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The extract of red yeast rice (RYR) is the most effective cholesterol-lowering nutraceutical on the market. In particular, its effectiveness is directly related to the amount of monacolin K within the extract (up to 10 mg/day). Consuming monacolin K on a daily basis reduces low-density lipoprotein (LDL) cholesterol plasma levels between 15% and 25% within 6 to 8 weeks. Certainly, the decrease in LDL-cholesterol is accompanied by a similar reduction in total cholesterol, non-high-density lipoprotein cholesterol, plasma apolipoprotein B, matrix metalloproteinases 2 and 9, and high-sensitivity C-reactive protein. Furthermore, the RYR lipid-lowering effect is associated with significant improvements in pulse wave velocity and endothelial function, which are validated and reliable biomarker tools able to detect vascular aging. Although it has a mechanism of action similar to statins, a daily consumption of between 3 and 10 mg monacolin K has only minimal associated risks, and mild myalgias are seen only in the frailest patients (those who also cannot tolerate minimal dosages of statin). The monacolin K found in RYR is a safe and effective supplement for managing mild to moderate hypercholesterolemia in people with no additional cardiovascular risk factors.

A healthy aorta exerts a powerful cushioning function, which limits arterial pulsatility and protects the microvasculature from potentially harmful fluctuations in pressure and blood flow. Large-artery (aortic) stiffening, which occurs with aging and various pathologic states, impairs this cushioning function, and has important consequences on cardiovascular health, including isolated systolic hypertension, excessive penetration of pulsatile energy into the microvasculature of target organs that operate at low vascular resistance, and abnormal ventricular-arterial interactions that promote left ventricular remodeling, dysfunction, and failure. Large-artery stiffness independently predicts cardiovascular risk and represents a high-priority therapeutic target to ameliorate the global burden of cardiovascular disease. This paper provides an overview of key physiologic and biophysical principles related to arterial stiffness, the impact of aortic stiffening on target organs, noninvasive methods for the measurement of arterial stiffness, mechanisms leading to aortic stiffening, therapeutic approaches to reduce it, and clinical applications of arterial stiffness measurements.

Cardiovascular disease (CVD) presents a great burden for elderly patients, their caregivers, and health systems. Structural and functional alterations of vessels accumulate throughout life, culminating in increased risk of developing CVD. The growing elderly population worldwide highlights the need to understand how aging promotes CVD in order to develop new strategies to confront this challenge. This review provides examples of some major unresolved clinical problems encountered in daily cardiovascular practice as we care for elderly patients. Next, the authors summarize the current understanding of the mechanisms implicated in cardiovascular aging, and the potential for targeting novel pathways implicated in endothelial dysfunction, mitochondrial oxidative stress, chromatin remodeling, and genomic instability. Lastly, the authors consider critical aspects of vascular repair, including autologous transplantation of bone marrow-derived stem cells in elderly patients.

History of a hypertensive disorder of pregnancy (HDP) among women may be useful to refine atherosclerotic cardiovascular disease risk assessments. However, future risk of diverse cardiovascular conditions in asymptomatic middle-aged women with prior HDP remains unknown.The purpose of this study was to examine the long-term incidence of diverse cardiovascular conditions among middle-aged women with and without prior HDP.Women in the prospective, observational UK Biobank age 40 to 69 years who reported ≥1 live birth were included. Noninvasive arterial stiffness measurement was performed in a subset of women. Cox models were fitted to associate HDP with incident cardiovascular diseases. Causal mediation analyses estimated the contribution of conventional risk factors to observed associations.Of 220,024 women included, 2,808 (1.3%) had prior HDP. The mean age at baseline was 57.4 ± 7.8 years, and women were followed for median 7 years (interquartile range: 6.3 to 7.7 years). Women with HDP had elevated arterial stiffness indexes and greater prevalence of chronic hypertension compared with women without HDP. Overall, 7.0 versus 5.3 age-adjusted incident cardiovascular conditions occurred per 1,000 women-years for women with versus without prior HDP, respectively (p = 0.001). In analysis of time-to-first incident cardiovascular diagnosis, prior HDP was associated with a hazard ratio (HR) of 1.3 (95% CI: 1.04 to 1.60; p = 0.02). HDP was associated with greater incidence of CAD (HR: 1.8; 95% CI: 1.3 to 2.6; p 0.001), heart failure (HR: 1.7; 95% CI: 1.04 to 2.60; p = 0.03), aortic stenosis (HR: 2.9; 95% CI: 1.5 to 5.4; p 0.001), and mitral regurgitation (HR: 5.0; 95% CI: 1.5 to 17.1; p = 0.01). In causal mediation analyses, chronic hypertension explained 64% of HDP's association with CAD and 49% of HDP's association with heart failure.Hypertensive disorders of pregnancy are associated with accelerated cardiovascular aging and more diverse cardiovascular conditions than previously appreciated, including valvular heart disease. Cardiovascular risk after HDP is largely but incompletely mediated by development of chronic hypertension.

The gut microbiota has been implicated as an environmental factor that modulates atherosclerosis, and recent evidence suggests that microbiota-mediated changes in bile acid profiles and signalling through the bile acid nuclear receptor farnesoid X receptor (FXR) contribute to impaired endothelial

Cardio-ankle vascular index (CAVI) has been recognized as a useful indicator to assess the arterial stiffness and atherosclerosis. Some reports show that the higher CAVI values predict the worse prognosis in patients with cardiovascular disease. Although it is already reported that ankle-brachial

Arterial stiffness assessed by cardio-ankle vascular index (CAVI) is commonly used as a surrogate marker of subclinical atherosclerosis. The aim of study is to demonstrate the association of CAVI and coronary artery calcification (CAC) or coronary stenosis in the asymptomatic metabolic syndrome (MS

Pulse pressure (PP), a marker of arterial stiffness, and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) have been associated with heart failure (HF) and cardiovascular disease (CVD). We examined whether the combination of PP and NT-proBNP identifies individuals at higher risk for

Lipoprotein-associated Phospholipase A2 (Lp-PLA2), has inflammatory and atherogenic effect on vasculature. Hence, we examine the impact of high Lp-PLA2 levels on endothelial function and arterial stiffness of patients with coronary artery disease (CAD). We enrolled 374 patients with stable CAD.

Although visceral fat accumulation (VFA) has been identified as a potential risk factor for arteriosclerosis progression, only a few studies have reported the association between them. The cardio-ankle vascular index (CAVI) has been proposed as a feasible method to assess arterial stiffness from the

BACKGROUND Carotid stiffening is considered a key element in the pathogenesis of stroke. However, results of studies evaluating the association between carotid stiffness and incident stroke have been inconsistent. OBJECTIVES This study investigated whether carotid stiffness (as determined by ultrasonography) is associated with incident stroke and whether this association is independent of aortic stiffness as estimated by carotid-femoral pulse wave velocity (cfPWV). Additionally, we evaluated the incremental value of carotid stiffness for stroke risk prediction beyond Framingham risk factors and cfPWV. METHODS This study included a systematic review and meta-analyses of aggregate and individual participant data (IPD), the latter of which was obtained by requesting individual-level data of all cohort studies with available data on carotid stiffness and cfPWV. RESULTS Ten studies (n = 22,472) were included in the aggregate data meta-analysis and 4 (n = 4,540) in the IPD meta-analysis. After adjusting for cardiovascular (CV) factors, the aggregate data meta-analysis showed that greater carotid stiffness (per SD) was associated with stroke (hazard ratio: 1.18; 95% confidence interval: 1.05 to 1.33). In addition, carotid stiffness was associated with total CV events and CV and all-cause mortality, but not with coronary heart disease events. In the IPD meta-analysis, additional adjustment for cfPWV did not materially change these associations. Carotid stiffness did improve stroke risk prediction beyond Framingham and cfPWV (integrative discrimination improvement: 0.4 percentage point [95% confidence interval: 0.1 to 0.6 percentage point] and continuous net reclassification improvement: 18.6% [95% confidence interval: 5.8% to 31.3%]). CONCLUSIONS Carotid stiffness is associated with incident stroke independently of CV factors and aortic stiffness. In addition, carotid stiffness improves stroke risk prediction beyond Framingham and aortic stiffness.

Background Carotid stiffening is considered a key element in the pathogenesis of stroke. However, results of studies evaluating the association between carotid stiffness and incident stroke have been inconsistent. Objectives This study investigated whether carotid stiffness (as determined by ultrasonography) is associated with incident stroke and whether this association is independent of aortic stiffness as estimated by carotid-femoral pulse wave velocity (cfPWV). Additionally, we evaluated the incremental value of carotid stiffness for stroke risk prediction beyond Framingham risk factors and cfPWV. Methods This study included a systematic review and meta-analyses of aggregate and individual participant data (IPD), the latter of which was obtained by requesting individual-level data of all cohort studies with available data on carotid stiffness and cfPWV. Results Ten studies (n = 22,472) were included in the aggregate data meta-analysis and 4 (n = 4,540) in the IPD meta-analysis. After adjusting for cardiovascular (CV) factors, the aggregate data meta-analysis showed that greater carotid stiffness (per SD) was associated with stroke (hazard ratio: 1.18; 95% confidence interval: 1.05 to 1.33). In addition, carotid stiffness was associated with total CV events and CV and all-cause mortality, but not with coronary heart disease events. In the IPD meta-analysis, additional adjustment for cfPWV did not materially change these associations. Carotid stiffness did improve stroke risk prediction beyond Framingham and cfPWV (integrative discrimination improvement: 0.4 percentage point [95% confidence interval: 0.1 to 0.6 percentage point] and continuous net reclassification improvement: 18.6% [95% confidence interval: 5.8% to 31.3%]). Conclusions Carotid stiffness is associated with incident stroke independently of CV factors and aortic stiffness. In addition, carotid stiffness improves stroke risk prediction beyond Framingham and aortic stiffness.

Objectives This study sought to investigate the association of local and segmental arterial stiffness with incident cardiovascular events and all-cause mortality. Background The association of different stiffness indices, in particular of carotid, brachial, and femoral stiffness, with cardiovascular disease and mortality is currently unknown. Methods In a population-based cohort (n = 579, mean age 67 years, 50% women, 23% with type 2 diabetes [by design]), we assessed local stiffness of carotid, femoral, and brachial arteries (by ultrasonography), carotid-femoral pulse wave velocity (cfPWV), aortic augmentation index, and systemic arterial compliance. Results After a median follow-up of 7.6 years, 130 participants had a cardiovascular event and 96 had died. The hazard ratios (HRs) (95% confidence intervals [CIs]) per 1 SD for cardiovascular events and all-cause mortality, respectively, were HR: 1.22 (95% CI: 0.95 to 1.56) and 1.51 (95% CI: 1.11 to 2.06) for lower carotid distensibility; HR: 1.19 (95% CI: 1.00 to 1.41) and 1.28 (95% CI: 1.07 to 1.53) for higher carotid elastic modulus; HR: 1.08 (95% CI: 0.88 to 1.31) and 1.43 (95% CI: 1.10 to 1.86) for lower carotid compliance; HR: 1.39 (95% CI: 1.06 to 1.83) and 1.27 (95% CI: 0.90 to 1.79) for lower femoral distensibility; HR: 1.25 (95% CI: 0.96 to 1.63) and 1.47 (95% CI: 1.01 to 2.13) for lower femoral compliance; and HR: 1.56 (95% CI: 1.23 to 1.98) and 1.13 (95% CI: 0.83 to 1.54) for higher cfPWV. These results were adjusted for age, sex, mean arterial pressure, and cardiovascular risk factors. Mutual adjustments for each of the other stiffness indices did not materially change these results. Brachial stiffness, augmentation index, and systemic arterial compliance were not associated with cardiovascular events or mortality. Conclusions Carotid and femoral stiffness indices are independently associated with incident cardiovascular events and all-cause mortality. The strength of these associations with events may differ per stiffness parameter.

Objectives This study sought to investigate the association of local and segmental arterial stiffness with incident cardiovascular events and all-cause mortality. Background The association of different stiffness indices, in particular of carotid, brachial, and femoral stiffness, with cardiovascular disease and mortality is currently unknown. Methods In a population-based cohort (n = 579, mean age 67 years, 50% women, 23% with type 2 diabetes [by design]), we assessed local stiffness of carotid, femoral, and brachial arteries (by ultrasonography), carotid-femoral pulse wave velocity (cfPWV), aortic augmentation index, and systemic arterial compliance. Results After a median follow-up of 7.6 years, 130 participants had a cardiovascular event and 96 had died. The hazard ratios (HRs) (95% confidence intervals [CIs]) per 1 SD for cardiovascular events and all-cause mortality, respectively, were HR: 1.22 (95% CI: 0.95 to 1.56) and 1.51 (95% CI: 1.11 to 2.06) for lower carotid distensibility; HR: 1.19 (95% CI: 1.00 to 1.41) and 1.28 (95% CI: 1.07 to 1.53) for higher carotid elastic modulus; HR: 1.08 (95% CI: 0.88 to 1.31) and 1.43 (95% CI: 1.10 to 1.86) for lower carotid compliance; HR: 1.39 (95% CI: 1.06 to 1.83) and 1.27 (95% CI: 0.90 to 1.79) for lower femoral distensibility; HR: 1.25 (95% CI: 0.96 to 1.63) and 1.47 (95% CI: 1.01 to 2.13) for lower femoral compliance; and HR: 1.56 (95% CI: 1.23 to 1.98) and 1.13 (95% CI: 0.83 to 1.54) for higher cfPWV. These results were adjusted for age, sex, mean arterial pressure, and cardiovascular risk factors. Mutual adjustments for each of the other stiffness indices did not materially change these results. Brachial stiffness, augmentation index, and systemic arterial compliance were not associated with cardiovascular events or mortality. Conclusions Carotid and femoral stiffness indices are independently associated with incident cardiovascular events and all-cause mortality. The strength of these associations with events may differ per stiffness parameter.

Objectives The goal of this study was to determine whether aortic pulse wave velocity (aPWV) improves prediction of cardiovascular disease (CVD) events beyond conventional risk factors. Background Several studies have shown that aPWV may be a useful risk factor for predicting CVD, but they have been underpowered to examine whether this is true for different subgroups. Methods We undertook a systematic review and obtained individual participant data from 16 studies. Study-specific associations of aPWV with CVD outcomes were determined using Cox proportional hazard models and random effect models to estimate pooled effects. Results Of 17,635 participants, a total of 1,785 (10%) had a CVD event. The pooled age- and sex-adjusted hazard ratios (HRs) per 1-SD change in log e aPWV were 1.35 (95% confidence interval [CI]: 1.22 to 1.50; p 70 years, respectively; p interaction Conclusions Consideration of aPWV improves model fit and reclassifies risk for future CVD events in models that include standard risk factors. aPWV may enable better identification of high-risk populations that might benefit from more aggressive CVD risk factor management.

Arterial stiffness is a well-established surrogate marker of vascular properties and arterial dysfunction in patients with type 2 diabetes mellitus (DM2). We aimed to investigate whether optimization of DM2 therapy with, additional to metformin, novel antiglycemic agents may improve arterial wall

Arterial stiffness is considered a surrogate marker of arterial dysfunction in type 2 diabetes mellitus (DM2). Antiplatelet therapy is the cornerstone of cardiovascular disease therapy. There exists little evidence about the influence of antiglycemic agents on arterial wall properties and

The Fuster-BEWAT Score (FBS) has been recently developed for use in lifestyle-based cardiovascular disease (CVD) prevention, presenting similar accuracy in predicting subclinical atherosclerosis with ideal cardiovascular health score (ICHS), but it is unclear whether both scores exhibit comparable

The progression of atherosclerosis versus arterial stiffness with age within and between arteries has not been defined. Systemic lupus erythematosus (SLE) is a human model of inflammation related accelerated arterial disease that may permit this determination. 77 SLE patients (70 women, age 37 ±

Large artery stiffness has been associated with both a reduction in myocardial perfusion and an increase in myocardial oxygen demand, so called the ‘aortocoronary relationship’. The impact of increased arterial stiffness on blood flow within ‘infarct’ and ‘non-infarct’ myocardium

The dietary patterns, in cardiovascular diseases has been challenged and the role of breakfast as an element of balance energy intake has gained research interest. However, the effects of dietary patterns on vascular function is unknown. Therefore, we examined the association of breakfast

Although HIV-infected patients on antiretroviral therapy (ART) containing abacavir (ABC) have been reported to have increased cardiovascular disease (CVD) mortality, studies of vascular function have reported inconsistent results. In this study, measures of vascular endothelial function and arterial

Stroke is a leading cause of morbidity, mortality, and disability worldwide, and the disease burden has progressively increased over the past decades. A rising interest in identifying risk factors for cerebrovascular disease may finally shift the focus to prevention of future events [(1)][1].

Objectives The study sought to evaluate the effects of endurance exercise training (ET) on endothelial-dependent flow-mediated arterial dilation (FMD) and carotid artery stiffness, and their potential contributions to the training-related increase in peak exercise oxygen consumption (Vo2) in older patients with heart failure with preserved ejection fraction (HFPEF). Background Elderly HFPEF patients have severely reduced peak Vo2, which improves with ET, however, the mechanisms of this improvement are unclear. FMD and arterial distensibility are critical components of the exercise response and are reduced with aging. However, it is unknown whether these improve with ET in elderly HFPEF or contribute to the training-related improvement in peak Vo2. Methods A total of 63 HFPEF patients (age 70 ± 7 years) were randomized to 16 weeks of ET (walking, arm and leg ergometry, n = 32) or attention control (CT) (n = 31). Peak Vo2, brachial artery FMD in response to cuff ischemia, carotid artery distensibility by high-resolution ultrasound, left ventricular function, and quality of life were measured at baseline and follow-up. Results ET increased peak Vo2 (ET: 15.8 ± 3.3 ml/kg/min vs. CT: 13.8 ± 3.1 ml/kg/min, p = 0.0001) and quality of life. However, brachial artery FMD (ET: 3.8 ± 3.0% vs. CT: 4.3 ± 3.5%, p = 0.88), and carotid arterial distensibility (ET: 0.97 ± 0.56 vs. CT: 1.07 ± 0.34 × 10(-3) mm·mm Hg(-2); p = 0.65) were unchanged. Resting left ventricular systolic and diastolic function were unchanged by ET. Conclusions In elderly HFPEF patients, 16 weeks of ET improved peak Vo2 without altering endothelial function or arterial stiffness. This suggests that other mechanisms, such as enhanced skeletal muscle perfusion and/or oxygen utilization, may be responsible for the ET-mediated increase in peak Vo2 in older HFPEF patients. (Prospective Aerobic Reconditioning Intervention Study [PARIS]; NCT01113840).

Objectives This study sought to test whether measures of pulsatile arterial function are useful for diagnosing heart failure with preserved ejection fraction (HFPEF), in comparison with and in addition to tissue Doppler echocardiography (TDE). Background Increased arterial stiffness and wave reflections are present in most patients with HFPEF. Methods Patients with dyspnea as a major symptom were categorized as having HFPEF or no HFPEF, based on invasively derived filling pressures and natriuretic peptide levels. Pulse wave velocity (PWV) was measured invasively (aortic PWV). Aortic pulse pressure (aoPP) and its components (incident pressure wave height, forward wave amplitude; augmented pressure; backward wave amplitude [Pb]) were quantified noninvasively. Results Seventy-one patients were classified as HFPEF and 65 as no HFPEF (223 patients had intermediate results). Patients with HFPEF were older, more often had hypertension and diabetes, and had larger left atria and higher left ventricular mass. Brachial pulse pressure (bPP), aoPP, and all measures of arterial stiffness and wave reflections were higher in HFPEF patients. Receiver-operating curve analysis–derived area under the curve (AUC) values for separating HFPEF from no HFPEF were 0.823 for E/E′ at the medial annulus, the best TDE parameter; 0.816 for bPP; and 0.867, 0.851, and 0.825 for aortic PWV, aoPP, and Pb, respectively. Adding measures of pulsatile function to TDE resulted in an increase in AUC to 0.875 (bPP; p = 0.03) and 0.901 (aoPP; p = 0.005). In comparison with a TDE-based algorithm, net reclassification improvement was 32.9% (p Conclusions Measures of pulsatile arterial hemodynamics may complement TDE for the diagnosis of HFPEF. (Pulsatile and Steady State Hemodynamics in Diastolic Heart Failure; NCT00720525 )

Objectives This study sought to assess sex differences in ventricular-arterial interactions. Background Heart failure with preserved ejection fraction is more prevalent in women than in men, but the basis for this difference remains unclear. Methods Echocardiography and arterial tonometry were performed to quantify arterial and ventricular stiffening and interaction in 461 participants without heart failure (189 men, age 67 ± 9 years; 272 women, age 65 ± 10 years). Aortic characteristic impedance (Z c ), total arterial compliance (pulsatile load), and systemic vascular resistance index (steady load) were compared between men and women, and sex-specific multivariable regression analyses were performed to assess associations of these arterial parameters with diastolic dysfunction and ventricular-arterial coupling (effective arterial elastance/left ventricular end-systolic elastance [Ea/Ees]) after adjustment for potential confounders. Results Z c was higher and total arterial compliance was lower in women, whereas systemic vascular resistance index was similar between sexes. In women but not men, higher log Z c was associated with mitral inflow E/A ratio (β ± SE: −0.17 ± 0.07), diastolic dysfunction (odds ratio: 7.8; 95% confidence interval: 2.0 to 30.2) and Ea/Ees (β ± SE: 0.13 ± 0.04) (p ≤ 0.01 for all). Similarly, total arterial compliance was associated with E/A ratio (β ± SE: 0.12 ± 0.04), diastolic dysfunction (odds ratio: 0.33; 95% confidence interval: 0.12 to 0.89), and Ea/Ees (β ± SE: −0.09 ± 0.03) in women only (p ≤ 0.03 for all). Systemic vascular resistance index was not associated with diastolic dysfunction or Ea/Ees. Conclusions Proximal aortic stiffness (Z c ) is greater in women than men, and women may be more susceptible to the deleterious effects of greater pulsatile and early arterial load on diastolic function and ventricular-arterial interaction. This may contribute to the greater risk of heart failure with preserved ejection fraction in women.

Metabolic syndrome (MetS), an important component of insulin resistance and cardiovascular (CV) risk, is defined by 3 or more of the following characteristics: abdominal obesity, hyperglycemia, hypertension, hypertriglyceridemia, and hypo-high-density lipoprotein cholesterolemia. Based on the previously published age- and sex-mediated DESIR (Data from an Epidemiological Study on the Insulin Resistance Syndrome) cohort and parallel central hemodynamic measurements, our goal was to evaluate the effects of MetS on brachial central pulse pressure (PP), PP amplification, aortic stiffness, and wave reflections. These data were then compared with those of patients with essential hypertension but without MetS for the same mean arterial pressure. Increased aortic stiffness, a major mechanical factor predicting CV risk, has been well identified as playing a role in MetS. Its age progression is proportional to the number of risk factors involved in MetS and is responsible for increased systolic blood pressure and decreased diastolic blood pressure with increasing age, the principal hallmarks of hypertension in the elderly. Beyond brachial pressure measurements, central hemodynamic parameters involve increased aortic stiffness, reduced wave reflections, and increased PP amplification, a parameter commonly associated with increased heart rate. With the exception of arterial stiffness, all these findings are opposite in direction to those observed in essential hypertension, in which MetS is absent. A divergent behavior of wave reflections and PP amplification, but not of arterial stiffness, is observed when hypertension is studied alone or when compared with MetS for the same mean arterial pressure. This pulsatile hemodynamic abnormality contributes independently to increase age- and sex-mediated CV risk, justifying new research regarding Framingham scores and drug treatment.

Objectives This study sought to assess the associations of childhood adiposity with vascular phenotype in pre-pubertal children. Background The early-life metabolic consequences have consistently been demonstrated in obese children, but the time course and development of any vascular changes remain largely unexplored. Methods A total of 6,576 children age 10 to 11 years from the ALSPAC (Avon Longitudinal Study of Parents and Children) were studied. Childhood overweight and obesity were based on body mass index contemporary to vascular measures and supported by other adiposity measures, including fat mass and waist circumference on dual-energy x-ray absorptiometry. Heart rate, blood pressure, flow-mediated dilation in the brachial artery, and carotid to radial pulse wave velocity were measured in all children. Results Overweight and obese children had higher heart rates (mean 72.4 ± 11 beats/min and 74.6 ± 12.2 beats/min vs. 71.7 ± 11 beats/min) and systolic blood pressures (mean 106.3 ± 9.1 mm Hg and 108 ± 10.2 mm Hg vs. 103.6 ± 9 mm Hg) compared with normal-weight peers. However, obese children had greater brachial diameters and resting and hyperemic blood flow, marginally increased endothelial function (higher flow-mediated dilation: mean 8.2 ± 3.2% vs. 8.1 ± 3.3%), and lower arterial stiffness (pulse wave velocity: mean 6.99 ± 1.0 m/s vs. 7.05 ± 1.23 m/s) compared with normal-weight children. These findings were not explained by metabolic differences. Conclusions Greater childhood adiposity is associated with adverse cardiometabolic risk factors, but with no evidence of vascular damage at age 9 to 11 years. This could represent physiological adaptation to the hyperemic state of adiposity in childhood.

Outcomes for heart failure (HF) patients remain suboptimal. No known therapy improves mortality in acute HF and HF with preserved ejection fraction; the most recent HF trial results have been negative or neutral. Improvement in surrogate markers has not necessarily translated into better outcomes. To translate breakthroughs with potential therapies into clinical benefit, a better understanding of the pathophysiology establishing the foundation of benefit is necessary. Vascular function plays a central role in the development and progression of HF. Endothelial function and nitric oxide availability affect myocardial function, systemic and pulmonary hemodynamics, and coronary and renal circulation. Arterial stiffness modulates ventricular loading conditions and diastolic function, key components of HF with preserved ejection. Endothelial function and arterial stiffness may therefore serve as important physiological targets for new HF therapies and facilitate patient selection for improved application of existing agents.

Objectives The goal of this study was to examine the progression of central arterial pulse pressure (cPP) in women and the degree to which this can be reversed by nitrovasodilation. Background cPP can be partitioned into height of the first systolic shoulder (P1), generated by a forward pressure wave and related to arterial stiffness, and augmentation pressure (AP), thought to be influenced by pressure wave reflection from muscular arteries and/or aortic reservoir. Methods Using a longitudinal cohort design, cPP, P1, and AP were estimated (using the SphygmoCor System [AtCor Medical Pty Ltd., West Ryde, Australia]) in 411 female twins over a mean follow-up of 10.8 years. In a subsample (n = 42), cPP, arterial stiffness (using pulse wave velocity [PWV]) and arterial diameters (using ultrasonography) were measured before and after nitroglycerin administration (400 μg s/l). Results cPP increased more than peripheral pulse pressure (10.3 and 9.2 mm Hg, respectively; p Conclusions Age-related widening of cPP is driven in large part by an increase in AP, which can be reversed by selective dilation of muscular arteries, independent of PWV.

We thank Dr. Messerli and colleagues for their interest in our paper examining the role of arterial stiffness in patients with heart failure with preserved ejection fraction (HFpEF) [(1)][1]. We found that although brachial and aortic pressures were similar at rest, there was an unmasking of

Excess cardiac and vascular disease complicates type 2 diabetes mellitus (T2DM) before diagnosis. Aortic pulse wave velocity (PWV) powerfully predicts mortality in those with and at risk of T2DM independent of blood pressure (BP) [(1)][1]. We tested the hypothesis that spironolactone, dietary

We appreciate Dr. Palatini’s interest in our review paper and would like to respond by making the following 4 points. First, we agree that the greater augmentation index associated with a lower heart rate implies but this cannot be translated “tout court” into increased arterial stiffness. The

The aorta stiffens with aging, a process that is accelerated by arterial hypertension. Decreased arterial compliance is one of the earliest detectable manifestations of adverse structural and functional changes within the vessel wall. The use of different imaging techniques optimized for assessment of vascular elasticity and quantification of luminal and vessel wall parameters allows for a comprehensive and detailed view of the vascular system. In addition, several studies have also documented the prognostic importance of arterial stiffness (AS) in various populations as an independent predictor of cardiovascular morbidity and all-cause mortality. Measurement of AS by applanation tonometry with pulse-wave velocity has been the gold-standard method and is well-validated in large populations as a strong predictor of adverse cardiovascular outcomes. Because aortic stiffness depends on the prevailing blood pressure, effective antihypertensive treatment is expected to reduce it in proportion to the blood pressure reduction. Nevertheless, drugs lowering blood pressure might differ in their effects on structure and function of the arterial walls. This review paper not only will discuss the current understanding and clinical significance of AS but also will review the effects of various pharmacological and nonpharmacological interventions that can be used to preserve the favorable profile of a more compliant and less stiff aorta.

ObjectivesThis study aimed to investigate sex differences in the association between arterial stiffness and left ventricular (LV) diastolic dysfunction.BackgroundHeart failure with preserved ejection fraction is more common in women. Arterial stiffness has been suggested as a significant contributor to the development of heart failure. We hypothesized that the association between arterial stiffness and LV diastolic function would be stronger in women than in men.MethodsTwo-dimensional, Doppler echocardiography and radial artery tonometry were performed simultaneously in 158 age-matched subjects (79 males, 79 females; mean age: 58 ± 10 years) without any structural heart disease or LV systolic dysfunction.ResultsThe peripheral blood pressure and pulse pressure (PP) were similar between sexes. However, central PP and augmentation index were significantly higher and PP amplification was significantly lower in women (1.31 vs. 1.19, p < 0.001). The associations of PP amplification with early diastolic mitral annular (Em) velocity and transmitral to mitral annular early diastolic velocity ratio (E/Em) were significant in women (r = 0.38, p = 0.001; r = −0.36, p = 0.001), whereas no significant association was found in men (r = 0.09, p = 0.428, r = −0.14, p = 0.215). Multiple regression analysis revealed that PP amplification had an independent correlation with Em velocity only in women.ConclusionsDespite similar peripheral PP, the central hemodynamics reflecting arterial stiffness were different between men and women. LV diastolic function correlates significantly with the parameters representing arterial stiffness only in women. We suggest that the effects of earlier wave reflection on central pressure may contribute to greater susceptibility to heart failure with preserved LV ejection fraction in women.

Objectives Our aim was to examine the relationship of arterial stiffness to measures of atherosclerosis, arterial calcification, and bone mineral density (BMD); the heritability of these measures; and the degree to which they are explained by common genetic influences. Background Arterial stiffening relates to arterial calcification, but this association could result from coexistent atherosclerosis. A reciprocal relationship between arterial stiffening/calcification and BMD could explain the association between cardiovascular morbidity and osteoporosis. Methods We examined, in 900 women from the Twins UK cohort, the relationship of carotid-femoral pulse wave velocity (cfPWV) to measures of atherosclerosis (carotid intima-media thickening; carotid/femoral plaque), calcification (calcified plaque [CP]; aortic calcification by computed tomography, performed in subsample of 40 age-matched women with low and high cfPWV), and BMD. Results The cfPWV independently correlated with CP but not with intima-media thickness or noncalcified plaque. Total aortic calcium, determined by computed tomography, was significantly greater in subjects with high cfPWV (median Agatston score 450.4 compared with 63.2 arbitrary units in subjects with low cfPWV, p = 0.001). There was no independent association between cfPWV and BMD. Adjusted heritability estimates of cfPWV and CP were 0.38 (95% confidence interval: 0.19 to 0.59) and 0.61 (95% confidence interval: 0.04 to 0.83), respectively. Shared genetic factors accounted for 92% of the observed correlation (0.38) between cfPWV and CP. Conclusions These results suggest that the association between increased arterial stiffness and the propensity of the arterial wall to calcify is explained by a common genetic etiology and is independent of noncalcified atheromatous plaque and independent of BMD.

Arterial stiffening is the hallmark of normal vascular aging, and early acceleration of the stiffening process represents 1 of the major pathologies of the cardiovascular system [(1,2)][1]. During the last 50 years, thanks to the development of easy to use and reasonably reproducible noninvasive

Objectives We prospectively and longitudinally determined the effects of smoking on the progression of arterial stiffening as well as the involvement of inflammation in this process. Background Smoking is an important avoidable risk factor for cardiovascular disease, and arterial stiffness might be involved in the pathophysiology. No prospective study has examined the effect of continuous smoking on the age-associated progression of arterial stiffening. Methods In 2,054 Japanese subjects (40 ± 8 years of age), brachial-ankle pulse wave velocity (baPWV) and serum C-reactive protein (CRP) levels were measured at the baseline and the end of a 5- to 6-year follow-up period. Results The annual rate of change of the baPWV during the study period was significantly greater in the continuous heavy smokers (11.0 ± 1.9 cm/s/year, n = 181) than in the never-smokers (5.5 ± 0.6 cm/s/year, n = 1,018). This difference remained significant even after adjustments for covariates, including age (p Conclusions Continuous smoking might accelerate the age-associated progression of structural stiffening of the large- to middle-size arteries. We also found a dose–response relationship between cigarette consumption and accelerated arterial stiffening. However, we failed to confirm any significant association between the rate of arterial stiffening and the serum CRP levels in the smokers.

Metabolic syndrome (MS) is associated with increasing in cardiovascular (CV) events and all-cause mortality. The aim of this study is to use arterial stiffness assessed by cardio-ankle vascular index (CAVI) to predict the CV events and all-cause mortality in MS patients. A total of 3,983 employee

The exact impact of chronic coffee consumption on atherosclerosis is not determined. We evaluate the association of coffee consumption with arterial stiffness. Corinthia study is a cross sectional epidemiological study based on 2043 inhabitants (age 40-99years) of Corinthia region in Greece.

Cigarette smoking is the commonest modifiable risk factor for coronary artery disease (CAD) and vascular inflammation may play an important role in the pathogenesis. However, the presence of confounding factors, particularly age and gender, makes it difficult to interpret vascular effects of smoking

Anthracyclines are the preferred agents for breast cancer chemotherapy, but their use is limited by their cardiotoxicity. Anthracyclines' effects on vascular function have been less well studied. We explored the effects of anthracycline chemotherapy on endothelial function and arterial stiffness in

Emotion and depression may affect atherosclerosis progression. We examined the association between depression, arterial stiffness and atheromatic burden in carotid arteries. Corinthia study is a cross sectional epidemiological study based on 2043 inhabitants (age 40-99years) of Corinthia region in

Strict glycaemic control in patients with type 2 diabetes mellitus (T2D) may attenuate progression of microvascular disease. We study the predictive value of endothelial function and arterial stiffness in T2D patients. A total of 80 T2D patients were screened for diabetic retinopathy. At baseline