Changes In Aortic Pulse Wave Velocity Research Articles

Aortic diastolic pressure decay modulates relation between worsened aortic stiffness and myocardial oxygen supply/demand balance after resistance exercise.

High-intensity resistance exercise (RE) increases aortic stiffness and decreases the index of myocardial oxygen supply/demand balance (Buckberg index, BI); there is a correlation between the changes in these parameters. Central hemodynamics during diastole can explain the correlation. We aimed to investigate whether the aortic diastolic decay index mediates the association between changes in aortic stiffness and BI by high-intensity RE. We evaluated the effect of high-intensity RE on aortic stiffness, BI, aortic decay index, and their associations in 52 young men. Subjects were studied under parallel experimental conditions on two separate days. The order of experiments was randomized between RE (5 sets of 10 repetitions at 75% of 1-repetition maximum) and sham control (seated rest). Aortic pulse wave velocity (PWV; index of aortic stiffness), BI, and aortic decay index were measured in all subjects. Aortic decay index was quantified by fitting an exponential curve: P(t) = P0e-λt (where λ is decay index, P0 is end-systolic pressure and t is time from end-systole). Aortic PWV and decay index increased and BI decreased after RE. RE conditions showed that change in the aortic decay index was associated with changes in aortic PWV and changes in aortic PWV were related to changes in BI, although the PWV-BI relationship was not significant after accounting for decay index change. Mediation analysis revealed the mediating effect of the aortic decay index on the relationship between changes in aortic PWV and BI. The present findings suggest that high-intensity RE-induced aortic stiffening worsens myocardial viability by accelerating aortic diastolic exponential decay.NEW & NOTEWORTHY Aortic pulse wave velocity (PWV) and diastolic decay index increased and Buckberg index (BI) decreased after resistance exercise (RE). Mediation analysis revealed a mediating effect of aortic decay index on the relationship between changes in aortic PWV and BI. The present study provides evidence that high-intensity RE-induced aortic stiffening accelerates aortic decay and aortic decay can account for the relationship between aortic stiffening and a deteriorated surrogate marker of myocardial oxygen supply/demand balance induced by high-intensity RE.

Favorable effects on arterial stiffness after renal sympathetic denervation for the treatment of resistant hypertension: a cardiovascular magnetic resonance study

Favorable effects on arterial stiffness after renal sympathetic denervation for the treatment of resistant hypertension: a cardiovascular magnetic resonance study Tommy Arild Hammer,1 Knut Asbjørn Rise Langlo,2 Pål Erik Goa,1,3 Fadl Elmula M Fadl Elmula,4,5 Pavel Hoffmann,6 Knut Haakon Stensaeth1,7 1Department of Radiology and Nuclear Medicine, 2Department of Nephrology, St Olav’s University Hospital, Trondheim, Norway; 3Department of Physics, Norwegian University of Science and Technology, Trondheim, Norway; 4Institute of Cardiovascular and Renal Research, Department of Cardiology, Oslo University Hospital, Oslo, Norway; 5Faculty of Clinical Medicine, University of Oslo, Oslo, Norway; 6Department of Cardiology, Oslo University Hospital, Oslo, Norway; 7Institute of Circulation and Medical Imaging, Norwegian University of Science and Technology, Trondheim, Norway Aims: Renal sympathetic denervation (RDN) has recently been suggested to be a novel treatment strategy for patients with treatment-resistant hypertension. However, the latest randomized studies have provided conflicting results and the influence of RDN on arterial stiffness remains unclear. Therefore, this study aimed to detect the effects of RDN on arterial stiffness as measured with aortic pulse wave velocity (PWV) and distensibility in addition to cardiac function and T1 mapping at baseline and at 6-month follow-up.Methods: RDN was performed in a total of 16 patients with treatment-resistant hypertension, and the procedures were conducted at two university hospitals using two different RDN devices. All patients and age-matched controls underwent a comprehensive clinical examination and cardiac magnetic resonance protocols both at baseline and at a 6-month follow-up.Results: In the treatment group, the systolic blood pressure (SBP) was found to be decreased at the follow-up visit (office SBP; 173±24 compared to 164±25 mmHg [P= 0.033]), the 24-hour ambulatory SBP had decreased (163±25 compared to 153±20 mmHg [P=0.057]), the aortic PWV had decreased from 8.24±3.34 to 6.54±1.31 m/s (P=0.053), and the aortic distensibility had increased from 2.33±1.34 to 3.96±3.05 10−3 mmHg−1 (P=0.013). The changes in aortic PWV and distensibility were independent of the observed reductions in SBP.Conclusion: The arterial stiffness, as assessed with aortic PWV, and distensibility were improved at 6 months after RDN. This improvement was independent of the reduction in SBP. Keywords: renal denervation, cardiovascular MR, arterial stiffness

Abstract P336: Changes in Arterial Pulse Wave Velocity, Effective Arterial Elastance, and Contractility in Hypertension Induced Cardiovascular Disease in Rats: Independent Prognostic Values

Hypertension is an established comorbidity in cardiovascular (CV) disease. Changes in aortic pulse-wave velocity (PWV) have been shown to predict the longitudinal development of hypertension, its underlying vascular alterations, and associated CV risks. However, as the heart and arterial tree are coupled, it has been shown that the successful monitoring of not only CV disease progression, but of its therapies, requires the evaluation of ventriculo-arterial uncoupling and its determinants. This study aimed to establish the relationships between PWV and changes in the estimated effective arterial elastance (Ea) and/or contractility over a wide-range of hypertension-induced CV pathologies in a controlled rodent model/environment. In a large series (n = 96) of anesthetized (pentobarbital) male Sprague-Dawley rats, PWV (carotid-to-femoral), systolic pressures, contractility (preload recruitable stroke work; PRSW), and Ea were evaluated using echocardiography, invasive hemodynamics, and left ventricular (LV) pressure-volume relationships. Data were collected in healthy animals (n = 37) and those with hypertension-induced chronic systolic/diastolic left-ventricular dysfunction (n = 59) (chronic beta-adrenergic stimulation and/or renoprival). A subset of each group, were also studied under common clinical cardio/vasoactive pharmacological interventions. Disease animals had significantly (P < 0.001) higher systolic pressures (141 ± 4 vs 116 ± 4 mmHg), faster PWV (9.0 ± 0.8 vs 5.1 ± 0.5 m/s), and depressed contractility (PRSW: 39 ± 1 vs. 49 ± 1 mmHg*). Both PWV (7.6 ± 0.7 to 4.3 ± 0.4 m/s) and Ea (95 ± 10 to 63 ± 8 mmHg/mL) decreased in response to vascular therapies in the diseased animals; only PWV was reduced in healthy rats. More interestingly, over all conditions, PWV was a poor predictor of both systolic pressures (R 2 =0.00009) and Ea (R 2 = 0.024). but yet was a moderate predictor of PRSW (R 2 =0.23, P < 0.001), suggesting a contractility-dependent velocity of propagation. Taken together, these data suggest that indices of ventriculo-arterial efficacy, cardiac afterload, and peripheral arterial stiffness while all are affected by CV disease, each cannot be used to predict one another, and all provide independent prognostic information in disease.

Cardiovascular and inflammatory effects of simvastatin therapy in patients with COPD: a randomized controlled trial

BackgroundThere is excess cardiovascular mortality in patients with chronic obstructive pulmonary disease. Aortic stiffness, an independent predictor of cardiovascular risk, and systemic and airway inflammation are increased in patients with the disease. Statins modulate aortic stiffness and have anti-inflammatory properties. A proof-of-principle, double-blind, randomized trial determined if 6 weeks of simvastatin 20 mg once daily reduced aortic stiffness and systemic and airway inflammation in patients with chronic obstructive pulmonary disease.MethodsStable patients (n=70) were randomized to simvastatin (active) or placebo. Pre-treatment and post-treatment aortic stiffness, blood pressure, spirometry, and circulating and airway inflammatory mediators and lipids were measured. A predefined subgroup analysis was performed where baseline aortic pulse wave velocity (PWV) was >10 m/sec.ResultsTotal cholesterol dropped in the active group. There was no significant change in aortic PWV between the active group and the placebo group (−0.7 m/sec, P=0.24). In those with aortic stiffness >10 m/sec (n=22), aortic PWV improved in the active group compared with the placebo group (−2.8 m/sec, P=0.03). Neither systemic nor airway inflammatory markers changed.ConclusionThere was a nonsignificant improvement in aortic PWV in those taking simvastatin 20 mg compared with placebo, but in those with higher baseline aortic stiffness (a higher risk group) a significant and clinically relevant reduction in PWV was shown.

Influence of single bout of aerobic exercise on aortic pulse pressure.

Regular aerobic exercise has come to the forefront of non-pharmacological treatment for hypertension. In this line, post-exercise hypotension may have a potential tool for efficient blood pressure management. However, less is known about the influence of acute aerobic exercise on aortic pulse pressure (PP), an important property underlying the pathophysiology of cardiovascular disease. We tested the hypotheses that aortic PP would be attenuated with a single aerobic exercise and that its extent would be associated with the delayed return of reflected wave and the leg vasodilatory capacity. In 23 apparent healthy men (22 ± 4 years), hemodynamic variables and aortic pulse wave velocity (PWV) were measured before and 20 and 50 min after a 60-min bout of cycling exercise at moderate intensity (corresponding to 65-75 % heart rate reserve). Aortic pressure was estimated from applanation tonometrically measured radial arterial pressure waveform via general transfer function. Peak calf vascular dilatory capacity was measured with the ischemic exercise-induced hyperemia (via venous occlusion plethysmography). Finger, brachial, and aortic PP were significantly attenuated following the exercise. At 20 min after the exercise cessation, individual changes in aortic PWV significantly correlated with corresponding changes in aortic PP (r = 0.541, P < 0.05), but this correlation was no longer significant at 50 min after the exercise cessation. Peak calf vascular dilatory capacity was not associated with change in aortic PP. We conclude that in young men the aortic PP would be attenuated with the moderate-intensity dynamic exercise partly due to the delayed return of reflection wave from periphery.

Short-term Aerobic Exercise and Vascular Function in CKD Stage 3: A Randomized Controlled Trial

The present study was designed to determine the effect of short-term moderate-intensity exercise training on arterial stiffness in patients with chronic kidney disease (CKD) stage3. Randomized controlled trial with a parallel-group design. Testing and training sessions were performed at Springfield College. 46 (treatment group, n=25; control group, n=21) patients with CKD with diabetes and/or hypertension completed the study. The aerobic training program consisted of 16 weeks of supervised exercise training at 50%-60% peak oxygen uptake (Vo2peak) 3 times per week, while the control group remained sedentary. Identical testing procedures were performed following the 16-week intervention. The primary outcome was arterial stiffness. Secondary outcomes were aerobic capacity, various blood parameters (endothelin 1, nitrate/nitrite, and high-sensitivity C-reactive protein), and health-related quality of life. Arterial stiffness was assessed with aortic pulse wave velocity (PWV), aerobic capacity by Vo2peak, blood parameters by enzyme-linked immunosorbent assays, and health-related quality of life by the 36-Item Short Form Health Survey (SF-36). Participants attended 4 sessions before being randomly assigned to either the treatment or control group. Participants gave consent during the first session, whereas a graded exercise test with measurement of Vo2peak was completed during the second session. During sessions 3 and 4, aortic PWV was measured at rest prior to 40 minutes of either moderate-intensity exercise training or seated rest. A venous blood sample was obtained prior to exercise or rest and participants completed the SF-36 questionnaire. 16 weeks of training led to an 8.2% increase in Vo2peak for the treatment group (P=0.05), but no changes in aortic PWV . Randomization was not concealed and was violated on one occasion; also, use of an indirect measurement of endothelial function and the short duration of the intervention. Short-term moderate-intensity exercise training does not alter arterial stiffness in patients with CKD, but seems to reduce endothelin 1 levels.

Arterial stiffness in patients with COPD: the role of systemic inflammation and the effects of pulmonary rehabilitation

Clear evidence for an association between systemic inflammation and increased arterial stiffness in patients with chronic obstructive pulmonary disease (COPD) is lacking. Moreover, the effects of pulmonary rehabilitation on arterial stiffness are not well studied. We aimed to 1) confirm increased arterial stiffness in COPD; 2) evaluate its correlates including systemic inflammation; and 3) study whether or not it is influenced by pulmonary rehabilitation. Aortic pulse-wave velocity (APWV) was determined in 168 healthy volunteers, and APWV and inflammatory markers were determined in 162 COPD patients during baseline evaluation of a pulmonary rehabilitation programme. A complete post-pulmonary rehabilitation dataset was collected in 129 patients. It was found that APWV was increased in COPD patients when compared with controls, blood pressure and age predicted baseline APWV, and systemic inflammatory markers were not independently related to APWV. Although baseline APWV was predictive for the change in APWV after pulmonary rehabilitation (r= -0.77), on average APWV did not change (10.7 ± 2.7 versus 10.9 ± 2.5 m·s(-1); p=0.339). Arterial stiffness in COPD is not related to systemic inflammation and does not respond to state-of-the-art pulmonary rehabilitation. These results emphasise the complexity of cardiovascular risk and its management in COPD.

P128 Cardiovascular Effects of Statin Therapy on Arterial Stiffness in Patients with COPD: A Double Blind Randomised Controlled Trial

BackgroundAs cardiovascular disease is a comorbidity and major cause of death in patients with COPD, primary preventative strategies are required. Arterial stiffness, as measured by aortic pulse wave velocity (PWV)...

Effect of whole-body mild-cold exposure on arterial stiffness and central haemodynamics: a randomised, cross-over trial in healthy men and women

Aortic pulse wave velocity (PWV) and augmentation index (AIx) are independent predictors of cardiovascular risk and mortality, but little is known about the effect of air temperature changes on these variables. Our study investigated the effect of exposure to whole-body mild-cold on measures of arterial stiffness (aortic and brachial PWV), and on central haemodynamics [including augmented pressure (AP), AIx], and aortic reservoir components [including reservoir and excess pressures (P ex)]. Sixteen healthy volunteers (10 men, age 43 ± 19 years; mean ± SD) were randomised to be studied under conditions of 12 °C (mild-cold) and 21 °C (control) on separate days. Supine resting measures were taken at baseline (ambient temperature) and after 10, 30, and 60 min exposure to each experimental condition in a climate chamber. There was no significant change in brachial blood pressure between mild-cold and control conditions. However, compared to control, AP [+2 mmHg, 95 % confidence interval (CI) 0.36-4.36; p = 0.01] and AIx (+6 %, 95 % CI 1.24-10.1; p = 0.02) increased, and time to maximum P ex (a component of reservoir function related to timing of peak aortic in-flow) decreased (-7 ms, 95 % CI -15.4 to 2.03; p = 0.01) compared to control. Yet there was no significant change in aortic PWV (+0.04 m/s, 95 % CI -0.47 to 0.55; p = 0.87) or brachial PWV (+0.36 m/s; -0.41 to 1.12; p = 0.35) between conditions. We conclude that mild-cold exposure increases central haemodynamic stress and alters timing of peak aortic in-flow without differentially affecting arterial stiffness.

Role of Birth Weight and Postnatal Growth on Pulse Wave Velocity in Teenagers

Low birth weight and accelerated postnatal growth appear to play a significant role in the pathogenesis of hypertension and cardiovascular disease in adulthood. The aim of the present study was to characterize the factors determining pulse wave velocity (PWV) in teenagers and, in particular, to verify the relationship with birth weight, postnatal growth, timing of adiposity rebound, lifestyle, and hemodynamic parameters. Carotid-femoral and carotid-radial pulse wave velocities of 558 healthy teenagers (age range: 16.2-19.9 years) were determined by means of a PulsePen tonometer. Birth weight and gestational age were obtained from obstetrical records, and data regarding postnatal growth were obtained from pediatric clinical records. No change in aortic PWV was found in association with birth weight, postnatal growth, and timing of adiposity rebound. However, the study showed a strong association between accelerated growth from 0 to 12 months and carotid-radial PWV (trend: p = .02). Subjects with birth weight values <2,500 g showed higher values of upper limb PWV (p < .05) and higher values of diastolic and mean arterial pressure (p < .05). Stepwise regression analysis revealed that mean arterial pressure, age, and height were the main independent factors determining aortic PWV in this young population. These results suggest that there is no linear correlation between birth weight and hemodynamic parameters in teenagers; however, subjects characterized by very low birth weight and accelerated postnatal weight gain appear to demonstrate increased upper limb PWV and diastolic and mean arterial pressure values.

Aortic stiffness is increased in polymyalgia rheumatica and improves after steroid treatment

BackgroundInflammatory rheumatic diseases have been associated with increased cardiovascular risk and arterial stiffness. Polymyalgia rheumatica (PMR), a disease which affects primarily older people, is characterised by a systemic inflammatory response...

Large-artery stiffness: A reversible marker of cardiovascular risk in primary hyperparathyroidism

ObjectivePatients with primary hyperparathyroidism (pHPT) are at increased risk of cardiovascular mortality. We investigated whether aortic stiffness, an early marker of arteriosclerosis and a strong predictor of cardiovascular risk, is increased in pHPT, and whether it improves after parathyroidectomy. MethodsTwenty-four patients with mild pHPT (age 56±10 years, blood pressure 136/85mmHg, serum calcium 2.55–3.00mmol/L) and 48 control subjects individually matched with cases by age, sex and blood pressure underwent aortic (carotid-femoral) and upper-limb (carotid-radial) pulse wave velocity (PWV) determination by applanation tonometry in a case-control study. Subjects with renal disease, diabetes, treated hypertension or overt cardiovascular disease were excluded from the study. Seventeen of the patients with pHPT were re-examined 4 weeks after surgical parathyroidectomy. ResultsAortic PWV was significantly higher among pHTP patients (11.4±2 vs 9.6±2m/s, p<0.001). In a conditional logistic regression analysis, pHPT was independently associated with an increased risk of having an aortic PWV >12m/s (odds ratio 3.28, 95% confidence interval 1.21–8.93). As expected, surgery was accompanied by a reduction in serum calcium (from 2.77±0.2 to 2.25±0.1mmol/L, p<0.001) and parathyroid hormone (from 29.6±10 to 3.3±2pmol/L, p<0.001). Aortic PWV decreased after surgery (from 10.9±2 to 9.8±2m/s, p=0.003). The change in aortic PWV remained significant also after adjustment for changes in blood pressure (p<0.01). Changes in upper-limb PWV generally paralleled those in aortic PWV. ConclusionpHPT is associated with increased aortic stiffness, which improves after parathyroidectomy. Our data demonstrate that aortic stiffness may improve upon removal of hyperparathyroid stimuli.

CENTRAL BLOOD PRESSURE AND AUGMENTATION INDEX DECREASE ARE DEPENDENT ON AORTIC PULSE WAVE VELOCITY IMPROVEMENT: THE EXPLOR STUDY: PP.10.406

Antihypertensive drugs have different effects on peripheral and central blood pressure (BP). In the EXPLOR trial, we have demonstrated that angiotensin-receptor blockers (ARBs) lower central BP more efficiently than atenolol, when amlodipine is given in association. In this analysis we investigated the interrelationship between decrease in central pressure and augmentation index and changes in pulse wave velocity. Methods: Central systolic BP (cSBP) was measured with applanation tonometry (Sphygmocor ®) after 28 weeks active treatment by the single pill combination valsartan-amlodipine (VA, 80/5 mg then 160/10 mg) or an atenolol-amlodipine combination (AA, 50/5 mg then 100/10 mg) in a prospective, randomized, parallel groups, PROBE design, multicentric trial. Data quality was controlled by a Core-Lab, blinded for center, visit and treatment allocation. VA or AA were were uptitrated from W8 to W24. We analyzed changes in central systolic pressure (cSBP), augmentation index (AIx), and carotid-to-femoral pulse wave velocity (PWV) between W24 and baseline. Results are expressed as slope (β), standardized slope (βs), % explained variance (%EV) and p values. Results: Data were adjusted on age, sex, treatment, changes in HR and baseline values. Change in cSBP was significantly associated with change in PWV (β: 2.4, βs: 0.35, EV%: 12%, p < 10–6). Similarly, change Aix was significantly associated with change in PWV (β: 0.27, βs: 0.12, EV%: 1.5%, p < 0.01). Changes in PWV were strongly dependent on changes in HR, cSBP or AIx. Correlation with change in cSBP was stronger than those with brachial SBP (EV% 8% and 0.9%, respectively). Interestingly, changes in cSBP and AIx remained significantly larger with valsartan-amlodipine, compared to atenolol-amlodipine when changes in PWV were accounted for. Conclusion: Changes in central systolic blood pressure and augmentation index are dependent on changes in aortic PWV. The differential effect of valsartan over atenolol on central SBP and augmentation index remained significant, even when adjusted on PWV.

Effect of Membrane Permeability on Inflammation and Arterial Stiffness

Both larger molecule removal and dialyzer biocompatibility have been implicated in the high-flux hemodialysis (HD)-associated favorable outcome. In an attempt to delineate the effect of membrane permeability, we performed a randomized, crossover study to compare the inflammatory biomarkers, lipid profile, and aortic pulse wave velocity (PWV) of two dialyzers that are composed of identical membranes but with different flux characteristics. Stable patients who had anuria and were on low-flux polysulfone membrane were randomly allocated either to HD with high-flux polyamide membrane (group A; 22 patients) or to HD with low-flux polyamide membrane (group B; 24 patients) for 24 weeks, then they were started on 24 weeks of the alternative HD treatment. Apart from the dialyzer, the dialysis prescription remained unchanged. Nineteen patients from group A and 23 patients from group B completed the study. Predialysis beta(2)-microglobulin levels decreased significantly when using the high-flux polyamide membrane. No difference between membranes was observed for serum albumin, high-sensitivity C-reactive protein, fibrinogen, IL-6, triglycerides, HDL cholesterol, LDL cholesterol, and lipoprotein(a) during the study. A significant increase in aortic PWV, a marker of aortic stiffness, was noted after patients switched from high-flux to low-flux polyamide membranes. Similarly, the rate of change in aortic PWV was significantly decreased with the use of the high-flux polyamide membrane. Our findings suggest that dialysis with polyamide membranes with different flux characteristics did not modify the inflammatory indices and lipid profile in stable HD patients; however, a seemingly beneficial effect on aortic stiffness was noted for patients who were maintained on high-flux polyamide membrane.

Opposite changes in carotid versus aortic stiffness during healthy human pregnancy

Systemic arterial compliance has been known to increase during healthy pregnancy, whereas, recently, the carotid artery has been reported to stiffen. To clarify this controversy, we simultaneously measured aortic PWV (pulse wave velocity) and carotid artery elastic parameters in a cohort of pregnant women. Twelve normotensive pregnant women were studied longitudinally during the three trimesters of pregnancy (T1, T2 and T3 respectively) and 12 weeks PP (postpartum). Carotid artery diastolic diameter and pulsatile distension was measured by an echo-wall tracking method and carotid pulse pressure by applanation tonometry. Carotid strain, compliance, distensibility coefficient, stiffness index beta, Einc (incremental elastic modulus) and augmentation index were calculated. Aortic PWV was determined to estimate aortic distensibility. All carotid artery elastic parameters indicated significant stiffening from T1 to T3 (1.8+/-0.2 versus 2.9+/-0.3 mmHg for Einc), which was reversed after delivery (2.3+/-0.2 mmHg). Aortic PWV decreased during pregnancy (6.2+/-0.2 versus 5.4+/-0.2 m/s) and increased in the PP period (6.7+/-0.2 m/s). No correlation was found between changes in carotid artery elastic parameters and changes in aortic PWV either from T1 to T3 or from T3 to PP. The carotid artery exhibits regionally specific stiffening during pregnancy, which appears to represent a qualitatively different change in arterial elastic behaviour.

Stiffening Our Resolve Against Adult Weight Gain

Increasing adiposity with a clinical endpoint of obesity is associated with a progressive increase in risk of cardiovascular diseases (CVD). However, we are only beginning to understand the physiological and pathophysiological mechanisms by which excessive body fat storage causes CVD. In this issue of Hypertension , the findings of Wildman et al1 extend and strengthen previous observations2–5 by showing that changes in arterial stiffness, as measured by aortic pulse-wave velocity (PWV), are related to changes in body weight over a 2-year follow-up period in healthy men and women aged 20 to 40 years. Weight gain was associated with an increase, whereas weight loss was associated with a decrease in aortic PWV, independent of changes in blood pressure. The greatest increases in aortic PWV were observed in those subjects who gained the most weight (≥4.5 kg). Importantly, the changes in aortic PWV were related to changes in body mass index (BMI), indicating that the associations with body weight were mediated by changes in adiposity (rather than fat-free mass). Changes in aortic PWV over time also were related to baseline body weight, BMI, and waist circumference (an indirect measure of abdominal adiposity), providing evidence that higher initial levels of total and abdominal body fatness are associated with greater future increases in arterial stiffness. The study included subjects with a broad range of BMI, suggesting that the findings are applicable to both nonobese and obese adults in the general population. An important finding was that black adults demonstrated greater increases in weight gain-adjusted and blood pressure-adjusted aortic PWV over time, suggesting that they undergo greater increases in arterial stiffness in response to the same age-associated weight gain compared with whites. These observations provide further support for the emerging concept that adiposity-driven weight gain during adulthood contributes significantly to the adverse changes …

Arterial Stiffness: Pathophysiology and Clinical Impact

The ill effects of hypertension are usually attributed to a reduction in the caliber or the number of arterioles, resulting in an increase in total peripheral resistance (TPR). This definition does not take into account the fact that BP is a cyclic phenomenon with systolic and diastolic BP being the limits of these oscillations. The appropriate term to define the arterial factor(s) opposing LV ejection is aortic input impedance which depends on TPR, arterial distensibility (D), and wave reflections (WR). D defines the capacitive properties of arterial stiffness, whose role is to dampen pressure and flow oscillations and to transform pulsatile flow and pressure in arteries into a steady flow and pressure in peripheral tissues. Stiffness is the reciprocal value of D. These parameters are BP dependent, and arteries become stiffer at high pressure. In to D which provides information about the <<elasticity>> of artery as a hollow structure, the elastic incremental modulus (Einc) characterizes the properties of the arterial wall biomaterials, independently of vessel geometry. As an alternative, arterial D can be evaluated by measuring the pulse wave velocity (PWV) which increases with the stiffening of arteries. Arterial stiffening increases left ventricular (LV) afterload and alters the coronary perfusion. With increased PWV, the WR impacts on the aorta during systole, increasing systolic pressures and myocardial oxygen consumption, and decreasing diastolic BP and coronary flow. The arterial stiffness is altered primarily in association with increased collagen content and alterations of extracellular matrix (arteriosclerosis) as classically observed during aging or in arterial hypertension. The arterial stiffening estimated by changes in aortic PWV and intensity of WR are independent predictors of survival in end stage renal disease (ESRD) and general population. Improvement of arterial stiffening could be obtained by antihypertensive treatmen as observed with the calcium-channel blocker and ACE inhibitors. ACE inhibitors increased AC and reduced WR, and it has been shown that reversibility of aortic stiffening and use of ACE inhbitors had favorable independent effect on survival in hypertensive patients with advanced renal disease.

Blood pressure reductions with exercise and sodium restriction in postmenopausal women with elevated systolic pressure: role of arterial stiffness

OBJECTIVES This study determined the relative efficacy of aerobic exercise (daily walking) and moderate dietary sodium restriction (sodium intake <100 mmol/day) for reducing systolic blood pressure (SBP) and pulse pressure (PP) in postmenopausal women with elevated initial levels, and the potential role of reductions in large artery stiffness in these changes. BACKGROUND Lifestyle behaviors are recommended for lowering blood pressure (BP) in adults with elevated baseline levels, but there is little information as to the relative efficacy of different interventions or the mechanisms underlying their potential beneficial effects. METHODS After baseline measurements and random assignment, 35 nonmedicated healthy postmenopausal women with SBP between 130 and 159 mm Hg completed three months of either aerobic (walking) exercise (n = 18; 62 ± 9 years, mean ± SD) or moderate dietary sodium restriction (SR) (n = 17; 65 ± 10 years, mean ± SD). RESULTS Body mass and composition, plasma volume, and fasting concentrations of metabolic coronary risk factors did not differ between the groups at baseline or change with intervention. Systolic BP and PP at rest decreased with both exercise and SR (p < 0.05); however, the reductions were three- to fourfold greater with SR (p < 0.05). Sodium restriction, but not exercise, also reduced 24-h SBP and PP (p < 0.05). Aortic pulse wave velocity (PWV) and carotid augmentation index were reduced only with SR (p < 0.05). Changes in SBP and PP at rest and over 24 h correlated with the corresponding changes in aortic PWV (r = 0.53 to 0.61, p < 0.01). CONCLUSIONS Moderate SR lowers SBP and PP in postmenopausal women with elevated baseline levels more than does daily walking. The greater blood pressure reductions with SR may be mediated in part by a decrease in the stiffness of the large elastic arteries.

Salt and water retention and calcium blockade in uremia.

Blood pressure, echocardiography, and aortic and peripheral arterial pulse-wave velocity were studied in 40 hypertensive patients on long-term hemodialysis during a 24-week administration of nitrendipine (1,4-dihydro-2,6-dimethyl-4-[m-nitrophenyl]-3,5-pyridine-dicarboxylic acid ethyl methylester) monotherapy. In a double-blind placebo-randomized study, nitredipine effectively lowered the blood pressure (p less than 0.001) before hemodialysis without causing postdialysis hypotension. The antihypertensive effect of nitrendipine was greater in patients with significant salt and water retention, as indicated by interdialytic body weight gain (delta BW), that is, a significant correlation was observed between delta BW and the decrease in blood pressure (r = 0.72; p less than 0.001). The antihypertensive effect was not related to age, pretreatment plasma renin activity, or serum-ionized calcium concentration. After nitrendipine, a time-related decrease in aortic (p less than 0.005) and femoral (p less than 0.05) pulse-wave velocity was observed with a significant time-treatment interaction (p less than 0.01). Nitrendipine treatment did not influence left ventricular mass (which was positively correlated with delta BW; p less than 0.01) but was associated with an increase in the left ventricular ejection fraction. The increase in ejection fraction was correlated with changes in aortic pulse-wave velocity (r = 0.548; p less than 0.02) but not with changes in blood pressure (r = 0.352; p = 0.19) or delta BW.(ABSTRACT TRUNCATED AT 250 WORDS)