Reduction In Arterial Stiffness Research Articles

Benefits of whole-body vibration training on arterial function and muscle strength in young overweight/obese women.

The early arterial dysfunction linked with obesity and a sedentary lifestyle heightens the likelihood of suffering from future cardiovascular events. Whole-body vibration training (WBVT) may improve systemic arterial stiffness (brachial-ankle pulse wave velocity (baPWV)) and muscle strength in pre- and post-menopausal women. However, the effectiveness of WBVT to impact the arterial segments included in baPWV is unknown. The aim of this study was to investigate the effects of WBVT on aortic and leg arterial stiffness in young sedentary overweight/obese women. Thirty-eight young (21 years) overweight/obese women were randomized to WBVT (n=25) or a nonexercising control (CON, n=13) groups for 6 weeks. PWV, brachial and aortic blood pressures (BP), wave reflection (augmentation index (AIx)) and leg muscle strength measurements were acquired before and after 6 weeks. WBVT significantly reduced carotid-femoral PWV (aortic stiffness, P<0.05), femoral-ankle (leg arterial stiffness, P<0.01) and baPWV (systemic arterial stiffness, P<0.01) compared with CON. The reduction in brachial systolic BP (SBP), heart rate, aortic SBP, aortic diastolic BP, AIx normalized to a heart rate of 75 beats per min (AIx@75; P<0.01) and AIx (P<0.05) following WBVT was significant compared with CON (P<0.05). WBVT increased leg muscle strength compared with CON (P<0.001). There was a significant negative correlation between changes in relative muscle strength and aortic stiffness (r=-0.41, P<0.05). WBVT led to reductions in arterial stiffness, central BP and wave reflection in young obese women. WBVT may be an effective intervention toward vascular health promotion and prevention in young overweight/obese women (ClinicalTrials.gov identifier: NCT02679898).

Medium-term effect of sublingual l-glutathione supplementation on flow-mediated dilation in subjects with cardiovascular risk factors.

Supplementation of glutathione (GSH) may be a positive strategy to improve the endogenous antioxidant defense required to counteract many acute and chronic diseases. However, the efficacy of GSH treatment seems to be closely related to type of administration, degree of absorption, and increase of its concentrations. The aim of this study was to test a new sublingual formulation of L-GSH, which enters directly the systemic circulation, to assess its efficacy on circulating biochemical markers of hepatic metabolism, lipid profile, and oxidative stress and on peripheral vascular function compared with placebo in patients with cardiovascular risk factors (CVRF). We enrolled 16 healthy men with CVRF in a double-blinded, randomized placebo-controlled crossover study. At each visit, blood samples were collected for biochemistry analyses and peripheral endothelial function (reactive hyperemia index [RHI]) and stiffness were measured by Endo-PAT2000. In the overall population, a decrease in total and low-density lipoprotein cholesterol was highlighted after L-GSH supplementation compared with placebo (P=0.023 and P=0.04, respectively). On the contrary, no difference was observed in RHI and oxidative stress markers between L-GSH and placebo in the study population. However, seven participants with baseline abnormal RHI (≤1.67) compared with those with normal RHI showed a significant reduction of arterial stiffness after L-GSH administration, (P=0.007 and P=0.037, respectively). Supplementation of L-GSH compared with placebo influences the lipid profile of patients with CVRF. Sublingual L-GSH may represent a valid prevention of vascular damage in patients with CVRF and endothelial dysfunction.

Современный подход к лечению больных высокого сердечно-сосудистого риска: возможности комбинированной терапии

Introduction. Lack of efficacy of treatment with several medications in patients with arterial hypertension (AH) and high cardiovascular disease (CVD) risk is often explained by low compliance to treatment. Using combined therapy (CT) is one of the ways to increase compliance. Objective. To evaluate the influence of CT consisting of amlodipine, lisinopril and rosuvastatin on arterial elastance and serum fibrosis marker levels in patients with high CVD risk. Materials and methods. The study included 66 patients (mean age 66.5 years, 5% male, 95% female) with atherosclerosis of the brachiocephalic arteries. Serum levels of cholesterol and low density lipoprotein (LDL); brachial and central blood pressure (BP); brachial-ankle and carotid-femoral pulse wave velocity (baPWV and cfPWV, respectively); and augmentation index (AI) were determined initially and after 6 months of CT. Results. Against the background of CT statistically significant reduction of levels of LDL from 4.1 (3.6; 4.7) to 2.2 (1.8; 2.5) mmol/L (p<0.01); systolic and diastolic brachial BP from 127 (116; 144) to 122 (115; 132) mm Hg (p<0.01) and from 79 (72; 89) to 75 (70; 83) mm Hg (p<0.01), respectively; systolic and diastolic central BP from 125 (112; 139) to 120 (110; 124) mm Hg (p<0.01) and from 80 (75; 87) to 76 (70; 81) mm Hg (p<0.01), respectively; baPWV from 13.6 (12.5; 15.9) to 12.9 (11.8; 14.2) m/s (p<0.01); cfPWV from 11 (9; 12.2) to 9,4 (8.4; 10.2) m/s (p<0.01); and AI from 31 (25; 35) to 26 (21; 32) (p<0,05) was observed. Conclusion. CT consisting of amlodipine, lisinopril and rosuvastatin resulted in BP and LDL target level achievement and arterial stiffness reduction in patients with AH and high CVD risk. Further research is also necessary to more thoroughly assess efficacy of CT.

Moderate Versus Heavy Intensity Interval Training For Vascular Health In Post-menopausal Women

PURPOSE: Whilst the menopause has been associated with a decline in vascular function, sedentary postmenopausal women report a dislike of heavy intensity exercise. This study aimed to compare the impact of moderate (MOD) versus heavy (HVY) intensity interval exercise training upon vascular function and endothelial integrity. METHODS: 27 sedentary post-menopausal women completed either MOD (90% lactate threshold (LT) 10:10 s duty cycle) or HVY (120% LT 30:30 s duty cycle) interval exercise training twice per week for 12 weeks. Endothelial function (FMD), peak oxygen uptake (VO2peak), LT, circulating angiogenic cell number (FACS) and adhesive capacity to cultured saphenous vein vascular smooth muscle cells (VSMCs) were recorded prior to and following training. Group and time differences were assessed via two-way mixed mode ANOVA. RESULTS: VO2peak and LT increased in HVY only (VO2peak: MOD: 29.97 ±5.5 to 29.65 ± 5.4; HVY: 30.18 ±5.3 to 32.25 ±6.5 ml/kg/min; interaction P=0.02; LT: MOD: 1.13 ±0.19 to 1.11 ±0.18; HVY 1.09 ±0.15 to 1.22 ±0.17 L/min; interaction P=0.005). FMD (group mean: 4.7 ±2.4 %), brachial diameter (group mean: 3.7 ±0.3 mm) and blood pressure were unaffected by training (P>0.05), whilst peripheral arterial stiffness decreased post training in both groups (-0.58 a.u). [CD34+CD45dim] increased after MOD but not after HVY intensity interval training (MOD: 5.3 ±3.8 to 8.9 ±6.3; HVY: 6.34 ±3.1 to 5.7 ±2.6 CAC/105 leucocytes: interaction P=0.02). The adhesive capacity of CACs to VSMCs was seen to increase by 70% following MOD but only 12 % following HVY (P>0.05), this capacity persisted over 60 min in the MOD group (time x group interaction: P=0.05). CONCLUSION: In post-menopausal women HVY intensity interval training provided greater benefits for cardiorespiratory fitness. However, MOD intensity intervals produced equivalent reductions in arterial stiffness and greater modulation of CAC function perceived as beneficial to endothelial integrity. Neither intensity was sufficient to produce significant changes in FMD. Varying the intensities used in interval exercise prescription may provide the most effective cardiovascular benefits in post-menopausal women.

Smooth muscle filamin A is a major determinant of conduit artery structure and function at the adult stage.

Human mutations in the X-linked FLNA gene are associated with a remarkably diverse phenotype, including severe arterial morphological anomalies. However, the role for filamin A (FlnA) in vascular cells remains partially understood. We used a smooth muscle (sm)-specific conditional mouse model to delete FlnA at the adult stage, thus avoiding the developmental effects of the knock-out. Inactivation of smFlnA in adult mice significantly lowered blood pressure, together with a decrease in pulse pressure. However, both the aorta and carotid arteries showed a major outward hypertrophic remodeling, resistant to losartan, and normally occurring in hypertensive conditions. Notably, arterial compliance was significantly enhanced in the absence of smFlnA. Moreover, reactivity of thoracic aorta rings to a variety of vasoconstrictors was elevated, while basal contractility in response to KCl depolarization was reduced. Enhanced reactivity to the thromboxane A2 receptor agonist U46619 was fully reversed by the ROCK inhibitor Y27632. We discuss the possibility that a reduction in arterial stiffness upon smFlnA inactivation might cause a compensatory increase in conduit artery diameter for normalization of parietal tension, independently of the ROCK pathway. In conclusion, deletion of smFlnA in adult mice recapitulates the vascular phenotype of human bilateral periventricular nodular heterotopia, culminating in aortic dilatation.

The effect of antihypertensive treatment on arterial stiffness and serum concentration of selected matrix metalloproteinases.

IntroductionThe aim of the study was to assess the arterial stiffness and serum levels of selected metalloproteinases (MMPs) in hypertensive patients and their changes following antihypertensive therapy.Material and methodsThe study group consisted of 95 patients with essential arterial hypertension (HT) stage 1 or 2 (mean age: 53.1 ±13.0 years). The control group consisted of 31 normotensives of the same age range. Hypertension patients were randomized to one of the following monotherapies for 6 months: quinapril, losartan, amlodipine, hydrochlorothiazide or bisoprolol. Carotid-femoral pulse wave velocity (PWV) was measured using a Complior device. Serum concentrations of MMPs (proMMP-1, MMP-2, MMP-3, MMP-9) and plasma concentration of tissue inhibitor of MMPs (TIMP-1) were measured using ELISA.ResultsPulse wave velocity and serum concentrations of MMP-2 and MMP-9 were higher in HT patients than in the control group. In HT patients PWV was significantly associated (R2 = 0.41) with age (B = 0.408, p = 0.00027), systolic blood pressure (SBP) (B = 0.441, p = 0.0011), and MMP-3 (B = 0.204, p = 0.0459). After 6 months of treatment, regardless of the agent used, we observed a significant decrease of PWV, SBP, MMP-2 and MMP-3 and an increase of TIMP-1 plasma concentration. The decrease of PWV was significantly associated with a decrease of SBP (R2 = 0.07, B = 0.260, p = 0.015) only.ConclusionsIn patients with arterial hypertension, beside age and systolic blood pressure, the determinants of arterial stiffness include serum MMP-3 concentration. For drugs compared in the study with the same hypotensive effect obtained, the arterial stiffness reduction effect is not dependent on the drug used. Systolic blood pressure is one of the independent factors responsible for the reduction of arterial stiffness in the course of antihypertensive treatment.

Abstract 17026: Serum Adropin Level is Associated With Exercise Training-induced Improvement of Arterial Stiffness in Obese Adults

Introduction: Obesity-induced deterioration of arterial stiffness is reduced by habitual exercise, and increased production of nitric oxide (NO) participates in this effect. Adropin is a regulator of endothelial NO synthase and NO release, and circulating adropin level decreases in obese patients. However, the association between exercise-training effects of arterial stiffness and circulating adropin level in obese subjects remains unclear. Hypothesis: This study aimed to determine the serum adropin level related to exercise-training effects of arterial stiffness in obese subjects. Methods: Eighteen Japanese obese subjects (age: 65.7 ± 1.6 years, % body fat: 34.8 ± 1.6 %) and nine Japanese non-obese subjects (age: 69.1 ± 1.0 years, % body fat: 19.9 ± 2.4 %) participated in this study. Obese subjects completed 8-week of aerobic exercise training (60-70% peak oxygen uptake [VO2peak] for 45 min, 3 days/week). Before and after the intervention, we evaluated plasma nitrite/nitrate (NOx) and serum adropin concentrations, carotid beta-stiffness as an indicator of arterial stiffness, and VO2peak as an index of cardiorespiratory fitness. VO2peak was measured using an incremental cycle exercise test on a cycle ergometer. Results: Serum adropin level in the obese subjects was lower than that in the non-obese subjects. After the 8-week intervention, VO2peak was significantly increased and carotid beta-stiffness was significantly decreased (P &lt; 0.05). Moreover, plasma NOx level and serum adropin level was significantly increased after the 8-week intervention (P &lt; 0.05). Additionally, the exercise training-induced reduction in beta-stiffness was negatively correlated with the training-induced changes in serum adropin (r = -0.481, P &lt; 0.05) and plasma NOx levels (r = -0.668, P &lt; 0.01). Furthermore, a significant correlation was observed between the training-induced changes in serum adropin and plasma NOx levels (r = 0.677, P &lt; 0.01). Conclusions: These results suggest that the plasma adropin level is increased by aerobic exercise training intervention and is associated with exercise training-induced alternation of arterial stiffness in obese subjects. Thus, the increase in adropin may participate in the exercise-induced reduction of arterial stiffness.

Elevated pentraxin 3 level at the early stage of exercise training is associated with reduction of arterial stiffness in middle-aged and older adults.

Regular exercise improves aging-induced deterioration of arterial stiffness, and is associated with elevated production of pentraxin 3 (PTX3) and anti-inflammatory as well as anti-atherosclerotic effects. However, the time-dependent effect of exercise training on arterial stiffness and PTX3 production remains unclear. The purpose of this study was to investigate the time course of the association between the effects of training on the circulating PTX3 level and arterial stiffness in middle-aged and older adults. Thirty-two healthy Japanese subjects (66.2±1.3 year) were randomly divided into two groups: training (exercise intervention) and sedentary controls. Subjects in the training group completed 8 weeks of aerobic exercise training (60-70% peak oxygen uptake (VO2peak) for 45 min, 3 days per week); during the training period, we evaluated plasma PTX3 concentration and carotid-femoral pulse wave velocity (cfPWV) every 2 wk. cfPWV gradually declined over the 8-week training period, and was significantly reduced after 6 and 8 week of exercise intervention (P<0.05). Plasma PTX3 level was significantly increased after 4 weeks of the intervention (P<0.05). In addition, the exercise training-induced reduction in cfPWV was negatively correlated with the percent change in plasma PTX3 level after 6 week (r=-0.54, P<0.05) and 8 weeks (r=-0.51, P<0.05) of the intervention, but not correlated at 4 weeks. Plasma PTX3 level was elevated at the early stage of the exercise training intervention, and was subsequently associated with training-induced alteration of arterial stiffness in middle-aged and older adults.

Four weeks of regular static stretching reduces arterial stiffness in middle-aged men.

Trunk flexibility may be associated with arterial stiffness in young, middle-aged, and older healthy men after adjusting for blood pressure. This study assessed the effects of 4 weeks of regular static stretching on arterial stiffness in middle-aged men. Sixteen healthy men (43 ± 3 years) were assigned to control or intervention groups (n = 8 each). The control group did not alter their physical activity levels throughout the study period. The intervention group participated in five supervised stretching sessions per week for 4 weeks. Each session comprised 30 min of mild stretching that moved the major muscle groups through the full range of motion and stretches were held three times for 20 s at the end range. Flexibility was assessed by sit-and-reach test. Arterial stiffness was assessed by brachial-ankle pulse wave velocity (baPWV) and cardio-ankle vascular index (CAVI). Four weeks of stretching increased sit-and-reach (Control, Pre: 31.4 ± 2.1, Post: 30.8 ± 2.7 vs. Intervention, Pre: 30.6 ± 5.3, Post: 43.9 ± 4.3 cm), and reduced baPWV (Control, Pre: 1204 ± 25, Post: 1205 ± 38 vs. Intervention, Pre: 1207 ± 28, Post: 1145 ± 19 cm/s) and CAVI (Control, Pre: 7.6 ± 0.3, Post: 7.5 ± 0.3 vs. Intervention, Pre: 7.7 ± 0.2, Post: 7.2 ± 0.2 units) in the intervention group. However, the change in sit-and-reach did not significantly correlate with the changes in arterial stiffness. These findings suggest that short-term regular stretching induces a significant reduction in arterial stiffness in middle-aged men.

Association between high arterial stiffness and left ventricular filling pressures in patients with acute myocardial infarction

High arterial stiffness increases the left ventricular (LV) filling pressures in different cardiac disorders. The association between arterial stiffness and LV filling pressures has not been studied so far in patients with acute myocardial infarction (MI). The aim of the study was to assess the association between arterial stiffness and LV filling pressures in patients with acute MI. Arterial stiffness, measured using the digital volume pulse stiffness index (SIDVP), and LV filling pressures, quantified as the ratio of early transmitral flow velocity to early diastolic septal mitral annulus velocity (E/e'), were evaluated in 263 patients with acute MI (mean age, 63.8 ±11 years; 69 women). The association between high E/e' (>15) and very stiff arteries (SIDVP >18 m/s) was analyzed by logistic regression, with data presented as odds ratios (OR s) and 95% confidence intervals (CIs). A multivariate logistic regression analysis revealed an association between E/e' >15 and SIDVP >18 m/s (OR, 4.7; 95% CI, 1.8-12.3), independently of female sex (OR, 4.3; 95% CI, 1.4-10.2), LV ejection fraction <35% (OR, 3.1; 95% CI, 1.2-8.2), left atrial volume >34 ml/m2 (OR, 17.4; 95% CI, 5.8-52.0). There was no significant association between E/e' >15 and previous MI (OR, 2.2; 95% CI, 0.9-5.7). High arterial stiffness is an independent risk factor for LV diastolic dysfunction in patients with acute MI. A reduction in arterial stiffness may improve LV diastolic function in this patient group.

Arterial stiffness and coronary artery disease.

The current traditional risk scores are not sufficient to predict the full incidence of cardiovascular disease. In this brief review, we discuss the pathophysiological mechanisms through which arterial stiffness affects cardiac function and the additive value of markers of arterial stiffness, to detect the presence of coronary artery disease (CAD) and predict adverse outcome in these patients. Arterial stiffness causes early arrival of wave reflections in systole instead of diastole and, thus, increases systolic afterload and reduces diastolic coronary perfusion pressure. Abnormal collagen turnover, cytokines, and metalloproteinase activity are common biochemical links between vascular and myocardial stiffness. Pulse wave velocity, augmentation index, and central pressures measured by simple noninvasive methods are related to atheromatic plaque vulnerability, incidence, severity, and extent of CAD. Recent meta-analyses have shown the additive value of markers of arterial stiffness, and particularly of pulse wave velocity, to detect CAD, predict cardiovascular events, and reclassify patients to a higher cardiovascular risk. Studies assessing whether reduction of arterial stiffness is associated with improved prognosis are lacking. Markers of arterial stiffness are useful tools to identify early atherosclerosis and adverse clinical outcomes in young adults and individuals with a modest risk factor profile. Assessing arterial stiffness may facilitate cardiovascular risk stratification beyond traditional risk scores.

Aortic Stiffness in Native Hypertension – Amlodipine versus LisinoprilAdministration (ASHALINA study)

Background: Hypertension is a well-recognizedcardiovascular risk factors. Arterial stiffness increases with ageand hypertensionand is also enhanced in subjects with diabetes mellitus,atherosclerosis,and end-stage renal disease. Arterial stiffness can be assessed noninvasively with the use of carotid-femoral pulse wave velocity (CF-PWV) measurement, that is, the velocity of the pulse wave to travel a given distance between carotid and femoral artery. Antihypertensive drugs such as calcium channel blocker with its “destiffening” effect have been widely known to reduce arterial stiffness. However, the renin-angiotensin system inhibitors proved to be superior to all other antihypertensive drugs in reducing arterial stiffness. Objective: The aim of this study was to examine the difference in arterial stiffness reduction in native hypertensive subjects that was given ace-inhibitor or calcium channel blockerfor four weeks,by measuring the CF-PWV. Methods: A double blind randomized clinical trial was conducted in National Cardiovascular Centre Harapan Kita (NCCHK) to 54 subjects with native hypertension between the age of 30–50 years old, from March to May 2015. Subjects were divided into two groups: lisinopril 1 × 5 mg (n = 27) and amlodipine 1 × 5 mg (n = 27). Blood pressure and CF-PWV were measured before and after 4 weeks of therapy. Statistical analysis was done using bivariate and multivariate analysis to determine the significance of arterial stiffness reduction. Results: There was a reduction in blood pressure (systole, diastole, mean arterial pressure) before and after the treatment for both groups, however although it was clinicaly significant, statistically it was not (P value >0.05). Nonetheless, CF-PWV for lisinopril and amlodipine showed significant reduction with both p-value were <0.001 (2.09 ± 0.280, CI 95% 1.80–2.2 and 1.77 ± 0.340, CI 95% 1.6–1.9). When both drugs were compared using multivariate analysis, lisinopril was proved to have a more significant decrease in CF-PWV (P value <0.001 CI 95% 0.2–0.5). Conclusion: This study proved that there was a statistically significant difference in CF-PWV reduction between lisinopril and amlodipine administration to patients with native hypertension, with lisinopril having the larger effect.

Serum Adropin Level Is Associated With Exercise Training-induced Reduction Of Arterial Stiffness In The Elderly

Serum Adropin Level Is Associated With Exercise Training-induced Reduction Of Arterial Stiffness In The Elderly

Effect of CPAP on Endothelial Function in Subjects With Obstructive Sleep Apnea: A Meta-Analysis.

Obstructive sleep apnea (OSA) is related to endothelial dysfunction. CPAP is the first-line treatment for OSA. We conducted a meta-analysis to evaluate the effect of CPAP on endothelial function in subjects with OSA. The PubMed, Embase, and Cochrane Library databases were searched. The overall effects were measured by the weighted mean difference with a 95% CI. Subgroup and meta-regression analyses were used to explore the sources of between-study heterogeneity. Eleven studies were eligible for the meta-analysis. A random-effects model revealed that CPAP significantly improved endothelial function as assessed by flow-mediated dilation (weighted mean difference of 2.92, 95% CI 2.21-3.63, P < .001), whereas there was no significant improvement in endothelial function in response to nitroglycerin-mediated dilation (weighted mean difference of 0.90, 95% CI -1.63 to 3.43, P = .48). Age, sex, CPAP compliance and duration, and sleep-related variables had no effect on reduction in arterial stiffness after CPAP. Sensitivity analyses indicated that the protective effect of CPAP on endothelial function was robust. CPAP significantly improved flow-mediated dilation in subjects with OSA. Long-term randomized controlled trials with larger sample sizes are needed to confirm the positive effect of CPAP on endothelial function in subjects with OSA.

Changes in arterial stiffness and nitric oxide production with Chlorella-derived multicomponent supplementation in middle-aged and older individuals.

Chlorella is a unicellular green alga, which contains a variety of nutrients including amino acids, dietary fibers, n-3 unsaturated fatty acid, vitamins, and minerals. We previously demonstrated that Chlorella-derived multicomponent supplementation decreases arterial stiffness in young men. However, mechanisms underlying the reduction in arterial stiffness by Chlorella-derived supplementation and the effect in middle-aged and older individuals have remained unexplored. This study tested our hypothesis that Chlorella-derived supplementation improves arterial stiffness via an increase in nitric oxide (NO, a endothelium-derived relaxing factor) production in middle-aged and older individuals. Thirty-two subjects between 45 and 75 years of age assigned to placebo and Chlorella groups in a double-blinded manner and took respective tablets for 4 weeks. Before and after the supplementations, brachial-ankle pulse wave velocity (baPWV, an index of arterial stiffness) and plasma nitrite/nitrate (NOx, end product of NO) concentration were measured. There was no difference in baPWV between before and after the placebo intake, but baPWV decreased after the Chlorella supplementation. Changes in baPWV with the Chlorella supplementation were correlated with those in plasma NOx concentration. We concluded that Chlorella-derived multicomponent supplementation decreases arterial stiffness in middle-aged and older individuals. It may be associated with increase in NO production by vascular endothelium.

THE POSSIBLE INFLUENCE OF BISPHOSPHONATE THERAPY AND ITS COMBINATION WITH STATINS ON PARAMETERS OF AORTIC STIFFNESS IN WOMEN WITH POSTMENOPAUSAL OSTEOPOROSIS

The study shows that addition of statins to osteoporotic therapy in postmenopausal women with different cardiovascular risk beside desired hypolipidemic effect and reduction of arterial stiffness also elevates BMD at femoral neck by 4,9% from the baseline (p&lt;0.05). Bisphosphonates therapy in postmenopausal women gives additional reduction of central systolic arterial pressure of 4.1 mm Hg with the tendency to improvement in the arterial stiffness. The dynamics of aortal stiffness was correlated with changers in intensity of bone remodeling (for N-terminal propeptides of type I procollagen (P1NP) p =0.47, p=0.019; for carboxyl-terminal telopeptide of collagen type I (CITP1) p=0.40, p=0.05) as well as systolic blood pressure (r=0.52, p=0.008). Conclusions. Bisphosphonate therapy and its combination with statins may influence the on parameters of blood pressure and aortic stiffness in women with postmenopausal osteoporosis.

Beneficial effects of low-dose aspirin on aortic stiffness in hypertensive patients.

While treatment with low-dose aspirin has been established as a therapeutic tool for secondary prevention, the role of aspirin on primary prevention remains controversial. Aortic stiffness and wave reflections are independent predictors of cardiovascular events. The aim of the present study was to investigate the effect of low-dose aspirin on aortic stiffness and wave reflections in hypertensive patients. We studied 30 patients with grade I hypertension. Fifteen patients were treated with 160 mg of aspirin and 15 patients with placebo. Aortic stiffness and wave reflections were assessed by measuring carotid-femoral pulse wave velocity (PWV) and heart rate-adjusted augmentation index (AIx75), respectively. All measurements were conducted at baseline and 2 weeks after treatment. In the aspirin group, there was a significant reduction in PWV compared to the placebo group (from 8.9±1.5 to 8.5±1.6 m/s for the aspirin group vs from 8.6±1.4 to 8.7±1.6 m/s for the placebo group, net change: -0.5 m/s; p=0.02). AIx75 showed a marginal decrease (from 28.0±5.4 to 26.2±5.0% for the aspirin group vs from 31.2±9.7 to 30.6±9.2% for the placebo group, net change: -1.2%; p=0.06). In conclusion, a 2-week course of aspirin administration has a favorable effect on aortic stiffness and, to a lesser extent, on wave reflections in hypertensive patients. Whether the reduction in arterial stiffness is translated to fewer cardiovascular events needs to be confirmed by future prospective studies.

Acute effects of moderate-intensity continuous and accumulated exercise on arterial stiffness in healthy young men.

To examine and compare the effects of acute moderate-intensity continuous and accumulated exercise with different intervals on arterial stiffness in humans. Healthy young men (n = 16) participated in four trials in a randomized crossover design: complete rest control (CON), continuous exercise (CE, 30-min cycling), accumulated exercise with 20 min of interval (AE20, 2 × 15-min cycling) and accumulated exercise with 60 min of interval (AE60, 2 × 15-min cycling). Exercise was performed at intensity of 50 % heart rate reserve. Measurements of cardio-ankle vascular index (CAVI), an indicator of systemic arterial stiffness in humans, were performed at baseline (BL), immediately (0 min) and 60 min after exercise in exercise trials, and at corresponding time points in CON trial. CAVI remained unaltered throughout the procedure in CON trial (6.8 ± 0.1, 6.9 ± 0.1, 6.9 ± 0.2 at BL, 0 and 60 min, respectively). Similar CAVI reductions were observed in CE, AE20 and AE60 trials at 0 min compared to CON trial (P < 0.001 for CE, AE20 and AE60 vs. CON, respectively). Though CAVI in CE and AE60 trial returned to baseline at 60 min, the CAVI reduction at 60 min persisted in AE20 trial (P < 0.05 for AE20 vs. Compared to continuous exercise, accumulated exercise with appropriate short interval results in superior effects on systemic arterial stiffness in healthy young men, with arterial stiffness reduction for longer duration. When the interval is long, the acute superior effects of accumulated exercise on arterial stiffness disappeared.

Impact of General and Central Adiposity on Ventricular-Arterial Aging in Women and Men

ObjectivesThe aim of this study was to assess the effects of central and general obesity measures on long-term longitudinal changes in ventricular-arterial mechanics. BackgroundObesity, female sex, and ventricular-arterial stiffening are associated with the development of heart failure with preserved ejection fraction. Fat distribution and chronic changes in body composition may affect longitudinal changes in LV properties, independent of arterial load. MethodsIn 1,402 subjects from a randomly selected, community-based population, comprehensive echo-Doppler echocardiography was performed at two examinations separated by 4 years. From this population, 788 subjects had paired data adequate for determining left ventricular end-systolic elastance (Ees), end-diastolic elastance (Eed), and effective arterial elastance (Ea). ResultsOver 4 years, Ea was decreased by 3% in tandem with improved blood pressure control, whereas Ees and Eed were increased by 14% and 8% (all, p < 0.001). Greater weight loss over 4 years was associated with progressively greater decreases in Ea in men and women. After adjustment for Ea change, weight gain was correlated with increases in Eed in both women and men. Central obesity was associated with greater age-related increases in Ees in women but not in men, independent of arterial load, but central obesity did not predict changes in Eed or Ea. ConclusionsIn these subjects, weight gain was associated with increases in LV diastolic stiffness, even after adjustment for changes in arterial afterload, whereas weight loss was associated with reductions in arterial stiffness. Age-related LV systolic stiffening was increased in women, but not in men, with central obesity. Strategies for promoting weight loss and reducing central adiposity may be effective in preventing heart failure with preserved ejection fraction, particularly in women.

Reduction of Arterial Stiffness by Exercise Training Is Associated with Increasing Plasma Apelin Level

Reduction of Arterial Stiffness by Exercise Training Is Associated with Increasing Plasma Apelin Level