean age ± SD = 73.1 ± 2.7 years, 48% men and 42% black). Aortic pulse wave velocity was assessed at baseline via Doppler-recorded carotid and femoral pulse waveforms. Global cognitive function, verbal memory, psychomotor, and perceptual speed were evaluated over 6 years.
After adjustment for demographics, vascular risk factors, and chronic conditions, each 1 SD higher aortic pulse wave velocity (389 cm/s) was associated with poorer cognitive function: −0.11 SD for global function (SE = 0.04, p < .01), −0.09 SD for psychomotor speed (SE = 0.04, p = .03), and −0.12 SD for perceptual speed (SE = 0.04, p < .01). Higher aortic pulse wave velocity was also associated with greater decline in psychomotor speed, defined as greater than 1 SD more than the mean change (odds ratio = 1.42 [95% confidence interval = 1.06, 1.90]) but not with verbal memory or longitudinal decline in global function, verbal memory, or perceptual speed. Results were consistent with mixed models of decline in each cognitive test.
In well-functioning older adults, central arterial stiffness may contribute to cognitive decline independent of hypertension and other vascular risk factors.
Aging; Arterial stiffness; Cognitive decline
Obesity is associated with increased risk of cardiovascular disease. Arterial stiffness assessed by carotid femoral pulse wave velocity (PWV) is an independent predictor of cardiovascular morbidity and mortality. We aimed to investigate how various measures of body composition affect arterial stiffness.
This is an analysis of cross-sectional baseline data from a controlled clinical trial addressing changes in arterial stiffness after either surgery or lifestyle intervention in a population of morbidly obese patients. High-fidelity applanation tonometry (Millar®, Sphygmocor®) was used to measure pulse wave velocity (PWV). Carotid femoral PWV is a direct measure of arterial stiffness and is considered to be the gold standard method. The Inbody 720 Body Composition Analyzer was used for bioelectrical impedance analysis (BIA). Spearman's correlation, independent samples t-test, chi-square tests, Fisher's exact test and multiple linear regression analyses were used as statistical methods.
A total of 133 patients (79 women), with a mean (SD) age of 43 (11) years were included in the study. Men had a significantly higher prevalence of obesity related comorbidities and significantly higher PWV, 9.1 (2.0) m/s vs. 8.1 (1.8) m/s, p = 0.003, than women. In the female group, PWV was positively correlated with WC, WHtR, BMI and visceral fat area. In the male group, PWV was negatively correlated with BMI. Multiple linear regression analysis showed that increasing BMI, WC, WHtR, visceral fat area and fat mass were independently associated with higher PWV in women, but not in men, after adjustment for age, hypertension and type 2 diabetes.
Most measures of general and abdominal obesity were predictors of arterial stiffness in female morbidly obese patients.
ClinicalTrials.gov Identifier NCT00626964
Arterial stiffness is an independent predictor of cardiovascular morbidity and mortality. This study aimed to compare the 7-week effect of a low-calorie diet (LCD) and an intensive lifestyle intervention program (ILI) on arterial stiffness in morbidly obese individuals.
Design and Methods
Nonrandomized clinical trial. The LCD provided 900 kcal/day, and participants in the LCD group were instructed to maintain their habitual physical activity level. The ILI included two 90-min supervised training sessions 3 days a week at moderate to high intensity (4-8 METs) and a caloric restriction of 1000 kcal/day.
A total of 179 individuals completed the study, 88 (56 women) in the ILI group and 91 (57 women) in the LCD group. High-fidelity applanation tonometry (Millar®, Sphygmocor®) was used to measure carotid-femoral pulse wave velocity (PWV). After adjustment for relevant confounders, the ILI group had a significantly greater reduction in PWV than the LCD group; −0.4 (−0.6, −0.1) m/s, P = 0.004. When compared to the LCD group, the ILI group showed a larger reduction in systolic and diastolic blood pressure −5 (−9, −1) and −5 (−7, −2) mmHg, P = 0.038 and P ≤ 0.001 respectively, whereas no difference was observed regarding pulse pressure, P = 0.661. No significant differences between groups were found regarding the loss of fat mass, P = 0.259, but the loss of muscle mass was larger in the LCD group, 0.8 (0.5, 1.1) kg, P ≤ 0.001.
Despite the limitations of a nonrandomized design, our findings indicate that for morbidly obese individuals a moderate caloric restriction combined with aerobic physical exercise is associated with a greater decline in PWV than a LCD alone.
We prospectively and longitudinally determined the effects of childhood obesity on arterial stiffening and vascular wall changes. Changes in arterial stiffness measured as pulse wave velocity (PWV) and vascular morphology of the radial (RA) and dorsal pedal arteries (DPA) were examined in obese adolescents compared to lean subjects in a 5-year follow-up study.
A total of 28 obese subjects and 14 lean controls participated in both baseline (14 years old) and follow-up studies. PWV was measured by tonometer (SphygmoCor®) and recorded at RA and carotid artery, respectively. Intima thickness (IT), intima-media thickness (IMT) and RA and DPA diameters were measured using high-resolution ultrasound (Vevo 770™). Over the course of 5 years, PWV increased by 25% in the obese subjects as compared to 3% in the controls (p = 0.01). Diastolic blood pressure (DBP) increased by 23% in the obese subjects as opposed to 6% in controls (p = 0.009). BMI increased similarly in both groups, as did the IT and IMT. The change in PWV was strongly associated to the baseline BMI z -score (r = 0.51, p<0.001), as was the change in DBP (r = 0.50, p = 0.001).
During the transition from early to late adolescence, there was a general increase in arterial stiffness, which was aggravated by childhood obesity. The increase in arterial stiffness and DBP after 5 years was closely correlated to the baseline BMI z -score, indicating that childhood obesity has an adverse impact on vascular adaptation.
Serum dehydroepiandrosterone (DHEA) concentrations decrease ~80% between ages 25 and 75 yr. Aging also results in an increase in arterial stiffness, which is an independent predictor of cardiovascular disease (CVD) risk and mortality. Therefore, it is conceivable that DHEA replacement in older adults could reduce arterial stiffness. We sought to determine if DHEA replacement therapy in older adults reduces carotid augmentation index (AI) and carotid-femoral pulse wave velocity (PWV) as indices of arterial stiffness.
A randomized, double-blind trial was conducted to study the effects of 50 mg/d DHEA replacement on AI (n=92) and PWV (n=51) in women and men aged 65–75 yr. Inflammatory cytokines and sex hormones were measured in fasting serum.
AI decreased in the DHEA group but not in the placebo group (difference between groups, −6±2 AI units, p=0.002). PWV also decreased (difference between groups, −3.5±1.0 m/sec, p=0.001); however, after adjusting for baseline values, the between-group comparison became non-significant (p=0.20). The reductions in AI and PWV were accompanied by decreases in inflammatory cytokines (TNFα and IL-6, p<0.05) and correlated with increases in serum DHEAS (r = −0.31 and −0.37, respectively, p<0.05). The reductions in AI also correlated with free testosterone index (r = −0.23, p=0.03).
DHEA replacement in elderly men and women improves indices of arterial stiffness. Arterial stiffness increases with age and is an independent risk factor for CVD. Therefore the improvements observed in the present study suggest that DHEA replacement might partly reverse arterial aging and reduce CVD risk.
vasculature; augmentation index; aging