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Objective: Blood pressure fluctuates during diastole to create a dicrotic wave but the mechanistic origin remains poorly understood. We sought to investigate the characteristics and determinants of diastolic pressure and flow fluctuations with a focus on stiffness gradients between the central aorta and peripheral arteries. Methods: Using applanation tonometry and duplex ultrasound, pulse waveforms were recorded on the femoral artery in 592 patients (age: 55=14years) to estimate the diastolic pressure fluctuation as a residual wave against the mono-exponential decay and the diastolic flow fluctuation as a bidirectional (forward and reverse) velocity wave. The radial, carotid, and dorsalis pedis pressures were also recorded to measure the peripheral/aortic pulse pressure (PP) and pulse wave velocity (PWV) ratios. Results: There were close resemblances between the femoral pressure and flow fluctuation waveforms. The pressure and flow fluctuations were mutually correlated in relative amplitude as indexed to the total pulse height (r=0.63), and the former temporally followed the latter. In multivariate-adjusted models, higher peripheral/aortic PP and PWV ratios were independently associated with greater pressure and flow fluctuation indices (P

Purpose The evidence linking waterpipe smoking to cardiovascular disease is limited. We evaluated the association of waterpipe smoking (WPS) with arterial stiffness and wave reflection measured by augmentation pressure (AP), augmentation index (AIx), and carotid-femoral pulse wave velocity (CFPWV), which are validated predictors of cardiovascular disease. Materials and methods Community-based, cross-sectional study including 205 exclusive waterpipe smokers and 199 matched never-smokers aged 35 years or older (mean age 51.7 ± 8.9 years, 36% females). Smoking and its extent were assessed using a validated questionnaire and urine cotinine levels. CFPWV, AP, AIx (AP/aortic pulse pressure) and heart rate adjusted AIx (AIx@75) were determined using tonometry and compared between smokers and non-smokers, and the association of WPS with tonometry measures was assessed using linear regression adjusting for possible confounders. Results Waterpipe smokers and non-smokers had similar mean age and sex distribution. Compared to non-smokers, waterpipe smokers had significantly higher adjusted AP (10.5 ± 3.9 vs. 9.4 ± 3.9 mmHg respectively; p = 0.01), AIx (28.1 ± 8.4 vs. 25.7 ± 8.5% respectively; p = 0.01) and AIx@75 (24.2 ± 8.7 vs. 21.8 ± 8.9% respectively; p = 0.01). AIx was significantly associated with WPS extent, measured by a number of waterpipe smoked/day (β = 1.04/waterpipe, 95%CI:[0.50-1.58]), duration of waterpipe smoking (β = 0.77/10-years, 95%CI:[0.16-1.38]), their products in waterpipe-years (β = 0.30/10-waterpipe-year, 95%CI:[0.12-0.47]) and plasma cotinine (β = 0.56/100 ng/ml, 95%CI:[0.14-0.98]), adjusting for possible confounders, and so were AP and AIx@75. CFPWV however, was not associated with waterpipe smoking. Conclusion In a community-based sample, exclusive WPS and its extent were associated with a dose-dependent increase in AIx and AP, accounting for other risk factors, suggesting that waterpipe smokers are at increased risk of cardiovascular disease.

Arterial stiffness is a risk factor for chronic kidney disease progression (CKD). Pulse pressure is a surrogate marker of arterial stiffness. It is unclear if pulse pressure predicts CKD progression in type 2 diabetes mellitus. This was prospective study involving 1494 patients with estimated glomerular filtration rate (eGFR) ≥ 15 ml/min/1.73 m2. Carotid-femoral pulse wave velocity was measured using applanation tonometry. Pulse pressure was calculated as difference between systolic and diastolic blood pressures. CKD progression was defined as worsening of eGFR categories (stage 1, ≥ 90 ml/min/1.73 m2; stage 2, 60–89 ml/min/1.73 m2; stage 3a, 45–59 ml/min/1.73 m2; stage 3b, 30–44 ml/min/1.73 m2; stage 4; 15–29 ml/min/1.73 m2; and stage 5

Cerebral arterial pulsatility is strongly associated with cerebral small vessel disease and lacunar stroke yet its dependence on central versus local haemodynamic processes is unclear. In a population-based study of patients on best medical managment, 4–6 weeks after a TIA or non-disabling stroke, arterial stiffness and aortic systolic, diastolic and pulse pressures were measured (Sphygmocor). Middle cerebral artery peak and trough flow velocities and Gosling’s pulsatility index were measured by transcranial ultrasound. In 981 participants, aortic and cerebral pulsatility rose strongly with age in both sexes, but aortic diastolic pressure fell more with age in men whilst cerebral trough velocity fell more in women. There was no significant association between aortic systolic or diastolic blood pressure with cerebral peak or trough flow velocity but aortic pulse pressure explained 37% of the variance in cerebral arterial pulsatility, before adjustment, whilst 49% of the variance was explained by aortic pulse pressure, arterial stiffness, age, gender and cardiovascular risk factors. Furthermore, arterial stiffness partially mediated the relationship between aortic and cerebral pulsatility. Overall, absolute aortic pressures and cerebral blood flow velocity were poorly correlated but aortic and cerebral pulsatility were strongly related, suggesting a key role for transmission of aortic pulsatility to the brain.

This article presents a primed left ventricle heart perfusion method to generate physiologic aortic pressure (AoP) and perform functional assessment. Isolated hearts of male Yorkshire pigs were used to study the hemodynamic behaviors of AoPs generated in the primed left ventricle heart perfusion (n = 6) and conventional (zero-loaded left ventricle) Langendorff perfusion (n = 6). The measurement results show that left ventricular pressure generated in the primed left ventricle heart perfusion is a determinant of physiologic AoP (i.e. systolic and diastolic pressures within physiologic range). The aortic pulse pressure (systolic pressure = 124.5 ± 1.7 mm Hg, diastolic pressure = 87.8 ± 0.9 mm Hg, aortic pulse pressure = 36.7 ± 2.6 mm Hg) from the primed left ventricle heart perfusion represents close match with the in vivo physiologic data. The volume in the left ventricle remains constant throughout the primed left ventricle heart perfusion, which allows us to perform isovolumetric left ventricular pressure measurement in ex vivo heart perfusion (EVHP). Left ventricular contractility measurements (maximum and minimum rates of left ventricular pressure change) were derived for cardiac assessment. In summary, the proposed primed left ventricle heart perfusion method is able to create physiologic AoP and enables left ventricular functional assessment in EVHP in porcine hearts.

Aquatic exercise is an attractive form of exercise that utilizes the various properties of water to improve physical health, including arterial stiffness. However, it is unclear whether regular head-out aquatic exercise affects aortic hemodynamics, the emerging risk factors for future cardiovascular disease. The purpose of this study was to investigate whether head-out aquatic exercise training improves aortic hemodynamics in middle-aged and elderly people. In addition, to shed light on the underlying mechanisms, we determined the contribution of change in arterial stiffness to the hypothesized changes in aortic hemodynamics. Twenty-three middle-aged and elderly subjects (62 ± 9 years) underwent a weekly aquatic exercise course for 15 weeks. Aortic hemodynamics were evaluated by pulse wave analysis via the general transfer function method. Using a polar coordinate description, companion metrics of aortic pulse pressure (PPC = √{(systolic blood pressure)2 + (diastolic blood pressure)2}) and augmentation index (AIxC = √{(augmentation pressure)2 + (pulse pressure)2}) were calculated as measures of arterial load. Brachial-ankle (baPWV, reflecting stiffness of the abdominal aorta and leg artery) and heart-ankle (haPWV, reflecting stiffness of the whole aortic and leg artery) pulse wave velocities were also measured. The rate of participation in the aquatic training program was 83.5 ± 13.0%. Aortic systolic blood pressure, pulse pressure, PPC, AIxC, baPWV, and haPWV decreased after the training (P < 0.05 for all), whereas augmentation index remained unchanged. Changes in aortic SBP were correlated with changes in haPWV (r = 0.613, P = 0.002) but not baPWV (r = 0.296, P = 0.170). These findings suggest that head-out aquatic exercise training may improve aortic hemodynamics in middle-aged and elderly people, with the particular benefits for reducing aortic SBP which is associated with proximal aortic stiffness.

Background The enlargement of aortic aneurysm can alters pulse wave propagation and reflection, which may influence to left ventricular (LV) afterload changes. The relevance of pulse wave velocity (PWV) and central blood pressure depending on the locus of the aneurysm for LV structure and diastolic function (DF) are not clearly unknown. Purpose Assess the relationship between central pulse pressure (CPP), PWV and LV structure and DF in patients with ascending aortic aneurysm (AA) and abdominal aortic aneurysm (AAA). Methods 121 patients (95 male, 63±12 years) with aortic aneurysms and preserved LV systolic function were enrolled before aortic repair. 51 patients (37 male, 54±13 years) had AA and 70 patients (58 male, 69±7 years) had AAA. CPP and PWV were measured using applanation tonometry. A echocardiographic exam was performed with a Vivid 7 GE (USA). LV mass index (LVMI) and relative wall thickness (RWT) were calculated according to standard formulas. LV filling pressure (E/Em) was estimated by Doppler-derived ratio of mitral inflow velocity (E) to septal (Em) by tissue Doppler. Transmitral flow patterns (E/A ratio of E to late (A) ventricular filling velocities) were measured with the pulsed doppler method. Results Concentric LV hypertrophy (LVH) was observed in 51 (42%), eccentric LVH – in 35 (29%) patients. CPP was positively related with LVMI (r=0.362, P=0.001), but PWV was inversely associated with LVMI (r=−0.244, P=0.029). CPP was not associated with RWT (P≥0.5), whereas PWV was positively related (r=0.223, P=0.004). PWV decreased with increasing aortic diameter in AA and AAA (r=−0.360, P=0.029 and r=−0.315, P=0.019, respectively). 12 (23%) patients with AA and 36 (56%) patients with AAA had grade I diastolic dysfunction, 20 (40%) patients with AA and 12 (18%) patients with AAA had grade II diastolic dysfunction (P Conclusions In patients with aortic aneurysm CPP and PWV were conjointly but differently related to LV structure. Eccentric LV hypertrophy was accompanied by a significant decrease of PWV. Reduced PWV and decreased CPP exhibited association with more severe LV diastolic dysfunction, possibly due to the apparent effect of increased aortic aneurysm diameter. LV DF was severely reduced in the patients with AA compared by patients with AAA. Funding Acknowledgement Type of funding sources: Public hospital(s). Main funding source(s): Almazov National Medical Research Centre

Introduction: Intracerebral hemorrhage (ICH) is the second most common subtype of stroke. Hypertension is a major cause of primary spontaneous ICH. However, sex difference in blood pressure (BP) and arterial stiffness among ICH patients is not well characterized. Methods: A prospective pilot study to investigate the feasibility of measuring arterial stiffness in acute primary ICH patients was approved by the institutional research board at Wake Forest Baptist Health. Eligible subjects with primary ICH were enrolled in the study within 7 days of onset. Non-invasive measurements of brachial BP, aortic BP, augmentation index at heart rate of 75 beats per minute (AIx75), and carotid-femoral pulse wave velocity (cf-PWV) were measured at the patient’s bedside, using the SphygmoCor XCEL System v1 (AtCor Medical Pty Ltd., Sydney, Australia). Results: A total of 20 patients have been enrolled in the study over 5 months. Over half the patients enrolled were female (55%, n = 11), including 82% (n = 9) White, 9% (n = 1) Asian and 9% (n = 1) Hispanic. There was increased diversity in the male patients (45%, n = 9) including 44% (n = 4) Black, 22% (n = 2) White, 22% (n = 2) Hispanic, and 11% (n = 1) Asian. Men were significantly younger than women (57 ± 5 years vs 74 ± 3 years, respectively, P = 0.009). There were no significant differences in BMI or ICH score. At the time of measurement, there were no significant sex differences in brachial or aortic blood pressures (systolic and diastolic), however, females had significantly higher AIx75 (35 ± 4 vs 20 ± 6, P = 0.036) and aortic PP (53 ± 2 mm Hg vs 42 ± 4 mm Hg, P = 0.020) than males. Sex difference in cf-PWV was not statistically significant (p = 0.054). Conclusion: In the current feasibility pilot study, preliminary data show that females had higher arterial stiffness measured as AIx75 and aortic PP than males in the acute setting of ICH. Further study will be required to ascertain whether this is related to higher age at presentation in females. Whether sex differences in arterial stiffness predict differences in the outcome among ICH patients is not well characterized; thus, assessment of 30-day functional and neurological outcomes will be performed with NIHSS and modified Rankin Scores.

OBJECTIVE We evaluated the possible correlation between pulse wave analysis (PWA) parameters measured during the first trimester of pregnancy in normotensive, low-risk women, and the development of hypertensive disorders later in pregnancy. Our hypothesis was that a still asymptomatic increase in arterial stiffness may potentially precede the onset of overt hypertension in pregnancy and that PWA could detect it. METHODS The study population (n = 1648) was recruited at the time of prenatal screening for chromosomal abnormalities (11-12 weeks of gestation). The radial pressure waveform was obtained with an applanation tonometer (Sphygmocor, Atcor Medical, West Ryde, Australia) on pregnant women in recumbent position. Arterial stiffness was evaluated using arterial PWA. The aortic systolic pressure (aSp), aortic diastolic pressure, and aortic mean pressure, the aortic pulse pressure, the augmentation pressure, and the augmentation index were calculated. The main outcome measure was the development of hypertensive disorders later in pregnancy. RESULTS The values of aSp (P

Introduction Structural and functional changes of the vascular wall in women occur already at the very early stages of reproductive aging. An emergence of applanation tonometry made it possible to evaluate arterial stiffness and central hemodynamic parameters non-invasively, which considerably expanded the information that had been provided previously by invasive methods used for studying these parameters during cardiac catheterization. Whereas a few studies have assessed central aortic pressure (CAP) parameters and reflected pulse wave in women at different phases of their reproductive aging, none investigated the daily profile of CAP and reflected pulse wave parameters in women undergoing different stages of the menopause. Background: assessment of the daily variability in CAP and daily profile of amplification and augmentation of pulse blood pressure (PBP) in women at different menopause phases. Methods The study involved 384 climacteric women. The first group included 168 women undergoing perimenopause, the second group comprised of 216 women in their early postmenopausal stage. A 24-h blood pressure (BP) monitoring in the brachial artery and aorta (BPLab® Vasotens® system, Petr Telegin LLC, Russia) was performed via the measurements of the following indicators: systolic blood pressure (SBP), pulse blood pressure (PBP), central aortic systolic pressure (CASP), central aortic pulse pressure (CAPP), aortic augmentation index (AIxao), and pulse pressure amplification (PPA). Results When investigating PPA values in the brachial artery and aorta, we detected smaller amplification and higher aortic augmentation index at night than in daytime, which reflected a disproportionately higher CAP level during night hours. This pattern was more pronounced in postmenopausal women. We calculated the logistic regression equation (adjusted R2 = 0.49, log-likelihood = − 50.3, chi-square (19) = 97.6, p Conclusion Rising CAP, in combination with declining PPA and augmenting reflected pulse wave amplitude, may be associated with an increased risk of cardiovascular complications.

OBJECTIVE: Aortic pulse pressure (PP) represents the hemodynamic cardiac and cerebral burden more directly than cuff PP. The objective of this study was to investigate whether invasively measured aortic PP confers additional prognostic value beyond cuff PP for cardiovascular events and death. With increasing age, cuff PP progressively underestimates aortic PP. Whether the prognostic association between cuff PP and outcomes is age-dependent remains to be elucidated.METHODS: Cuff PP and invasively measured aortic PP were recorded in 21 908 patients (mean age 63 years, 58% men, 14% with diabetes) with stable angina pectoris undergoing elective coronary angiography during January 2001--December 2012. Multivariate Cox models were used to assess the association with incident myocardial infarction, stroke, and death. Discrimination was assessed using Harrell's C-index.RESULTS: During a median follow-up period of 3.7 years (range 0.1-10.8 years), 422 strokes, 511 myocardial infarctions, and 1530 deaths occurred. Both cuff and aortic PP were associated with stroke, myocardial infarction, and death in crude analyses. However, only cuff PP remained associated with stroke (hazard ratio per 10 mmHg, 1.06 (95% confidence interval (CI) 1.01--1.12)] and myocardial infarction [hazard ratio per 10 mmHg 1.05 (95% CI 1.01--1.11)] in multivariate Cox models. Both cuff and aortic PP lost significance as predictors of death in multivariate models. Age did not modify the prognostic association between cuff PP and stroke, myocardial infarction, and death.CONCLUSION: Invasively measured aortic PP did not add prognostic information about cardiovascular outcomes and death beyond cuff PP in patients with stable angina pectoris.

Increasing central blood pressure is an independent predictor of cardiovascular disease and is an acute effect of high-intensity resistance exercise. It has been shown that classical music suppresses increased peripheral pressure during exercise. We hypothesized that classical music would suppress increased central pressure induced by high-intensity resistance exercise. To confirm this hypothesis, we examined the effect of classical music on central pressure following high-intensity resistance exercise in 18 young men. A randomized, single-blinded, sham-controlled, crossover trial was conducted under parallel experimental conditions on four separate days. The order of experiments was randomized between sham control (seated rest), music (20-min classical music track compilation), resistance exercise (5 sets of 10 repetitions at 75% of 1 repetition maximum), and resistance exercise with music conditions. Aortic pressure was measured in all subjects. No significant interaction between time, music, and resistance exercise was observed for aortic systolic pressure and diastolic pressure. In contrast, aortic pulse pressure showed a significant interaction; that is, aortic pulse pressure significantly widened after resistance exercise, whereas music significantly attenuated this widening. No significant change was observed in aortic pulse pressure in sham control and music conditions. The present findings suggest that music attenuates resistance exercise-induced increase in central pressure.

Dynamic arterial elastance (Eadyn), the ratio between arterial pulse pressure and stroke volume changes during respiration, has been postulated as an index of the coupling between the left ventricle (LV) and the arterial system. We aimed to confirm this hypothesis using the gold-standard for defining LV contractility, afterload, and evaluating ventricular-arterial (VA) coupling and LV efficiency during different loading and contractile experimental conditions. Twelve Yorkshire healthy female pigs submitted to three consecutive stages with two opposite interventions each: changes in afterload (phenylephrine/nitroprusside), preload (bleeding/fluid bolus), and contractility (esmolol/dobutamine). LV pressure-volume data was obtained with a conductance catheter, and arterial pressures were measured via a fluid-filled catheter in the proximal aorta and the radial artery. End-systolic elastance (Ees), a load-independent index of myocardial contractility, was calculated during an inferior vena cava occlusion. Effective arterial elastance (Ea, an index of LV afterload) was calculated as LV end-systolic pressure/stroke volume. VA coupling was defined as the ratio Ea/Ees. LV efficiency (LVeff) was defined as the ratio between stroke work and the LV pressure-volume area. Eadyn was calculated as the ratio between the aortic pulse pressure variation (PPV) and conductance-derived stroke volume variation (SVV). A linear mixed model was used for evaluating the relationship between Ees, Ea, VA coupling, LVeff with Eadyn. Eadyn was inversely related to VA coupling and directly to LVeff. The higher the Eadyn, the higher the LVeff and the lower the VA coupling. Thus, Eadyn, an easily measured parameter at the bedside, may be of clinical relevance for hemodynamic assessment of the unstable patient.

Background and aims: Increased arterial stiffness contributes to diabetic vascular complications. We identified dietary factors related to arterial stiffness in individuals with type 1 diabetes, a population with high risk of cardiovascular disease. Methods and results: Altogether, 612 participants (40% men, mean +/- standard deviation age 45 +/- 13 years) completed a validated diet questionnaire and underwent measurements of arterial stiffness. Of these, 470 additionally completed a food record. Exploratory factor analysis was applied to identify dietary patterns from the diet questionnaires, and nutrient intakes were calculated from food record entries. Arterial stiffness was measured by applanation tonometry. Of the seven dietary factors formed, the factor scores of "Full-fat cheese and eggs" and "Sweet" patterns were negatively associated with measures of arterial stiffness. In the multivariable macronutrient substitution models, favouring carbohydrates over fats was associated with higher aortic mean arterial pressure and aortic pulse wave velocity. When carbohydrates were consumed in place of proteins, higher aortic pulse pressure, aortic mean arterial pressure, and augmentation index were recorded. Replacing energy from alcohol with proteins, was associated with lower aortic pulse pressure, aortic mean arterial pressure, and augmentation index. Relative distributions of dietary fatty acids were neutral with respect to the measures of arterial stiffness. Conclusion: The macronutrient distribution of the diet is likely to affect the resilience of the arteries. Our observations suggest that reducing energy intake from carbohydrates and alcohol may be beneficial. These observations, especially those dealing with dietary patterns, need to be confirmed in a longitudinal study. (C) 2018 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.

Objectives Central systolic blood pressure (CSBP) is the pressure in the root of aorta, which directly influences organs such as brain, heart and kidneys and is related to organ damage. Its value increases with the aortic stiffness. The aim of this study was to analyze the relationships of CSBP to aortic stiffness parameters. Methods Central blood pressure (BP) and related parameters were measured by Arteriograph, working based on oscillometric principle, using pulse wave analysis (PWA) approach. We examined 123 patients (69 females, 54 males) with a primary hypertension. Results Using a linear correlation analysis, we found that CSBP was correlated to aortic pulse wave velocity (PWV), aortic and brachial pulse pressure (PP), aortic augmentation index, return time of reflected pressure wave (RT) and aortic and brachial augmentation indexes. Multivariate analysis defines the aortic pulse pressure (PPao) as the most powerful parameter influencing CSBP. By an individual analysis of BP in each patient separately, we defined two different types of central hemodynamics; those with a higher CSBP than brachial SBP occur in stiffer aorta. Conclusion The CSBP increases with aortic PP, the most powerful stiffness parameter of aorta. Higher CSBP than brachial SBP usually accompanies a stiffer aorta (Tab. 5, Ref. 19).

We recently read the article, “Acute Effects of Exercise Mode on Arterial Stiffness and Wave Reflection in Healthy Young Adults: A Systematic Review and Meta-Analysis” by Doris R. Pierce, Kenji Doma and Anthony S. Leicht (volume 13, 2018). This particular article was a review and meta-analysis that focused on changes in arterial stiffness and measures of pulse wave reflection in response to different exercise modalities. The aim of this commentary is to highlight, and to make note, on some of the data that was presented in their manuscript. Increases in measures of pulse wave reflection, primarily the augmentation index (AIx), and the AIx at normalized to 75 beats per minute (AIx@75), are associated with increased cardiovascular mortality and morbidity (Weber et al., 2004). The AIx is defined as augmentation pressure expressed as a percentage of aortic pulse pressure. It is influenced by the timing and the amplitude of the forward traveling wave and the reflected wave (Wilkinson et al., 2000). Following resistance exercise there appears to be a significant impact on measures of pulse wave reflection (Fahs et al., 2009; Yoon et al., 2010; Kingsley et al., 2017; Tai et al., 2018). This is further supported by the meta-analysis of Pierce et al. (2018).

BACKGROUND Aortic knob width (AKW), which can be measured easily in simple radiography, is associated with the degree of dilatation and tortuosity of the aortic arch. Pulsatile stress influences aortic geometry. This study was carried out to investigate whether AKW can represent invasively measured aortic pulse pressure (APP). METHODS A total of 252 patients who underwent invasive coronary angiography (ICA) for the evaluation of coronary artery disease were enrolled. AKW was defined as the perpendicular length from the lateral margin of the main bronchus to the most prominent edge of the aortic knob on chest radiography. APP was measured at the ascending aorta using a pigtail catheter immediately before ICA. RESULTS When patients were divided into two groups according to the median value of APP (69 mmHg), AKW was significantly greater in patients with higher APP (≥69 mmHg) than in those with lower APP (

Background:Arterial stiffness is a strong predictor of mortality in hemodialysis patients. In this study, we aimed to investigate possible relations of arterial stiffness with volume status determined by bioimpedance analysis and aortic blood pressure parameters. Also, effects of a single hemodialysis session on these parameters were studied.Methods:A total of 75 hemodialysis patients (M/F: 43/32; mean age: 53 ± 17) were enrolled. Carotid-femoral pulse wave velocity, augmentation index, and aortic pulse pressure were measured by applanation tonometry before and after hemodialysis. Extracellular fluid and total body fluid volumes were determined by bioimpedance analysis.Results:Carotid-femoral pulse wave velocity (9.30 ± 3.30 vs 7.59 ± 2.66 m/s, p 2 = 0.15, p = 0.01), total cholesterol (r2 = 0.06, p = 0.02), peripheral mean blood pressure (r2 = 0.10, p = 0.005), aortic-mean blood pressure (r2 = 0.06, p = 0.02), aortic pulse pressure (r2 = 0.14, p = 0.001), and extracellular fluid/total body fluid (r2 = 0.30, p 2 = 0.06, p = 0,02), aortic-mean blood pressure (r2 = 0.16, p 2 = 0.22, p 2 = 0.06, p = 0.02) and inversely correlated with baseline carotid-femoral pulse wave velocity (r2 = 0.29, p 2 = 0.09, p = 0.009) and Δaortic pulse pressure (r2 = 0.06, p = 0.03) and inversely associated with baseline augmentation index (r2 = 0.14, p = 0.001). In multiple linear regression analysis (adjusted R2 = 0.46, p Conclusion:Carotid-femoral pulse wave velocity, augmentation index, and aortic pulse pressure significantly decreased after hemodialysis. Arterial stiffness was associated with both peripheral and aortic blood pressure. Furthermore, reduction in arterial stiffness parameters was related to reduction in aortic blood pressure. Pre-dialysis carotid-femoral pulse wave velocity was associated with volume status determined by bioimpedance analysis. Volume control may improve not only the aortic blood pressure measurements but also arterial stiffness in hemodialysis patients.

The aim is to study pulse wave velocity (PWV) and other parameters of arterial stiffness in patients with comorbid arterial hypertension (AH) and chronic obstructive pulmonary disease (COPD). Materials and methods. 32 patients with a combination of AH and COPD (group 1), 30 patients with isolated hypertension (group 2), 18 patients with isolated COPD (group 3), 30 healthy subjects (control group) were examined. Applanation tonometry and pulse wave contour analysis at the carotid-femoral segment were made by SphygmoCor (AtCor Medical). Results. Aortic systolic blood pressure in patients with the combination of hypertension and COPD was higher compared to the group of the patients with isolated hypertension by 9.83% (p=0.02), and the patients with COPD by 41.5% (p = 0.000042), respectively. Central pulse pressure in the first group was higher compared to the second group by 29.58% (p=0.00022), in the third group - by 53.4% (p=0.0029). The combination of hypertension and COPD (β=0.42, p=0.00019), age (β=0.39, p=0.0002) and the level of aortic pulse pressure (β=0.54, p=0.001) were marked as independent factors of PWV increasing according to the multiple regression analysis. Conclusion. In patients with a combination of hypertension and COPD the increase in PWV, systolic and pulse pressure in the ascending aorta was observed, compared to patients with isolated hypertension, isolated COPD and the control group during applanation tonometry.

Asymmetric dimethylarginine (ADMA) is a robust marker of endothelial dysfunction in patients with essential hypertension. We investigated ADMA levels and their association with vascular damage in untreated hypertension. We enrolled consecutive patients with untreated, recently diagnosed hypertension and age‐matched normotensive individuals. 24‐hour blood pressure, central hemodynamics, and arterial stiffness were recorded. A total of 311 individuals were studied: 165 with essential hypertension, 50 with masked hypertension, 25 with white‐coat hypertension, and 71 normotensive individuals. ADMA levels significantly correlated with aortic augmentation index (AIx75) (r = .156, P = .006), aortic pulse pressure (r = .153, P = .007) and marginally with carotid‐femoral pulse wave velocity (r = .110, P = .051), as well as with diastolic office BP. In the multivariate model, aortic AIx75 and age were the only statistically significant predictors of ADMA. This is the largest study to document an independent association between ADMA and aortic AIx75 but not with other indices of arterial stiffness.

The aim was to study the dynamics of renal function in relation to the fibrosis activity and the arterial stiffness in young and middle-aged patients with atrial fibrillation (AF). Materials and methods. 50 young and middle-aged men with AF were examined. The average age was 53.0 (48.0-58.0). The serum levels of creatinine and cystatin C (Cys C) were determined and the glomerular filtration rate (eGFR) was calculated initially and after 12 months. The activity of systemic fibrosis was assessed by serum metalloproteinase-2 (MMP-2) and transforming growth factor-s1 (TGF-s1) determining. To assess systemic vascular stiffness central aortic pressure and pulse wave velocity (PWV) were measured. Results. Renal impairment defined as eGFR decrease by more than 10 ml/min/1.73 m 2 or to the level below than 60 ml/min/1.73 m 2 throughout the year was registered in 10 (20.0 %) patients. The concentration of MMP-2 and TGF-s1 was higher in the subgroup with the eGFR decline compared to the patients without renal function impairment (21.1 (17.4-25.9) and 16.5 (13.0-19.2) ng/ml (p = 0.038); 3.01 (0.09-17.4), and 0.08 (0-1.3) ng/ml (p = 0.041). Central aortic pulse pressure was also higher in the patients with eGFR decline (45.5 (42.0-49.0) and 38.0 (31.0-41.0) mmHg; p = 0.036). The PWV levels did not differ in the subgroups. Conclusion. The renal function impairment throughout a follow-up period of 12 months was registered in 20.0 % of young and middle-aged patients with AF. This subgroup of AF patients was characterized by increased activity of systemic fibrosis and vascular stiffness in terms of matrix metalloproteinase-2, transforming growth factor-s1 and central aortic pulse pressure levels.

Although brachial-ankle pulse wave velocity (baPWV) has been widely used as an index of arterial stiffness, no consensus exists about whether baPWV can reflect central aortic stiffness. The authors investigated the association between baPWV and invasively measured aortic pulse pressure (APP) in a total of 109 consecutive patients (mean age, 62.3 ± 11.3 years; 67.9% men). Most patients (91%) had obstructive coronary artery disease, and mean baPWV and APP values were 1535 ± 303 cm/s and 66.8 ± 22.5 mm Hg, respectively. In univariate analysis, there was a significant linear correlation between baPWV and APP (r = .635, P < .001). The correlation between baPWV and APP remained significant even after controlling for potential confounders (β = 0.574, P < .001; R2 = .469). Arterial stiffness measured by baPWV showed a strong positive correlation with invasively measured APP, independent of clinical confounders. Therefore, baPWV can be a good marker of central aortic stiffness.

BACKGROUND Pulsatile hemodynamics are associated with left ventricular filling pressures and diastolic dysfunction. We investigated their relationship with maximum workload and peak oxygen uptake (peak VO2) in patients with exertional dyspnea and preserved left ventricular ejection fraction (LVEF). METHODS Radial waveforms from tonometry were processed with a transfer function, pulse wave analysis and wave separation analysis, yielding central aortic pressures and measures of forward (amplitude of forward wave-Pf) and reflected waves (augmentation index-AIx, augmentation pressure-AP, amplitude of backward wave-Pb) and their ratio (reflection magnitude). Aortic pulse wave velocity (aoPWV) was estimated with a validated formula from single-point waveforms. Ergospirometry for assessment of exercise capacity was performed on a bicycle ergometer, using a ramp protocol. RESULTS Sixty-six patients were included (43 females; mean age 66 years; 83% hypertensives; mean body mass index 28.3 kg/m2). Mean peak VO2 was 17.0 ml/min/kg, mean achieved maximum workload 104.5 watts (80.9% of a reference population). Maximum workload and peak VO2 showed significant inverse relationships with AIx, AP, Pb, and aoPWV (r = −0.26 to −0.57). In multiple adjusted regression models, brachial and aortic pulse pressure, AP, Pf, Pb, and aoPWV were significant independent predictors of maximum workload, whereas AP, AIx75, Pf, Pb, and aoPWV were independently related to peak VO2. CONCLUSIONS Pulsatile hemodynamics are independently associated with objective measures of exercise capacity in patients with normal LVEF.

This study aims to examine the changes in arterial stiffness immediately following sub-maximal exercise in people with metabolic syndrome.Ninety-four adult participants (19-80 years) with metabolic syndrome gave written consent and were measured for arterial stiffness using a SphygmoCor (SCOR-PVx, Version 8.0, Atcor Medical Private Ltd, USA) immediately before and within 5-10min after an incremental shuttle walk test. The arterial stiffness measures used were pulse wave velocity (PWV), aortic pulse pressure (PP), augmentation pressure, augmentation index (AI), subendocardial viability ratio (SEVR) and ejection duration (ED).There was a significant increase (p0.05) in most of the arterial stiffness variables following exercise. Exercise capacity had a strong inverse correlation with arterial stiffness and age (p0.01).Age influences arterial stiffness. Exercise capacity is inversely related to arterial stiffness and age in people with metabolic syndrome. Exercise induced changes in arterial stiffness measured using pulse wave analysis is an important tool that provides further evidence in studying cardiovascular risk in metabolic syndrome.

Purpose: Multiple studies have shown pulse pressure (PP) to be a strong predictor of aortic calcification. However, no studies are available that correlate PP with aortic calcification at the segmental level. Methods: We identified 37 patients with aortic PP measured during cardiac catheterization. Their noncontrast chest computed tomography scans were evaluated for the presence of calcium in different segments (ascending aorta, arch of aorta [arch], descending aorta) and quantified. Patients with calcification (Calcified Group A) were compared against patients without calcification (Noncalcified Group B) in terms of PP, calcification and compliance. Results: The mean of the total calcium score was higher in the descending aorta than the arch or ascending aorta (691 vs 571 vs 131, respectively, P < 0.0001). PP had the strongest correlation with calcification in the descending aorta (r = 0.47, P = 0.004). Calcified Group A had a much higher PP than Noncalcified Group B, with the greatest difference in the descending aorta (20 mmHg, P < 0.0001), lesser in the ascending aorta (10 mmHg, P = 0.12) and the least in the arch (5 mmHg, P = 0.38). Calcified Group A patients also had much lower compliance than Noncalcified Group B patients, with the greatest difference among groups seen in the descending aorta (0.7 mL/mmHg, P = 0.002), followed by the ascending aorta, then arch. Conclusions: These are the first data to evaluate the relative impact of aortic segments in PP. Finding the greatest amount of calcification along with greatest change in PP and compliance in the descending aorta makes a case that the descending aorta plays a major role in PP as compared to other segments of the thoracic aorta.

High central aortic pulse pressure (CPP) and thrombin-induced platelet-fibrin clot strength (TIP-FCS) have been associated with ischemic outcomes in patients with coronary artery disease in separate studies. But, the ischemic risk associated with these factors has never been analyzed in a single study and their interrelation is unknown. The primary aim of the study was to establish cut points for CPP and TIP-FCS measured at the time of catheterization associated with long term major adverse cardiovascular events. We enrolled 334 consecutive patients undergoing cardiac catheterization and assessed thrombogenicity by thrombelastography. Patients were followed up to 3 years. The primary endpoint was a composite of cardiovascular death, myocardial infarction, and ischemic stroke and the secondary endpoint was occurrence of the primary endpoint or recurrent ischemic events requiring hospitalization. Patients with primary and secondary endpoint occurrence had higher CPP (83 ± 20 vs. 60 ± 18 mmHg, p 0.0001; 70 ± 21 vs. 59 ± 18 mmHg, p 0.0001, respectively) and TIP-FCS (68.5 ± 5.8 vs. 65.5 ± 5.0 mm, p = 0.008; 67.4 ± 5.9 vs. 65.2 ± 4.8 mm, p = 0.001, respectively). CPP60 mmHg and TIP-FCS69 mm were both independent predictors of primary endpoint occurrence (p = 0.0001 and p = 0.02, respectively). ROC analysis for CPP and TIP-FCS showed a C-statistic of 0.81 (p 0.0001) and 0.68 (p = 0.007) for the primary endpoint, respectively. Patients with CPP60 mmHg had higher TIP-FCS (66.8 ± 5.1 vs. 64.8 ± 5.0 mm, p 0.001) and primary and secondary endpoint occurrence (13 vs. 1.1%, p 0.0001 and 31.8 vs. 14.4%, p = 0.0002, respectively). CPP60 mmHg + TIP-FCS 69 mm was associated with a markedly increased risk of primary endpoint occurrence [HR (95% CI) 5.4(2.3-12.5), p = 0.0001]. High CPP and thrombogenicity are interrelated; each are independently associated with increased cardiovascular risk; and simultaneous presence markedly enhances risk. The mechanistic link between CPP and thrombogenicity deserves further study.

Introduction:A peripheral pulse pressure (PP) is larger than a central PP (PP amplification). The phenomenon has been examined in adult, but not in children.Methods:Fifty-four patients with a normal aorta were enrolled. The ascending and descending aorta pressure waveforms were recorded by a pressur

Effective treatment of systolic hypertension in elderly patients remains a major therapeutic challenge. A multicenter, double-blind, randomized controlled trial with sacubitril/valsartan (LCZ696), a first-in-class angiotensin receptor neprilysin inhibitor, was conducted to determine its effects versus olmesartan (angiotensin receptor blocker) on central aortic pressures, in elderly patients (aged ≥60 years) with systolic hypertension and pulse pressure >60 mm Hg, indicative of arterial stiffness. Patients (n=454; mean age, 67.7 years; mean seated systolic blood pressure, 158.6 mm Hg; mean seated pulse pressure, 69.7 mm Hg) were randomized to receive once-daily sacubitril/valsartan 200 mg or olmesartan 20 mg, force titrated to double the initial doses after 4 weeks, before primary assessment at 12 weeks. The study extended double-blind treatment for 12 to 52 weeks, during which amlodipine (2.5–5 mg) and subsequently hydrochlorothiazide (6.25–25 mg) were added-on for patients not achieving blood pressure target (P =0.010), further corroborated by secondary assessments at week 12 (central aortic pulse pressure, −2.4 mm Hg, P P P P

Central (aortic) blood pressure, arterial stiffness, and sympathetic nerve activity increase with age in women. However, it is unknown if the age-related increase in sympathetic activity influences aortic hemodynamics and carotid-femoral pulse wave velocity (cfPWV), an index of central aortic stiffness. The goal of this study was to determine if aortic hemodynamics and cfPWV are directly influenced by sympathetic nerve activity by measuring aortic hemodynamics, cfPWV, and muscle sympathetic nerve activity (MSNA) in women before and during autonomic ganglionic blockade with trimethaphan camsylate. We studied 12 young premenopausal (23 ± 4 yr) and 12 older postmenopausal (57 ± 3 yr) women. These women did not differ in body mass index or mean arterial pressure ( P > 0.05 for both). At baseline, postmenopausal women had higher aortic pulse pressure, augmented pressure, augmentation index adjusted for a heart rate of 75 beats/min, wasted left ventricular pressure energy, and cfPWV than young women ( P < 0.05). During ganglionic blockade, postmenopausal women had a greater decrease in these variables in comparison to young women ( P < 0.05). Additionally, baseline MSNA was negatively correlated with the reductions in aortic pulse pressure, augmented pressure, and wasted left ventricular pressure energy during ganglionic blockade in postmenopausal women ( P < 0.05) but not young women. Baseline MSNA was not correlated with the changes in augmentation index adjusted for a heart rate of 75 beats/min or cfPWV in either group ( P > 0.05 for all). Our results suggest that some aortic hemodynamic parameters are influenced by sympathetic activity to a greater extent in older postmenopausal women than in young premenopausal women.NEW & NOTEWORTHY Autonomic ganglionic blockade results in significant decreases in multiple aortic pulse wave characteristics (e.g., augmented pressure) and central pulse wave velocity in older postmenopausal women but not in young premenopausal women. Certain aortic pulse wave parameters are negatively influenced by sympathetic activity to a greater extent in older postmenopausal women.

AIM To determine the degree to which an extended time to the peak of the aortic forward wave or early wave reflection time enhance associations between aortic backward wave pressure and hence central aortic pulse pressure (PPc) and left ventricular mass index (LVMI). METHODS In 701 adult participants from a community sample either receiving no antihypertensive therapy or receiving low-dose thiazide diuretic monotherapy for at least a year (the major therapy employed), we assessed aortic haemodynamics (SphygmoCor software and wave separation analysis; AtCor Medical, West Ryder, New South Wales, Australia) and LVMI (echocardiography). RESULTS An interaction between time to the peak of the aortic forward wave and aortic backward wave pressure was independently associated with aortic augmented pressure (P

Objective. To elucidate the association between polymorphic markers of the genes of C-reactive protein (CRP), interleukin 10 (IL10), interleukin 6 (IL6), lymphotoxin alpha (LTA) and tumor necrosis factor (TNFA) and changes of arterial stiffness in hypertensive patients. Design and methods. The study included 130 patients with hypertension (HTN) (64 (49,3%) men and 66 (50,7%) women), average age 63,7 ± 12,87 years. The intima-media thickness was measured by the method proposed by P. Pignolli. The arterial stiffness was assessed by the carotidfemoral and carotid-radial pulse wave velocity (PWV). Central aortic pulse pressure (PP) was calculated using pulse contour analysis. Results. An association of polymorphic markers of A (-3872)G, G (-2667)C, A (-5237) G CRP gene, G (-1082)A gene IL10, C (-174)G gene IL6, and A (-308)G gene TNFA with pulse wave velocity, PP in the aorta, the presence of atherosclerotic plaques of carotid arteries was found. Among patients with aortic PP > 50 mmHg the frequency of AA genotype carriers of polymorphic marker C804A LTA gene was higher (p = 0,037). Carriers AA genotype had a significantly greater carotid-femoral PWV as compared with native CC genotype (13,4 and 11,9 m/s, p = 0,042) and higher PP in the aorta. Also, higher PP and aortic PWV were found in carriers of GG genotype of A (252)G LTA gene. Among patients with the presence of atherosclerotic plaques of carotid arteries the frequency of AA genotype of the G (-3014)A CRP gene was higher (p = 0,031). Conclusion. Thus, we have shown that CRP gene polymorphism is associated with the development of carotid atherosclerosis and increased central PP, while lymphotoxin alpha gene polymorphism is associated with the increase in arterial stiffness in high risk hypertensive patients. Our data confirm the involvement of pro-inflammatory cytokines in the development of atherosclerosis and endothelial dysfunction.

Objective Data on ventricular-arterial coupling using invasive hemodynamic studies are limited. This study was performed to clarify the interaction between aortic pressures and left ventricular end-diastolic pressure (LVEDP) using invasive catheterization. Patients and methods A total of 104 consecutive stable patients (mean age, 65.8 ± 10.0 years; 56% men) undergoing invasive coronary angiography (ICA) were prospectively evaluated. LVEDP and central aortic pressures [systolic blood pressure (aSBP) and diastolic blood pressure (aDBP)] were sequentially measured using a pigtail catheter before ICA. Aortic pulse pressure (aPP) was defined by the difference between aSBP and aDBP. Results A total of 82 patients (79%) had obstructive coronary artery disease (≥50% stenosis). The mean LVEDP value was 18.7 ± 6.4 mmHg. Univariable analyses showed that aSBP (r = 0.309, P = 0.001) and aPP (r = 0.286, P = 0.003) significantly correlated with LVEDP, whereas aDBP was not correlated with LVEDP (P > 0.05). Multivariable analysis revealed that aSBP (β = 0.345, P = 0.001) and aPP (β = 0.276, P = 0.018) remained independent predictors of LVEDP even after controlling for potential confounders. Conclusion Invasively measured aSBP and aPP were independently associated with invasively measured LVEDP in patients undergoing ICA. This result provides additional evidence of a close interaction between central aortic pressure and LV diastolic function in this population.

Underlying pathophysiology of orthostatic hypotension has been poorly understood. We hypothesized that aortic pulse pressure (APP) reflecting aortic stiffness may be involved in the development of orthostatic hypotension.A total of 200 patients (age 64.3 ± 10.9 years, 62.5% men) who underwent invasive coronary angiography (ICA) were prospectively recruited. Orthostatic hypotension was defined as SBP drop at least 20 mmHg or DBP drop at least 10 mmHg within 3 min of the standing position compared with the supine position. Hemodynamic parameters were measured at the ascending aorta using a pig-tail catheter immediately before ICA. APP was calculated as a difference between the aortic peak systolic pressure and the end-diastolic pressure.A total of 156 patients (78.0%) had obstructive coronary artery disease on ICA. Orthostatic hypotension was present in 58 patients (29.0%). Diabetes mellitus was more prevalent in patients with orthostatic hypotension than those without (48.3% vs. 23.2%; P 0.001). Other clinical parameters including age, cardiovascular risk factors, laboratory findings and concomitant medications were not different between patients with and without orthostatic hypotension (P 0.05 for each). In hemodynamic parameters, APP was higher in patients with orthostatic hypotension than those without (78.4 ± 25.8 vs. 68.3 ± 21.3 mmHg; P = 0.005). Higher APP was significantly associated with the presence of orthostatic hypotension even after controlling for potential confounders (odds ratio, 2.99; 95% confidence interval 1.15-7.78; P = 0.025).In patients undergoing ICA, APP was associated with increased risk of orthostatic hypotension. Central aortic stiffness may play a role in the development of orthostatic hypotension.

Objective: Coronary slow flow (CSF) phenomenon is characterized by delayed opacification of coronary vessels in a normal coronary angiogram. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully understood yet. Aortic elastic properties have a predictive value in detecting early stages of atherosclerosis. In this study, we aimed to the evaluate the elastic properties of ascending aorta in patients with CSF. Materials and Methods: This single-center study enrolled 50 angiographically identified patients with CSF (23 female, mean age: 51.6 ± 9.7 years), along with 50 controls (19 female, mean age: 53.5 ± 8.7 years) with normal coronary flow. The quantitative measurement of coronary blood flow was performed using the thrombolysis in myocardial infarction frame count method. Aortic elastic parameters including aortic strain, aortic distensibility, aortic stiffness index and aortic compliance were calculated using M-mode echocardiography derived aortic diameters using accepted formulae. Results: There was no significant difference in terms of clinical, demographic, echocardiographic and laboratory parameters between the patients with CSF and the controls. The hemodynamic parameters including aortic pulse pressure, aortic mean pressure, aortic fractional pulse pressure and aortic pulsatility index were similar between patients with CSF and controls. Systolic and diastolic aortic diameters and pulsatile aortic diameter change were similar between the groups. There was also no significant difference in terms of aortic strain, aortic distensibility, aortic stiffness index and aortic compliance between the groups. Conclusion: The results demonstrated that there was no significant difference in terms of hemodynamic parameters and elastic properties of ascending aorta between CSF patients and control group with a similar risk profile and demographic characteristics. Further large scale studies are required to determine the relationship between CSF and elastic properties of aorta.

Background Peripheral mean arterial pressure (MAP) responses to muscle metaboreflex activation using postexercise muscle ischemia (PEMI) in type 2 diabetes patients (T2D) are contradictory. Given that aortic pulse pressure (PP) and wave reflections are better indicators of cardiac load than peripheral MAP, we evaluated aortic blood pressure (BP) and wave amplitude during PEMI. METHODS Aortic BP and pressure wave amplitudes were measured at rest and during PEMI following isometric handgrip at 30% maximum voluntary contraction (MVC) in 16 T2D and 15 controls. Resting aortic stiffness (carotid-femoral pulse wave velocity, cfPWV) and fasting blood glucose (FBG) were measured. RESULTS Increases in aortic MAP (Δ26 ± 2 mmHg vs. Δ17 ± 2 mmHg), PP (Δ15 ± 2 mmHg vs. Δ10 ± 1 mmHg), augmentation index (AIx) (Δ8.2 ± 1.0% vs. Δ4.5 ± 1.3%), augmented pressure (AP) (Δ11 ± 1 mmHg vs. Δ5 ± 1 mmHg), forward (Pf) (Δ9 ± 1 mmHg vs. Δ5 ± 1 mmHg), and backward pressure waves (Pb) (Δ10 ± 1 mmHg vs. Δ5 ± 1 mmHg) responses to PEMI were greater in T2D than controls (P < 0.05). Aortic PP, but not MAP, response to PEMI was correlated to Pf (r = 0.63, P < 0.001) and Pb (r = 0.82, P < 0.001) responses and cfPWV (r = 0.37, P < 0.05). CONCLUSIONS Aortic BP and pressure wave responses to muscle metaboreflex activation are exaggerated in T2D. Aortic PP during PEMI was related to increased wave reflection, forward wave amplitude, and aortic stiffness in T2D patients.

Background: Maternal obesity is associated with adverse cardiometabolic outcome in the offspring. We aimed to assess whether prenatal exposure to metformin can improve the cardiovascular profile and body composition in the offspring of obese mothers. Methods: In 151 children from the MOP trial we measured body composition, peripheral blood pressure and arterial pulse wave velocity. Central haemodynamics (central blood pressure and augmentation index) were estimated using the Vicorder device. Left ventricular cardiac function and structure were assessed by echocardiography. In 39 children from each group the metabolic profile was assessed. Findings: Children were 3.9±1.0 years of age and 77 were exposed to metformin prenatally. There was no significant difference in peripheral blood pressure, arterial stiffness and body composition apart from gluteal and tricep circumferences which were lower in the metformin group (p

Quantifying local aortic stiffness properties in vivo is acknowledged as essential to assess the severity of an ascending thoracic aortic aneurysm (ATAA). Recently, the LESI (local extensional stiffness identification) methodology has been established to quantify non-invasively local stiffness properties of ATAAs using electrocardiographic-gated computed tomography (ECG-gated CT) scans. The aim of the current study was to determine the most sensitive markers of local ATAA stiffness estimation with the hypothesis that direct measures of local ATAA stiffness could better detect the high-risk patients. A cohort of 30 patients (12 BAV and 18 TAV) referred for aortic size evaluation by ECG-gated CT were recruited. For each patient, the extensional stiffness Q was evaluated by the LESI methodology whilst computational flow analyses were also performed to derive hemodynamics markers such as the wall shear stress (WSS). A strong positive correlation was found between the extensional stiffness and the aortic pulse pressure (R = 0.644 and p < 0.001). Interestingly, a significant positive correlation was also found between the extensional stiffness and patients age for BAV ATAAs (R = 0.619 and p = 0.032), but not for TAV ATAAs (R = −0.117 and p = 0.645). No significant correlation was found between the extensional stiffness and WSS evaluated locally. There was no significant difference either in the extensional stiffness between BAV ATAAs and TAV ATAAs (Q = 3.6 ± 2.5 MPa.mm for BAV ATAAs vs Q = 5.3 ± 3.1 MPa.mm for TAV ATAAs, p = 0.094). Future work will focus on relating the extensional stiffness to the patient-specific rupture risk of ATAAs on larger cohorts to confirm the promising interest of the LESI methodology.

Aortic pulse pressure arises from the interaction of the heart, the systemic arterial system, and peripheral microcirculations. The complex interaction between hemodynamics and arterial remodeling precludes the ability to experimentally ascribe changes in aortic pulse pressure to particular adaptive responses. Therefore, the purpose of the present work was to use a human systemic arterial system model to test the hypothesis that pulse pressure homeostasis can emerge from physiological adaptation of systemic arteries to local mechanical stresses. First, we assumed a systemic arterial system that had a realistic topology consisting of 121 arterial segments. Then the relationships of pulsatile blood pressures and flows in arterial segments were characterized by standard pulse transmission equations. Finally, each arterial segment was assumed to remodel to local stresses following three simple rules: 1) increases in endothelial shear stress increases radius, 2) increases in wall circumferential stress increases wall thickness, and 3) increases in wall circumferential stress decreases wall stiffness. Simulation of adaptation by iteratively calculating pulsatile hemodynamics, mechanical stresses, and vascular remodeling led to a general behavior in response to mechanical perturbations: initial increases in pulse pressure led to increased arterial compliances, and decreases in pulse pressure led to decreased compliances. Consequently, vascular adaptation returned pulse pressures back toward baseline conditions. This behavior manifested when modeling physiological adaptive responses to changes in cardiac output, changes in peripheral resistances, and changes in local arterial radii. The present work, thus, revealed that pulse pressure homeostasis emerges from physiological adaptation of systemic arteries to local mechanical stresses.

Objective Digital ulcers (DU) are a burden in systemic sclerosis (SSc). Microangiopathy is a cardinal feature of SSc that plays a critical role in the development of DU. However, whether injury of medium or large vessels also contributes to DU in SSc remains controversial. Methods To measure concomitantly in SSc patients with and without active DU: (i) the Augmentation Index of the reflected wave (Aix_75) by radial applanation tonometry, an index of small and medium arterial function; (II) the aortic pulse wave velocity (PWV), a marker of large vessel injury (aortic stiffness). Results Sixty-three consecutive SSc patients were included (49 females, aged 60 [49–65] years, disease duration of 8.5 [5–13] years), including 10 (15.9%) with active DU. Patients with active DU versus those without had increased Aix_75 (35% [28–38] versus 28% [20–34], P = 0.041) whereas no difference existed in PWV (7.0 m/s [6.7–10.1] versus 7.6 m/s [6.8–8.7], P = 0.887), in systolic, diastolic, as well as aortic pulse pressure ( P = 0.126, 0.592, and 0.161, respectively). When compared to patients in the low tertile, patients having Aix_75 in the highest tertile had 10-fold more DU (OR = 10.23; 95% CI 1.12 to 93.34, P = 0.039). Conclusion The presence of DU is associated with increased Aix_75 whereas there is no relation with PWV. These data suggest that small and medium arteries are involved in the occurrence of DU whether large vessel stiffness does not contribute. Whether Aix_75 is predictive of further DU remained to be studied.

BACKGROUND Whether the impact of backward wave pressures (Pbs) on left ventricular (LV) diastolic dysfunction (DD) antedates the effects of aortic stiffness is uncertain. We compared the relative contribution of various aortic hemodynamic parameters to preclinical DD in a predominantly young-to-middle-aged community-based sample. METHODS In 524 randomly selected participants of African ancestry (mean age = 46.8±18.4 years), we assessed central aortic pulse pressure (PPc), forward wave pressure (Pf), Pb, augmented pressure (Pa), the time-to-wave reflection (Rt), and aortic pulse wave velocity (PWV) using applanation tonometry (SphygmoCor software). LV mass index (LVMI), early to late transmitral velocity (E/A), and E/velocity of myocardial tissue lengthening (E/e') were determined using echocardiography. RESULTS Independent of age, sex, mean arterial pressure, body mass index, diabetes mellitus and/or HbA1c > 6.1%, regular smoking, regular alcohol intake, treatment for hypertension, pulse rate, and LVMI; PPc (P < 0.002), Pb (P < 0.0005), Pa (P < 0.002), and Pf (P < 0.02), but not Rt or PWV were independently associated with E/e' (but not with E/A). With adjustments for confounders, PPc (P < 0.005), Pb (P < 0.002), and Pa (P < 0.001), but not Pf, Rt, or PWV were independently associated with E/e' ≥ 12 (moderate-to-severe DD, n = 69). The independent relations between PPc and E/e' or moderate-to-severe DD were not affected by adjustments for PWV, Pf, or Rt, but were abolished with adjustments for Pb. CONCLUSIONS In a predominantly young-to-middle-aged community sample, the impact of Pbs on LV DD antedates the effects of aortic stiffness, the time-to-wave reflection, or Pfs.

Controversial data exist on acute and chronic effects of competitive sports on central hemodynamics and arterial stiffness. We investigated chronic as well as acute training effects in professional rowers. The trial was planned as a non-randomized, controlled pilot-study comparing athletes and controls. 13 German national team rowers (24.1 ± 1.5 years) and 12 controls (23.8 ± 0.8 years) participated. Aortic, brachial hemodynamics and arterial stiffness were measured (Arteriograph, TensioMed(®), Hungary) before and after a standardized exercise test. Chronic heart rate (49 [Formula: see text] 2 bpm versus 70 [Formula: see text] 2 bpm, p

Background: Aortic pulse pressure is a significant marker of cardiovascular morbidity independently of mean blood pressure and pulse pressure of 60 mm Hg should be considered as the threshold at risk both in normotensives and hypertensives. Coronary perfusion is dependent on diastolic blood pressure and patients with CAD may be susceptible to the adverse effects of low diastolic blood pressure. This study conducted to examine the relation between central aortic pulse pressure and the prevalence and extent of CAD.Methods: A cross sectional, hospital-based study conducted in Sri Jayadeva Institute of Cardiovascular Sciences and Research, Bengaluru, among patients undergoing diagnostic coronary angiography.Results: Risk factors like Diabetes, Hypertension, Dyslipidemia and smoking rates were significantly higher in patients with PP of >60 mmHg (p60 mmHg, 4 patients had left main coronary artery (LMCA) disease, 20 patients had single vessel disease, 11 patients had two vessel disease and 20 patients had triple vessel disease.Conclusions: In this study it was demonstrated aortic pulse pressure of more than 60 mm Hg is associated with significant CAD.

BACKGROUND Through the impact of conventional risk factors on arteries, several changes in aortic function contribute to cardiovascular events. It is nevertheless uncertain whether these effects are accurately reflected by changes in central aortic pulse pressure (PPc). We, therefore, aimed to determine the extent to which relations between modifiable risk factors and aortic function translate into increases in PPc. METHODS In 1,232 black South Africans from the South West Township (SOWETO) of Johannesburg, we determined risk factors and aortic function from carotid-femoral pulse wave velocity (PWV), aortic PPc, forward wave pressures (Pf), and reflected (backward) wave pressures (Pb) (applanation tonometry and SphygmoCor software). RESULTS With adjustments for alternative risk factors and distending pressure (mean arterial pressure (MAP)), diabetes mellitus (treatment or HbA1c > 6.5%, n = 151) was associated with an increased PWV (7.10 ± 2.09 vs. 6.17 ± 2.00 m/s, P < 0.0001), and Pf (26 ± 8 vs. 24 ± 8 mm Hg, P < 0.005), but neither brachial PP (46 ± 14 vs. 45 ± 13, P = 0.19), PPc (36 ± 12 vs. 35 ± 11 mm Hg, P = 0.48), nor Pb (17 ± 6 vs. 17 ± 6 mm Hg, P = 0.83). Moreover, independent of alternative risk factors and MAP, uncontrolled hypertension (office blood pressure > 140/90 mm Hg, n = 433) was associated with an increased Pf (26 ± 12 vs. 24 ± 10 mm Hg, P < 0.01), but not with changes in brachial PP (45 ± 19 vs. 44 ± 17, P = 0.75), PPc (35 ± 16 vs. 35 ± 15 mm Hg, P = 0.93), or Pb (18 ± 8 vs. 17 ± 8 mm Hg, P = 0.46). CONCLUSIONS Neither brachial nor aortic PP are adequate indexes of relations between the modifiable conventional risk factors, uncontrolled hypertension or diabetes mellitus, and risk-related aortic functional changes.

Aorta effectively buffers cardiac pulsatile fluctuation generated from the left ventricular (LV) which could be a mechanical force to high blood flow and low-resistance end-organs such as the brain. A dynamic orthostatic challenge may evoke substantial cardiac pulsatile fluctuation via the transient increases in venous return and stroke volume (SV). Particularly, this response may be greater in endurance-trained athletes (ET) who exhibit LV eccentric remodeling. The aim of this study was to determine the contribution of aortic compliance to the response of cerebral blood flow fluctuation to dynamic orthostatic challenge in ET and age-matched sedentary (SED) young healthy men. ET (n = 10) and SED (n = 10) underwent lower body negative pressure (LBNP) (−30 mmHg for 4 min) stimulation and release the pressure that initiates a rapid regain of limited venous return and consequent increase in SV. The recovery responses of central and middle cerebral arterial (MCA) hemodynamics from the release of LBNP (~15 s) were evaluated. SV (via Modeflow method) and pulsatile and systolic MCA (via transcranial Doppler) normalized by mean MCA velocity (MCAv) significantly increased after the cessation of LBNP in both groups. ET exhibited the higher ratio of SV to aortic pulse pressure (SV/AoPP), an index of aortic compliance, at the baseline compared with SED (P < 0.01). Following the LBNP release, SV was significantly increased in SED by 14 ± 7% (mean ± SD) and more in ET by 30 ± 15%; nevertheless, normalized pulsatile, systolic, and diastolic MCAv remained constant in both groups. These results might be attributed to the concomitant with the increase in aortic compliance assessed by SV/AoPP. Importantly, the increase in SV/AoPP following the LBNP release was greater in ET than in SED (P < 0.01), and significantly correlated with the baseline SV/AoPP (r = 0.636, P < 0.01). These results suggest that the aortic compliance in the endurance athletes is able to accommodate the additional SV and buffer the potential increase in pulsatility at end-organs such as the brain.

The interrelationship between endothelial function and arterial stiffness may be different for central and peripheral arteries due to their structural and functional differences. The study aims to assess the interrelationship between central and peripheral vascular function and haemodynamics in metabolic syndrome. Thirty-seven patients [63.0 (57.5-66.0) years, 68.4% males] of metabolic syndrome (National Cholesterol Education Program - Adult Treatment Panel-III criteria) were studied. Carotid-femoral, carotid-radial pulse wave velocity and augmentation index (AIx@75) were assessed using applanation tonometry. Endothelial function was evaluated by brachial flow-mediated dilation using B-mode ultrasonography. Central and peripheral pressures were measured by radial tonometry and sphygmomanometer, respectively. Carotid-radial pulse wave velocity correlated significantly with peripheral diastolic blood pressure ( r = 0.33, p = 0.04) and inversely with flow-mediated dilation ( r = -0.61, p = 0.0001). AIx@75 correlated significantly with carotid-femoral pulse wave velocity ( r = 0.35, p = 0.03) and with aortic pulse pressure ( r = 0.43, p = 0.01). In principal component analysis, an inverse relationship was observed between flow-mediated dilation and carotid-radial pulse wave velocity but not with carotid-femoral pulse wave velocity. Regional arterial stiffness assessed by pulse wave velocity in central-elastic and peripheral-muscular arteries differentially relates to endothelial dysfunction. The central arteries might be predominantly influenced by endothelial dysfunction-induced structural changes, while the peripheral arteries are majorly affected by functional alterations.

Abstract. Increased arterial stiffness results from reduced elasticity of the arterial wall and is an independent predictor for cardiovascular risk. The gold standard for assessment of arterial stiffness is the carotid-femoral pulse wave velocity. Other parameters such as central aortic pulse pressure and aortic augmentation index are indirect, surrogate markers of arterial stiffness, but provide additional information on the characteristics of wave reflection. Peripheral arterial disease (PAD) is characterised by its association with systolic hypertension, increased arterial stiffness, disturbed wave reflexion and prognosis depending on ankle-brachial pressure index. This review summarises the physiology of pulse wave propagation and reflection and its changes due to aging and atherosclerosis. We discuss different non-invasive assessment techniques and highlight the importance of the understanding of arterial pulse wave analysis for each vascular specialist and primary care physician alike in the context of PAD.

Epicardial adipose tissue (EAT), metabolically active visceral fat, is easily measurable using transthoracic echocardiography (TTE). This study aimed to clarify the relationship between EAT thickness and parameters for target organ damage (TOD). A total of 338 consecutive patients (64.5 ± 10.9 years, 58.0% men) undergoing invasive coronary angiography in a stable condition were prospectively enrolled. TTE was performed, and the EAT thickness was measured perpendicular to the right ventricular free wall at end-systole. We investigated TOD parameters, including the estimated glomerular filtration rate, proteinuria, left ventricular (LV) mass index (LVMI), septal e' velocity, E/e', brachial-ankle pulse wave velocity, ankle-brachial index, aortic pulse pressure (APP), and presence of coronary artery disease (CAD). APP and CAD were assessed by invasive cardiac catheterization. Most patients (77.5%) had significant CAD (≥50% stenosis). In Pearson's bivariate correlation analyses, the EAT thickness was significantly correlated with the septal e' velocity (r = -0.203, P 0.001) and E/e' (r = 0.217, P 0.001), but not with other TOD parameters (P 0.05). Multiple linear regression analysis showed that the correlations of the EAT thickness with septal e' velocity (β = -0.172, P = 0.047) and E/e' (β = 0.207, P = 0.011) remained significant even after adjusting for potential confounders. EAT thickness is more closely related to LV diastolic function than other TOD parameters, including renal function, LVMI, arterial stiffness, peripheral artery disease, and CAD. These findings provide additional evidence for the potential role of EAT in the pathogenesis of LV diastolic dysfunction.

Various control and monitoring algorithms have been proposed to improve the left-ventricular assist device (LVAD) therapy by reducing the still-occurring adverse events. We developed a novel multi-objective physiological control system that relies on the pump inlet pressure (PIP). Signal-processing algorithms have been implemented to extract the required features from the PIP. These features then serve for meeting various objectives: pump flow adaptation to the perfusion requirements, aortic valve opening for a predefined time, augmentation of the aortic pulse pressure, and monitoring of the LV pre- and afterload conditions as well as the cardiac rhythm. Controllers were also implemented to ensure a safe operation and prevent LV suction, overload, and pump backflow. The performance of the control system was evaluated in vitro, under preload, afterload and contractility variations. The pump flow adapted in a physiological manner, following the preload changes, while the aortic pulse pressure yielded a threefold increase compared to a constant-speed operation. The status of the aortic valve was detected with an overall accuracy of 86% and was controlled as desired. The proposed system showed its potential for a safe physiological response to varying perfusion requirements that reduces the risk of myocardial atrophy and offers important hemodynamic indices for patient monitoring during LVAD therapy.

Reports on the contribution of aortic forward (Pf) and backward (Pb) wave pressures to age-related increases in central aortic pulse pressure (PPc) have been confounded by the use of participants receiving antihypertensive therapy. We assessed the relative contribution of Pf and Pb to age-related increases in PPc (radial applanation tonometry and SphygmoCor software using an assumed triangular wave for wave separation analysis) in 892 community participants not receiving antihypertensive therapy. We validated our results using aortic flow waves (echocardiography) for wave separation analysis in 254 of these participants. In multivariate regression models in those aged50 years, adjustments for both Pb and a Pf-independent measure of reflected wave function (RM = Pb/Pf), but not Pf abolished the impact of age on PPc. However, in those aged50 years, adjustments for Pf (β-coefficient: 0.25 ± 0.06 vs. 0.74 ± 0.08; P .0001) and Pb (0.04 ± 0.04 vs. 0.74 ± 0.08; P .0001), but not RM markedly decreased the relationship between age and PPc. On product of coefficient mediation analysis, whether assessed in men or in women, in those participants aged50 years, independent of several confounders and mean arterial pressure, Pb (P .005), but not Pf contributed to age-related increases in PPc. In contrast, in those participants aged ≥50 years, independent of several confounders and mean arterial pressure, Pb (P .005) and Pf (P .01) contributed to age-related increases in PPc, and Pb effects were markedly diminished by adjustments for Pf (0.26 ± 0.002 vs. 0.52 ± 0.003 mm Hg per year, P .0001 for comparison). In conclusion, independent of the effects of antihypertensive therapy, aortic backward waves contribute to age-related increases in aortic PPc across the adult lifespan, but at an older age, this effect may be attributed in part to the impact of forward on backward wave pressures.

Aim Although the diastolic flow reversal of the descending aorta has been recognized in patients with aortic regurgitation, its generation without this condition is still unknown. This study was performed to investigate whether flow patterns of the descending thoracic aorta, as measured by echocardiography, can represent invasively measured aortic pulse pressure (APP). Methods A total of 100 patients (age, 62.3±11.0 years; men, 62.0%) undergoing invasive coronary angiography (ICA) was analyzed. APP was measured at ascending thoracic aorta using pigtail catheter before ICA. Flow in the descending thoracic aorta was assessed using pulse wave Doppler echocardiography, and R/F ratio was defined as reverse peak velocity (R)/forward peak velocity (F). Results Eighty patients (80.0%) had obstructive coronary artery disease (CAD) (≥50% stenosis of one or more epicardial coronary arteries) in ICA. APP and R/F ratio were significantly higher in patients with obstructive CAD than those without (P