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A number of circulating and imaging biomarkers are robustly associated with cardiovascular (CV) risk. The overall expectation from a biomarker in the erectile dysfunction (ED) setting is to enhance the optimal management of a man with this disorder but no clinical atherosclerosis. Evidence demonstrating that these biomarkers enhance risk prediction for individuals with ED is at this stage still limited for most of them. A better identification of the subsets of the ED population that require further risk stratification, as well as the initiation of randomized trials that will formally test the ability of biomarkers to predict CV risk, could make biomarker-guided prevention an attainable goal.

Purpose/Background/Objectives: Hypertension is associated with higher cardiovascular risk as well as several markers of subclinical target organ damage (TOD). Albumin to creatinine ratio (ACR) in urine has been recognised as an independent risk factor for cardiovascular events. We hypothesised that there is a relationship between ACR and markers of TOD in never- treated hypertensives. Methods: We enrolled 924 consecutive essential hypertensives (mean age 53±12 years, 486 males) without known cardiovascular disease (CVD). Markers of subclinical TOD [left ventricular mass index (LVMI), pulse wave velocity (PWV), ankle-brachial index (ABI) and estimated glomerular filtration rate (eGFR)] were evaluated in all patients. LVMI was assessed echocardiographically using the Devereux formula. Carotid-femoral PWV was estimated with the Complior device. eGFR was calculated by the Cockcroft-Gault formula. ABI was calculated by dividing the highest ankle systolic blood pressure by the highest brachial systolic blood pressure. Results: ACR exhibited significant association with LVMI (r = 0.277, p < 0.001), PWV (r = 0.277, p < 0.001) ABI (r = −0.078, p = 0.018) and eGFR (r = −0.100, p = 0.002). In further analysis, ACR was associated with TOD as suggested by the 2013 European Guidelines for Hypertension [left ventricular hypertrophy (LVMI > 115 g/m2 in men and >95 g/m2 in women), increased PWV (PWV > 10m/s), decreased ABI (ABI < 0.9) and decreased renal function (eGFR < 60ml/min)]. Specifically, ACR exhibited a significant association with the number of TOD and this association was independent of age and gender (p < 0.05). Conclusions: Our findings support the close relationship between ACR and TOD in hypertension, as well as, the predictive ability of ACR for TOD.

Purpose/Background/Objectives: Aortic stiffness and hemodynamics are independent predictors of adverse cardiovascular events. Transcatheter aortic valve implantation (TAVI) is growingly used in elderly patients with aortic stenosis. We sought to investigate the effect of TAVI upon aortic vascular function and hemodynamics as well as the interplay between genders. Methods: Twenty high-risk patients (mean age 82.2±5.3 years, 13 female) with severe symptomatic aortic stenosis undergoing TAVI were included. Aortic stiffness was estimated through carotid-femoral pulse wave velocity (PWV). Aortic hemodynamics (aortic pressures, aortic augmentation index [AIx]) and subendocardial viability ratio (SEVR) were measured with Sphygmocor. Measurements were conducted prior to the implantation and at discharge. Results: PWV prior to the implantation was 8.6±1.5 m/s and aortic AIx = 33.0±14.0% for the overall population. There was no statistically significant change in peripheral or aortic pressures as well as on aortic stiffness after implantation of TAVI. However, there was a marginally non-significant trend for an increase in SEVR (116±28 vs 131±40%, p = 0.067). Results to the male population were similar to the overall population. Conversely, in the female population, there was a significant increase in PWV after TAVI (8.4±1.2 m/s vs 8.9±1.3% with p = 0.034, respectively). Furthermore, there was a significant increase in SEVR after TAVI (107±28 vs 125±24% with p = 0.002, respectively). All other variables did not change significantly in the female population. Conclusion: Our study shows that shortly after TAVI female subjects experience an increase in aortic stiffness with an improvement of myocardial perfusion. These findings further elucidate the short-term hemodynamic consequences of aortic valve repair.

Purpose/Background/Objectives: Proprotein convertase subtilisin/kexin type 9 (PCSK9) levels are modestly but significantly associated with increased risk of total cardiovascular events. Aortic stiffness and wave reflections are also important predictors of cardiovascular events. The aim of this pilot study was to determine if PCSK9 levels are associated with aortic elastic properties in patients with familial dyslipidemia. Methods: Thirty-three patients with familial dyslipidemia (mean age 45 ± 12 years, 21 men, 14 with heterozygous familial hypercholesterolemia and 19 with familial combined hyperlipidemia) without known cardiovascular disease were enrolled. PCSK9 levels were measured with ELISA. Aortic stiffness was assessed with carotid-femoral pulse wave velocity (cfPWV) and wave reflections were assessed with aortic augmentation index corrected for heart rate (AIx@75). High-sensitivity C-reactive protein (hsCRP) levels were determined as a marker of subclinical inflammation. Results: There was a positive correlation between AIx@75 and PCSK9 levels (r = 0.371, p = 0.034). (Figure) No association was found between levels PCSK9 and cfPWV (r = 0.043, p = 0.813) or hsCRP (r = 0.199, p = 0.274). In multivariate regression analysis, after adjustment for potential confounders such as age and sex, AIx@75 showed a significant positive correlation with PCSK9 levels (Adjusted R2 = 0.23, p = 0.007). Even after further adjustment for possible confounders such as the type of familial dyslipidemia, low-density lipoprotein levels, cfPWV and hsCRP this association remained statistically significant (Adjusted R2 = 0.16, p = 0.03). Gender was also significantly associated with levels of PCSK9 (p = 0.029). Conclusions: In a group of patients with familial dyslipidemia PCSK9 levels were positively associated with wave reflections but not aortic stiffness.

Purpose/Background/Objectives: Aim of the study is to examine the possible differentiation of aortic stiffness, carotid atherosclerosis and penile vascular function among patients with erectile dysfunction (ED) according to cholesterol level and statin therapy. Methods: We measured carotid intima-media thickness (IMT), carotid-femoral pulse wave velocity (PWV) and penile peak systolic velocity (PSV) 20 min after intracavernous injection of prostaglandin E1 in 356 consecutive ED patients (mean age 57±9 years). Lipid parameters and total testosterone were measured in all patients. Results: 95 (26.7%) ED patients are treated with statins. The patients not receiving statin therapy (n = 261) were subsequently divided into three groups according to LDL level (group 1: LDL < 100 mg/dl, group 2: LDL: 100–155 mg/dl, group 3: LDL > 155 mg/dl). Patients with statin therapy and subjects in group 2 have similar mean LDL level. Carotid IMT was higher in patients with LDL >155 mg/dl (group 3) compared to patients treated with statins (P = 0.01) and subjects with LDL: 100–155 mg/dl (P = 0.005) and LDL < 100 mg/dl (left plot, P < 0.001). Post hoc analysis showed that patients treated with a statin and subjects in group 3 had comparable penile PSV and lower mean value compared to that of patients in group 1 and group 2 (right plot). Carotid-femoral PWV was similar between the studied groups. Testosterone levels were similar between patients treated with a statin and males not receiving hypolipidemic therapy (groups 2 and 3). Conclusions: Although treated hypercholesterolemic patients exhibited lower atherosclerotic burden compared to untreated individuals with high LDL levels, penile blood inflow remains significantly impaired.

Purpose/Background/Objectives: Hypertension is associated with several markers of subclinical target organ damage (TOD). Short-term blood pressure variability (SBPV) is a prognostic factor for cardiovascular events in hypertensives. We hypothesised that there is a relationship between SBPV and TOD in never-treated hypertensives. Methods: We enrolled 943 consecutive essential hypertensives (mean age 53±12 years, 497 males). Markers of subclinical TOD [left ventricular mass index (LVMI), pulse wave velocity (PWV), total arterial compliance (TAC), aortic augmentation index (AIx@75), ankle-brachial index (ABI) and estimated glomerular filtration rate (eGFR)] and 24-h ambulatory blood pressure were evaluated in all patients. SBPV was calculated as follows: 1) SD of 24-hour, daytime, or nighttime SBP and 2) weighted SD of 24-hour SBP. Results: In multivariable regression analysis, all four variables of SBPV exhibited significant association with LVMI (p = 0.014, p = 0.002, p = 0.002 and p < 0.001, respectively), PWV (p = 0.021, p = 0.015, p = 0.055 and p = 0.006, respectively) and TAC (p = 0.048, p = 0.020, p = 0.036 and p = 0.006, respectively). In multivariable analysis, ABI and eGFR were not associated with indices of SBPV. We assessed TOD based on 2013 European Guidelines for Hypertension [left ventricular hypertrophy (LVMI > 115 g/m2 in men and >95 g/m2 in women), increased PWV (PWV > 10m/s), increased AIx@75 (AIx@75 > 28%), decreased ABI (ABI < 0.9) and decreased renal function (eGFR < 60ml/min)]. In multivariable logistic regression analysis, SBPV indices were not associated with markers of TOD (P > 0.05). Conclusions: Our findings support a complex relationship between SBPV and TOD in hypertension. Specifically, SBPV is more closely related to markers of ventricular and vascular compliance than other markers of TOD in hypertension.

Purpose/Background/Objectives: We investigated the acute effect of electronic cigarette (EC) smoking on the aortic pressure waveform amplification. We also sought to compare the effect of EC and combustible cigarette (TC) smoking on central haemodynamics. Methods: We studied 24 smokers (age: 30±8 years) on 3 separate occasions: a) tobacco cigarette (nicotine content, 1.2 mg) over 5 minutes, b) EC (18 mg E-liquid) for a period of 30 minutes, and c) nothing (sham procedure) for 60 minutes. Smoking EC for 30 min (15 puffs) was chosen to mimic the common pattern of EC smoking. Results: Both TC and EC smoking caused a significant increase in brachial pressures and heart rate (HR), and the differences in blood pressure (BP) and HR responses between the two smoking forms were not significant. The aortic pressures also increased significantly after smoking both TC and EC, with the greatest changes seen in the first 5 minutes after TC smoking and 15 minutes EC smoking (figures 1A– C, all P < 0.05). Although AIx, decreased in both two smoking forms, by applying a correction factor for changes in HR, the AIx increased significantly after TC (by 3.0% at 5 minutes, P < 0.05) and EC (by 2.9% at 15 minutes, P < 0.05) (figure 1D). Conclusions: Electronic cigarette smoking exerts an unfavourable and comparable to that of TC smoking acute effect on aortic pressure waveform amplification. Given the prognostic role of central haemodynamics on cardiovascular disease risk, EC may still be considered a hazardous smoking method.

Brachial cuff blood pressure (BP) is clinically important, but may be an inaccurate substitute for central BP. Many non-invasive devices have been developed that purport to estimate central BP from peripheral artery sites, yet with no standardized guidelines; the accuracy testing of these new devices has not been undertaken in a uniform fashion with comparable protocols. This is an abridged paper describing the recommendations reached by an international task force convened to identify issues that need to be addressed and reach consensus relating to methods for assessing and reporting the accuracy (validation) of central BP devices. The recommendations are endorsed by the Association for Research into Arterial Structure and Physiology (ARTERY) Society, as well as the European Society of Hypertension (ESH) Working Group on Arterial Structure and Function, and the ESH Working Group on Blood Pressure Monitoring and Cardiovascular Variability. Researchers interested in validating central BP monitors should read the full version of the statement.

Arterial hypertension and dyslipidemia often coexist and constitute major risk factors of ischemic heart disease. Aggressive treatment of both comorbidities is of paramount importance to decrease global risk. Low adherence is a determinant of poor risk factor control and increases adverse cardiovascular outcomes. Regarding treatment of hypertension, combination therapy is superior in achieving target BP values compared to up-titrating monotherapy and it is recommended in hypertension guidelines. The combined use of drugs in a single pill formulation increases adherence and reduces cardiovascular risk. Our review of the literature indicates that triple therapy with an angiotensin converting enzyme inhibitor, a calcium channel blocker and a statin is associated with a significant reduction in major cardiovascular events. This is attributed to synergy at the vascular, and is translated into efficacy at the clinical level.

A strong heritage of science has been handed down in Britain from outstanding individuals, promoted and encouraged by strong scientific and medical societies. Application to clinical practice in recent years has been slow but can be expected to advance in the present and future age of new sensors, fast computing and clinical problems awaiting explanation. Agreement on terminology and physical mechanisms needs be fostered.

Purpose: Erectile dysfunction (ED) confers an independent risk for cardiovascular events and total mortality. Central pressures and wave reflection indices independently predict cardiovascular events. Aim of this study is to investigate whether central haemodynamics predict major adverse cardiovascular events (MACEs) in ED patients beyond traditional risk factors. Methods: MACEs in relation to aortic pressures and Augmentation index (AIx) were analyzed with proportional hazards models in 398 patients (mean age, 56 years) without established cardiovascular disease (CVD). Results: During the mean follow-up period of 6.5 years, a total of 29 (6.5%) MACEs occurred. The adjusted relative risk (RR) of MACEs was 1.062 (95% CI 1.016–1.117) for a 10-mmHg increase of aortic systolic pressure, 1.117 (95% CI 1.038–1.153) for a 10-mmHg increase of aortic pulse pressure (PP), and 1.191 (95% CI 1.056–1.372) for a 10% absolute increase of AIx. The based on categories for 10-year coronary heart disease risk and adapted at 6.5 years overall net reclassification index (NRI) showed marginal and indicative risk reclassification for AIx (15.7%, P=0.12) and aortic PP (7.2%, P=0.20) respectively. Conclusions: Our results show for the first time that higher central pressures and wave reflections indices are associated with increased risk for a MACE in patients with ED without known cardiovascular disease. Considering the adverse prognostic role of central haemodynamics on outcomes, the present findings may explain part of the increased cardiovascular risk associated with ED.

Purpose/Background/Objectives: Patients with rheumatoid arthritis (RA) have a higher arterial stiffness than their age-matched healthy counterparts and an increased inflammatory burden that might be associated with their increased cardiovascular risk. Tumor necrosis factor alpha (TNF)-antagonists have been found to reduce inflammatory markers in RA however it is debatable if they have favorable effects on surrogate markers of cardiovascular outcomes. We conducted a meta-analysis to assess the effect of TNF-antagonists on arterial stiffness, a predictor of cardiovascular events and mortality, in RA patients. Methods: A search of PUBMED was conducted to identify studies into the effect of TNF-antagonists on arterial stiffness in RA patients. Data were available on 3 TNF-antagonists: infliximab, adalimumab, and etanercept. Results: 10 studies (n=208 patients) out of 14 eligible studies in total, measured changes in carotid-femoral PWV after treatment with anti-TNFs. Subjects under therapy with anti-TNFs significantly decreased their arterial stiffness (mean change in PWV: -0.53 m/s, p=0.001)(Figure). No significant heterogeneity was observed across the studies (I2=8.5%, p=0.364). By subgroup analysis, improvement in PWV after therapy was independent of age, sex, nationality and clinical response to treatment and dependent of the type of the TNF- antagonist used. Conclusions: The balance of evidence suggests that TNF-antagonists may have a beneficial effect on arterial stiffness in RA patients. Given the predictive role of aortic stiffness for adverse cardiovascular outcomes, TNF-antagonists might confer reduction of the cardiovascular risk of these patients beyond their anti-inflammatory effect. However, larger longitudinal studies are warranted to confirm recent findings.

Purpose/Background/Objectives: Smoking increases aortic stiffness which is an important predictor of cardiovascular risk. Electronic cigarettes (EC) simulate tobacco cigarette (TC) and have been advocated as a less harmful alternative. We investigated the acute effect of EC smoking on aortic stiffness compared to the effect of TC smoking. Methods: We studied 24 healthy smokers (mean age 30±8 years, 13 females), who were free of risk factors X from smoking. Each participant visited our unit on four separate occasions (96 in total) and smoked: a) TC over 5 minutes b) EC over 5 minutes c) EC for a period of 30 minutes. During the sham procedure, participants did not smoke anything. Carotid-femoral pulse wave velocity (PWV) was used to assess aortic stiffness. Results: Both TC and EC smoking increased systolic and diastolic BP, and the differences in changes of BP responses between the two smoking forms were not significant. Compared to TC, EC5 min smoking resulted in a less potent PWV increase throughout the study (F=4.425, P=0.005). On the other hand, EC30min resulted in a PWV increase similar to that of TC smoking throughout the study period (F=0.268, P=0.615). EC30 min smoking resulted in a more potent effect on PWV compared to EC5 min smoking (F=3.167, P=0.030). Conclusions: EC over 30 minutes induces an unfavorable effect on aortic stiffness similar to TC smoking. The influence of EC smoking over 5 minutes on aortic stiffness is not as prompt and is less potent compared to the effect of TC smoking.

Measures of arterial aging have the potential to improve risk prediction beyond traditional risk scores. Such biomarkers that fulfil most, or some of the strict criteria of a surrogate end-point are aortic stiffness (IIa level of recommendation in European Guidelines and Position Papers) and central haemodynamics (IIb level of recommendation). Early intervention towards improving aortic elastic properties acquires particular importance since evidence suggests that arterial stiffening may occur before the onset of hypertension. Part of the beneficial effects of antihypertensive treatment in risk reduction may be mediated through improvement in aortic stiffness and central haemodynamics. However, not all antihypertensive drugs affect aortic stiffness and central haemodynamics in a similar way. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARB) and calcium channel blockers (CCB) have beneficial effects on such parameters. Meta-analytical approaches have shown that ACE inhibitors reduce mortality in hypertension, whereas ARBs do not exhibit such a benefit. Furthermore, ACE inhibitors have been shown to reduce the risk of coronary artery disease, and CCBs to reduce the risk of stroke independently of blood pressure reduction. Combining an ACE inhibitor with a CCB has the potential to reduce cardiovascular risk (synergy at the clinical level) by reducing aortic stiffness and improving central haemodynamics (synergy at the vascular level).

Purpose: Erectile dysfunction (ED) is an independent predictor of future cardiovascular (CV) events. Aortic pressures (central) and low testosterone independently predict future CV events and mortality. The relationship between testosterone, central pressures and wave reflection indices in ED patients is unknown. Methods: Total testosterone (TT) levels were measured in 407 consecutive ED patients (55 ± 8 y/o) without CVD. Central (aortic) systolic and pulse pressure, augmentation index (AIx) and augmented pressure (AP) as indices of pulse wave amplification across the arterial tree were measured with SphygmoCor device (AtCor Medical). Results: TT levels were inversely correlated with systolic and pulse central pressures (r = −0.195 and r = −0.249, respectively) and wave reflection indices (AIx: r = −0.208 and AP: r = −0.168) (all P < 0.001). In multivariate regression models adjusting for age and risk factors, TT was an independent predictor of central pressures and wave reflection indices (all P < 0.001). The combination of low TT level (40 mmHg) and AIx (>27%) values showed greater effect on 10-year risk of a CV event (figure). Conclusions: Our study is the first, to the best of our knowledge, to demonstrate in ED patients the independent association of low testosterone with central pressures and indices of pulse wave amplification across the arterial tree. This observation highlights the role of testosterone as a marker of arterial disease and predictor of CV events and imply a pathophysiological contribution of testosterone deficiency to age and blood pressure-related processes associated with generalized arterial disease.

Purpose: Testosterone levels are decreased in hypertensive patients compared to normotensive subjects with similar age. Measurements of carotid IMT or aortic stiffness are reasonable for detecting vascular organ damage (OD) in patients with arterial hypertension. We investigated whether low testosterone concentration is associated with vascular OD in hypertensive patients. Methods: 178 consecutive asymptomatic hypertensive males (40–60 y/o) were evaluated using exercise treadmill test and stress echocardiography. Men with positive one or both of the two tests were referred for coronary angiography in order to document coronary artery disease (CAD). All patients underwent carotid-femoral pulse wave velocity (PWV) and carotid IMT evaluation. Vascular OD was detected when IMT>0.9 mm (or plaque) and/or PWV>10 m/s. Total testosterone (TT) levels were measured in all participants. Testosterone deficiency (TD) was defined when TT levels were below 3.4 ng/ml. Results: Coronary angiography revealed significant stenosis in 31 (17%) patients. The prevalence of Grade II/III hypertension was not different between CAD patients and subjects without CAD. Subjects without CAD were further divided according to presence/absence of vascular OD. Patients with vascular OD had lower TT level (p

Objectives: Smoking has an unfavorable effect on arterial properties. Vascular aging is an independent predictor of cardiovascular risk. We examined the effect of quitting smoking on the progression of arterial stiffness. Methods: 142 subjects (mean age 51.9 ± 10.8 years, 94 men) with no established cardiovascular disease were investigated in 2 examinations over a 2-year period. Subjects were categorized in current smokers, non-smokers and ex-smokers. Ex–smokers were further categorized according to the time elapsed since smoking ( 15 years). Subjects had at the beginning and end of the study determinations of carotid-femoral pulse wave velocity (PWV) and common carotid intima-media thickness. Based on these measurements the annual absolute changes were calculated. Results: Smoking at baseline was not associated with statistically significant differences in PWV and CIMT. However, the annual change of PWV was statistically different between the groups of smokers, non-smokers and the 3 groups of ex-smokers (p = 0.041) after adjustment for relevant confounders. Specifically, smokers had 0.23 m/s/year (95% CI: 0.10 to 0.35), non-smokers 0.17 m/s/year (95% CI: 0.08 to 0.25), quitters (15 years) −0.07 m/s/year (95% CI:−0.26 to 0.13). Similar trend for slower progression was observed for CIMT in past smokers (>5 years) but this was not statistically significant. Conclusions: Quitting smoking slows down progression of vascular aging after many years, implying a period of adjustment for former deleterious effects of smoking.

Background: Human immunodeficiency virus (HIV) infection is associated with subclinical inflammation and increased cardiovascular risk. Arterial stiffness and enhanced wave reflections are markers of cardiovascular disease and independent predictors of cardiovascular risk. The effect of HIV infection, per se, on aortic stiffness and wave reflections has not been clearly defined. Methods: We studied 51 adults with a recent HIV infection, free of antiretroviral treatment and AIDS diagnosis, as well as 35 controls matched for age, sex and smoking status. Carotid-femoral pulse wave velocity (PWV) and timing of the reflected wave (Tr) were measured as indices of aortic stiffness, while aortic augmentation index (AIx) and augmented pressure (AP) were measured as indices of wave reflections. Results: While PWV was similar in the two populations, Tr was significantly lower in HIV-infected subjects compared to controls (by 16.5ms, p=0.002). In addition, AIx and AP were decreased (by 6.4%, p=0.048 and by 3.3mmHg, p=0.010, respectively) in subjects with HIV infection. Moreover, HIV-infected patients compared with controls had increased values of hs-CRP [1.37 (0.85–2.53) vs. 0.75 (0.41–1.90) mg/l, p=0.007] and interleukin-6 [1.90 (0.91–3.9) vs. 1.28 (0.80–2.65) pg/ml, p=0.048]. Tr was negatively correlated with hs-CRP (r=−0.283, p=0.010) and interleukin-6 (r=−0.278, p=0.018). Conclusions: Our study provides evidence of decreased wave reflections and similar aortic stiffness, as assessed by PWV, in the early stages of HIV infection in treatment-naive patients compared to controls. Subclinical inflammation and resultant peripheral vasodilatation constitute potential mediators of the whole pathophysiological process.

Introduction: Inflammatory state is activated in metabolic syndrome and may explain part of the adverse prognosis of this entity. Arterial stiffness, central blood pressures and wave reflections are independent predictors of cardiovascular risk. This study investigates the relation between low-grade inflammation and arterial stiffness and central hemodynamics in patients with metabolic syndrome. Methods: We studied 106 consecutive hypertensive patients with metabolic syndrome. Arterial stiffness was assessed by carotid-femoral (c-f) and carotid-radial (c-r) pulse wave velocity (PWV). Central blood pressures were evaluated by pulse wave analysis and heart rate corrected augmentation index (AIx75) was used as a measure of wave reflections. White blood cell count (WBC), high sensitivity C-reactive protein (hsCRP) and fibrinogen were measured as inflammatory markers. Results: In univariable analysis, PWVc-f correlated with both hsCRP (p

This review deals with the effect of several components of the broad term “lifestyle” on arterial stiffness and wave reflections. Caffeine and coffee have an unfavourable effect on aortic stiffness and wave reflections both on an acute and on a chronic basis. Acute consumption of tea, which contains not only a great amount of flavonoids but also caffeine, stiffens the arteries less than its caffeine content. Dark chocolate, also rich in flavonoids, has a beneficial acute effect on wave reflections, while its habitual consumption appears to have a beneficial effect both on aortic stiffness and wave reflections. Alcohol consumption has a J- or U-shaped effect on arterial stiffness and wave reflections; moderate consumption is beneficial, while high consumption may be deleterious. Salt restriction results in a rapid amelioration of arterial elastic properties. Smoking has been extensively associated with a deterioration of arterial stiffness and wave reflections both on an acute and on a chronic basis. Obesity (especially central) is generally associated with impaired arterial elastic properties, and weight loss is accompanied with improvement in arterial stiffness. Aerobic exercise is beneficial to arterial function, while resistance exercise has the opposite results. Data suggest that acute mental stress has a prolonged unfavorable effect on aortic stiffness and wave reflections. Lifestyle has a significant, and increasingly recognised, impact on cardiovascular risk. An important part of this impact may be mediated through its effect on arterial stiffness and wave reflections given their important pathophysiological and prognostic role.