Alterations In Arterial Stiffness Research Articles

Arterial Stiffness Changes in Adult Cancer Patients Receiving Anticancer Chemotherapy: A Real-World Bicentric Experience.

Background Chemotherapy correlates to acute and long-term cardiotoxicity, is reflected clinically by myocardial and vascular endothelial dysfunction, and can cause cardiovascular complications. Thus, early diagnosis of cardiovascular disease in cancer patients undergoing anti-cancer treatment is necessary to enhance long-term survival. Our principal objective in this study was to discern the impact of specific anti-cancer chemotherapeutics and biologics on arterial stiffness alterations before and after the administration. Methods Conducted at Mustafa Bacha University Hospital, Algeria, the study focused on arterial stiffness in anti-cancer chemotherapy patients. Assessments included blood pressure, diabetes, and dyslipidemia, with precise measurements using validated systems, particularly pulse wave velocity (PWV). Various chemotherapy protocols were applied, and statistical analysis with R software (R Foundation for Statistical Computing, Vienna, Austria) maintained a significance level of p=0.05. Key outcomes centered on carotid-femoral PWV and secondary endpoints such as central and peripheral pressures and pulse pressure (PP). Univariate and bivariate analyses were conducted using appropriate statistical tests. Results A comparative prospective observational study was completed on 58 patients (34 women and 24 men; mean age: 52.64 +/- 12.12 years) treated with anti-cancer chemotherapy agents. Our evaluation included a complete clinical exam, electrocardiogram, Doppler echocardiography, and applanation tonometry with arterial stiffness measurement using PWV. Patients presented significantly higher levels of carotid-femoral PWV, regardless of the chosen chemotherapy protocol, with no return to the initial level after one year of stopping treatment (p-value < 0.01). Moreover, this increase was more significant in patients with diabetes and hypertension and patients treated with monoclonal antibodies or intercalants. Conclusion This prospective study shows that chemotherapy patients have elevated arterial stiffness, emphasizing the need to assess PWV and monitor cardiovascular risk factors. PP measurement with PWV could improve risk management.

SARS-CoV-2 is associated withabnormal biomarkers of oxidative stress,and endothelial function linked with cardiovascular dysfunction four months after the infection

Abstract Introduction COVID-19 infection has been associated with increase arterial stiffness, endothelialdysfunction, and impairment in coronary and cardiac performance. Inflammation and oxidative stress have beensuggested as possible pathophysiological mechanisms leading to vascular and endothelial deregulation afterCOVID-19 infection. Purpose The objective of our study is to evaluate premature alterations in arterial stiffness, endothelial,coronary, and myocardial function markers four months after SARS-CoV-2 infection. Methods In a case-control prospective study, we included 70 patients 4 months after COVID-19 infection, 70 age- and sex-matched untreated hypertensive patients (positive control) and 70 healthy individuals. We measured (i) perfused boundary region (PBR) of the sublingual arterial microvessels (increased PBR indicates reduced endothelial glycocalyx thickness), (ii) flow-mediated dilatation (FMD), (iii) coronary flow reserve (CFR) by Doppler echocardiography, (iv) pulse wave velocity (PWV) and central systolic blood pressure (cSBP), (v) global left and right ventricular longitudinal strain (GLS), (vi) malondialdehyde (MDA), an oxidative stress marker, thrombomodulin and von Willebrand factor as endothelial biomarkers. Results COVID-19 patients had similar CFR and FMD with hypertensives (2.48±0.41 vs 2.58±0.88, p=0.562, 5.86±2.82% vs 5.80±2.07%, p=0.872 respectively) but lower values than controls (3.42±0.65, p=0.0135, 9.06±2.11%, p=0.002 respectively). Compared to controls, both COVID-19 and hypertensives had greater PBR5–25 (2.07±0.15μm and 2.07±0.26μm p=0.8 vs 1.89±0.17μm, p=0.001), higher PWV, (12.09±2.50 vs 11.92±2.94, p=0.7 vs 10.04±1.80m/sec, p=0.036) increased cSBP (128.43±17.39 vs 135.17±16.83 vs 117.89±18.85) and impaired LV and RV GLS (−19.50±2.56% vs −19.23±2.67%, p=0.864 vs −21.98±1.51%, p=0.020 and −16.99±3.17% vs −18.63±3.20%, p=0.002 vs −20.51±2.28%, p&amp;lt;0.001). MDA and thrombomodulin were higher in COVID-19 patients than both hypertensives and controls (10.67±2.75 vs 1.76±0.30, p=0.003 vs 1.01±0.50nmole/L, p=0.001 and 3716.63±188.36 vs 3114.46±179.18, p=0.017 vs 2590.02±156.51pg/ml, p&amp;lt;0.001). COVID-19 patients displayed similar vWF values with hypertensives but higher compared with healthy controls (4018.03±474.31 vs 3756.65±293.28 vs 2079.33±855.10 ng/ml, p=0.718 and p=0.016 respectively). Conclusions SARS-CoV-2 infection is associated with oxidative stress, endothelial and vascular dysfunction, which are linked to impaired longitudinal myocardial deformation 4 months after COVID-19 infection. Funding Acknowledgement Type of funding sources: None.

Arterial Stiffness Alterations in Simulated Microgravity and Reactive Sledge as a Countermeasure.

Experiments during spaceflight and simulated microgravity as head-down tilt bedrest, demonstrated the role of arterial stiffness among others, in microgravity induced cardiovascular pathologies and emphasized the need for a robust countermeasure. The purpose of the present study was to evaluate the use of a new countermeasure, consisting of a high intensity Reactive Sledge (RSL) jumps training protocol, to counteract changes in arterial stiffness during long term head down tilt bedrest (LTBR). The participants enrolled in the study were 23 male, healthy volunteers, aged between 20 and 45years, subjected to LTBR for 60days and randomly assigned either to a control (11) or to a training sledge (12) group using RSL 3-4 times per week, as a countermeasure. Recorded values were systolic and diastolic blood pressure, heart rate and the user's arterial stiffness index. Compared to baseline measurements, there was a deterioration in the values of arterial stiffness, systolic and diastolic blood pressure and heart rate, in both groups until day 35 of LTBR, interpreted as adaptation to the microgravity environment. From this day until the end of the experiment, arterial stiffness of the control group was constantly fluctuating, while constantly improving for the training group. During the recovery period, arterial stiffness values returned to the pre-experimental levels in both groups. Overall, arterial stiffness increased the longer the time spent in LTBR and the countermeasure was partially effective in preventing the observed phenomenon. German Clinical Trials Register (DRKS), DRKS00012946, September 18, 2017, retrospectively registered.

COVID-19 patients present impaired endothelial glycocalyx, vascular dysfunction and myocardial deformation resembling those observed in hypertensives four months after infection

Background/IntroductionCOVID-19 infection has been associated with increase arterial stiffness, endothelial dysfunction, and impairment in coronary and cardiac performance. Inflammation and oxidative stress have been suggested as possible pathophysiological mechanisms leading to vascular and endothelial deregulation after COVID-19 infection.PurposeThe objective of our study is to evaluate premature alterations in arterial stiffness, endothelial, coronary, and myocardial function markers four months after SARS-CoV-2 infection.MethodsWe conducted a case-control prospective study, including 70 patients four months after COVID-19 infection, 70 age- and sex-matched untreated hypertensive patients (positive control) and 70 healthy individuals. We measured a) perfused boundary region (PBR) of the sublingual arterial microvessels (increased PBR indicates reduced endothelial glycocalyx thickness b) flow-mediated dilation (FMD), c) coronary Flow Reserve (CFR) by Doppler echocardiography d) pulse wave velocity (PWV) and central systolic (SBP) e) global LV longitudinal strain (GLS) by speckle tracking imaging and f) malondialdehyde (MDA) as oxidative stress marker.ResultsCOVID-19 patients had similar CFR and FMD with hypertensives (2.48±0.41 vs 2.58±0.88, p=0.562, 5.86±2.82% vs 5.80±2.07%, p=0.872 respectively), but lower CFR and FMD than controls (3.42±0.65, p=0.0135 9.06±2.11%, p=0.002 respectively) Both COVID-19 and hypertensive group had greater PBR than controls (PBR5–25: 2.07±0.15 μm and 2.07±0.26 μm p=0.8 vs 1.89±0.17 μm, p=0.001). COVID-19 patients and hypertensives had higher PWV and central SBP than controls (PWVcf 12.09±2.50 and 11.92±2.94, p=0.7 vs 10.04±1.80 m/sec, p=0.036). COVID-19 patients and hypertensives had impaired values of GLS compared to controls (−19.50±2.56% and −19.23±2.67%, p=0.864 vs −21.98±1.51%, p=0.020). Increased PBR5–25 was associated with increased SBP central which in turn was related with impaired GLS (p<0.05). MDA was found increased in COVID-19 patients compared to both hypertensives and controls (10.67±2.75 vs 1.76±0.30, p=0.003 vs 1.01±0.50 nmole/L, p=0.001).ConclusionsSARS-CoV-2 may cause impaired coronary microcirculatory, endothelial and vascular deregulation which remain four months after initial infection and are associated with reduced cardiac performance. The 10-fold increase of MDA compared to healthy individuals four months after COVID-19 infection indicate oxidative stress as possible pathophysiological mechanism.FUNDunding AcknowledgementType of funding sources: None.

Carotid Arterial Stiffness and Hemodynamic Responses to Acute Cycling Intervention at Different Times during 12-Week Supervised Exercise Training Period.

This paper studied the alterations in arterial stiffness and hemodynamic responses during resting state and immediately following acute cycling intervention at different times across 12-week supervised exercise training. Twenty-six sedentary young males participated in the exercise training program at moderate intensity. Arterial stiffness and hemodynamic variables of the right common carotid artery were measured and computed during resting state and immediately following acute cycling intervention at weeks 0, 4, 8, and 12. Across the 12-week exercise training, carotid arterial stiffness was decreased at weeks 8 and 12 and hemodynamic variables were improved at week 12 during resting state. In response to acute cycling intervention, carotid arterial stiffness exhibited an acute increase foremost at 8 weeks, and arterial maximal and mean diameters showed acute decreases at weeks 0 and 4. Despite significant differences in arterial stiffness and hemodynamic variables between resting state and immediately after acute intervention for each time period, these differences presented a progressive decrease across the 12-week exercise training. In conclusion, long-term exercise training not only improved carotid arterial stiffness and hemodynamic alterations when at rest but also negated the acute responses of carotid arterial stiffness and hemodynamic variables to acute cycling intervention.

Metabolomic profile of arterial stiffness in aged adults

Increasing arterial stiffness is an important contributor to declining cardiovascular health in ageing. Changes in whole-body fuel metabolism could be related to alterations in arterial stiffness in ageing adults. Targeted high-performance liquid and gas chromatography mass spectrometry were used to measure 84 circulating metabolites in a group of community elderly adults ( n = 141, 58% men; mean age = 70.6 ± 11.2 years) without cardiovascular disease. In basic and adjusted models, we correlated the measured metabolites to carotid-femoral pulse wave velocity assessed by applanation tonometry. Age ( β = 0.10, p < 0.0001), smoking status ( β = 1.32, p = 0.02), dyslipidemia ( β = 1.22, p = 0.01), central systolic blood pressure ( β = 0.05, p < 0.0001), central mean arterial pressure ( β = 0.04, p = 0.03) and central pulse pressure ( β = 0.05, p < 0.0001) were significantly associated with pulse wave velocity. Amino acids such as histidine, methionine and valine correlated with pulse wave velocity. In multivariable models adjusted for clinical covariates, only Factor 5, comprising the medium- and long-chain dicarboxyl and hydroxyl acylcarnitines was independently associated with pulse wave velocity ( β = 0.24, p = 0.015). An upstream metabolic perturbation comprising medium- and long-chain dicarboxyl and hydroxyl acylcarnitines, likely reflecting changes in cellular fatty acid oxidation, was associated with arterial stiffness among aged adults. This advances mechanistic understanding of arterial stiffness among aged adults before clinical disease.

Arterial Stiffness and Cardiovascular Autonomic Dysfunction in Patients with Parkinson's Disease

Background: Pulse wave velocity is a marker of arterial stiffness and a surrogate marker of vascular damage. Autonomic abnormalities associated with blood pressure are relatively commonly observed in patients with Parkinson's disease (PD). Objective: The purpose of this study was to compare arterial stiffness between patients with PD and controls and investigate the associations between cardiovascular autonomic dysfunction and pulse wave velocity in PD. Methods: One hundred twenty-five PD patients without diabetes mellitus were enrolled into this study, along with 22 age-matched controls. Orthostatic vital signs and ambulatory 24-hour blood pressure monitoring values were recorded. Pulse wave velocity was used to evaluate arterial stiffness. Results: In PD, greater arterial stiffness was associated with orthostatic hypotension, supine hypertension, nocturnal hypertension, and nondipping. Dopaminergic treatment did not influence cardiovascular autonomic dysfunction or arterial stiffness. Although pulse wave velocity was mildly increased in patients with PD compared to controls, the arterial stiffness in PD patients without autonomic failure was similar to that in normal controls. Stiffer arteries were found only in patients with PD and autonomic failure. Conclusion: These findings suggest that cardiovascular autonomic dysfunction is associated with arterial stiffness in PD. PD itself does not affect arterial stiffness, whereas autonomic blood pressure disturbances influence alterations in arterial stiffness and architectural changes in the arteries of PD patients.

Plasma homocysteine levels are independently associated with alterations of large artery stiffness in men but not in women.

ObjectivesTo investigate the associations of the plasma homocysteine levels with the alterations in arterial stiffness in a community-based cohort. The gender differences in these associations were examined.MethodsWe evaluated the relationship between plasma homocysteine levels to three measures of vascular function [carotid-femoral pulse wave velocity (CF-PWV), carotid-ankle PWV (CA-PWV) and heart rate corrected augmentation index (AI)] in 1680 participants (mean age: 61.5 years; 709 men, 971 women) from communities of Beijing, China.ResultsIn univariate analysis, plasma homocysteine levels was positively related to the CF-PWV (r = 0.211, P < 0.0001) and CA-PWV (r = 0.148, P < 0.0001), whereas inversely associated with AI (r = −0.052, P = 0.016). In multiple linear regression models adjusting for covariants, plasma homocysteine remained positively related to the CF-PWV (standardized β = 0.065, P = 0.007) in total cases. When the groups of men and women were examined separately, plasma homocysteine remained positively associated with the CF-PWV (standardized β = 0.082, P = 0.023) in men, whereas the relations between homocysteine and any of the arterial stiffness indices were not further present in women.ConclusionsIn Chinese population, plasma homocysteine levels are independently associated with alterations of large artery stiffness in men but not in women.

Arterial stiffness results from eccentrically biased downhill running exercise

There is increasing evidence that select forms of exercise are associated with vascular changes that are in opposition to the well-accepted beneficial effects of moderate intensity aerobic exercise. To determine if alterations in arterial stiffness occur following eccentrically accentuated aerobic exercise, and if changes are associated with measures of muscle soreness. Repeated measures experimental cohort. Twelve (m=8/f=4) moderately trained (VO₂max=52.2 ± 7.4 ml kg(-1)min(-1)) participants performed a downhill run at -12° grade using a speed that elicited 60% VO₂max for 40 min. Cardiovascular and muscle soreness measures were collected at baseline and up to 72 h post-running. Muscle soreness peaked at 48 h (p=<0.001). Arterial stiffness similarly peaked at 48 h (p=0.04) and remained significantly elevated above baseline through 72 h. Eccentrically accentuated downhill running is associated with arterial stiffening in the absence of an extremely prolonged duration or fast pace. The timing of alterations coincides with the well-documented inflammatory response that occurs from the muscular insult of downhill running, but whether the observed changes are a result of either systemic or local inflammation is yet unclear. These findings may help to explain evidence of arterial stiffening in long-term runners and following prolonged duration races wherein cumulative eccentric loading is high.

Type 2 Diabetes Is Associated With Increased Pulse Wave Velocity Measured at Different Sites of the Arterial System but Not Augmentation Index in a Chinese Population

Patients with type 2 diabetes have increased stiffness of central elastic arteries. However, whether peripheral muscular artery stiffness is equally affected by the disease remains sparsely examined. Moreover, the association between pulse wave velocity (PWV) and augmentation index (AIx) in diabetes is poorly understood. Type 2 diabetes is associated with the alterations in arterial stiffness (PWV and AIx) in a community-based population. A total of 79 Chinese patients with type 2 diabetes and 79 sex-, age- (±3 years), and body mass index- (±2 kg/m(2) ) matched healthy controls were studied. Carotid-femoral pulse wave velocity (CF-PWV), carotid-radial pulse wave velocity (CR-PWV), and carotid-ankle pulse wave velocity (CA-PWV) were calculated from tonometry waveforms and body surface measurements, whereas AIx was assessed using pulse wave analyses. In univariate analysis, patients with type 2 diabetes showed increased CF-PWV (P < 0.001), CR-PWV (P = 0.012), and CA-PWV (P = 0.016), and lower AIx (P = 0.017) than the control group. In multiple linear regression models adjusting for covariates, type 2 diabetes remained a significant determinant of CF-PWV. Fasting glucose was associated with CR-PWV but was not related to CA-PWV or AIx. Our findings suggest that patients with type 2 diabetes have increased central and peripheral artery stiffness, but preserved AIx compared to controls. Diabetes was a predictor of central artery stiffness, and glucose was a determinant of peripheral artery stiffness.

Arterial stiffness is associated with minimally elevated high-sensitivity cardiac troponin T levels in a community-dwelling population

ObjectivesArterial stiffness predicts an excess risk of future cardiovascular events, supposedly via myocardial damage. Minimally elevated levels of plasma cardiac troponin T (TnT), a marker of cardiomyocyte injury, can be...

Arterial stiffness is associated with minimally elevated high-sensitivity cardiac, troponin T levels in a community-dwelling population

ObjectivesArterial stiffness predicts an increased risk of future cardiovascular events, possibly via myocardial damage. Minimally elevated levels of plasma cardiac troponin T (TnT), a marker of cardiomyocyte injury, can be detected by the high-sensitivity TnT (hsTnT) assay. The current study investigated the relationship between plasma hsTnT levels and alterations in arterial stiffness in a community-based population. MethodsWe related levels of plasma hsTnT to measures of arterial stiffness (carotid–femoral pulse wave velocity [PWV], office pulse pressure [PP] and carotid–radial PWV) in 1479 participants (mean age, 62.3 years; 619 men, 860 women) from a community-based population in Beijing, China. ResultsIn multiple logistic regression models, carotid–femoral PWV (OR: 1.84; 95% CI: 1.06–3.17; P=0.028) and office PP (OR: 2.02; 95% CI: 1.31–3.11; P=0.002) were associated with a higher likelihood of detectable hsTnT. In addition, carotid–femoral PWV (OR: 2.34; 95% CI: 1.03–5.30; P=0.042) and office PP (OR: 2.30; 95% CI: 1.13–4.66; P=0.022) were significantly related to elevated hsTnT levels. A subsequent subgroup analysis found that, in subjects aged 60 years and older, the associations between carotid–femoral PWV and office PP and hsTnT levels were strengthened. The associations between hsTnT with any of the arterial stiffness measures were not present in the younger subgroup (<60 years old). ConclusionsCarotid–femoral PWV and office PP are associated with minimally elevated hsTnT levels in the elderly, indicating a relationship between central artery stiffness and subclinical myocardial damage.

Contribution of nitric oxide to the blood pressure and arterial responses to incremental maximal exercise in humans

We sought to determine the contribution of nitric oxide (NO) to the blood pressure (BP) responses to exercise and post‐exercise alterations in arterial stiffness. In 10 healthy subjects (31±5 years), BP, heart rate (HR) and oxygen consumption were measured before, during and after an incremental cycling exercise test. Trials were performed with placebo (saline) or following acute inhibition of NO synthase with NG‐monomethyl‐L‐arginine (L‐NMMA) on separate days, in a randomized, double blind, cross‐over design. Central (aortic) and peripheral (femoral) arterial stiffness was assessed with pulse wave velocity (PWV). BP was increased with L‐NMMA at rest and during sub‐maximal exercise, but not at maximal exercise (mean BP 118±8 vs. 117±5 mmHg, saline vs. L‐NMMA, P&gt;0.05). L‐NMMA had no influence on exercising HR or maximal oxygen consumption (P=ns). Post‐exercise reductions in femoral PWV were attenuated with L‐NMMA (P&lt;0.05), while aortic PWV was increased similarly with either saline or L‐NMMA (P=ns). Our findings suggest that reductions in NO bioavailability cause augmented BP responses to sub‐maximal exercise, but do not lead to exaggerated BP responses to maximal exercise or reduce maximal oxygen consumption. Furthermore, NO is an important contributor to reductions in femoral artery stiffness following maximal exercise in healthy individuals.This research was supported by the BHF.

Cardio-Ankle Vascular Index for Evaluating Immunosuppressive Therapy in a Patient with Aortitis Syndrome

Aortitis syndrome is a chronic vasculitis that leads to arterial wall thickening and stiffening in large elastic arteries. However, there are no established markers for assessing arterial stiffening in aortitis syndrome. The cardio-ankle vascular index (CAVI) has recently been utilized to assess arterial stiffening that is associated with atherosclerosis-related diseases. We hypothesized that CAVI can be applicable for assessing alterations in arterial stiffness during immunosuppressive therapy for aortitis syndrome. A 69-year-old woman with a 2-month history of recurrent fever, fatigue, and malaise, showed intense 18F-fluorodeoxyglucose (18F-FDG) uptake in the thoracic aorta and common carotid arteries in 18F-FDG-positron emission tomography. These clinical and imaging findings resulted in the diagnosis of aortitis syndrome. The patient also showed the elevated CAVIs on both sides (right, 10.3; left, 10.4) (normal value for her age, 9.1 +/- 0.8), indicating the arterial stiffness due to aortitis syndrome. The patient was treated for 34 weeks with immunosuppressive therapy, which included oral prednisolone and methotrexate. C-reactive protein (from 4.24 to 0.49 mg/dL) and immunoglobulin G (from 2,627 to 1,524 mg/dL) were decreased by 7 weeks after initiation of the treatment. The decrease in these inflammatory parameters suggests the effectiveness of the immunosuppressive therapy. In addition, after the 34-week treatment, the CAVIs on both sides (right, 9.3; left, 9.2) were within the normal range. These data indicate that the immunosuppressive therapy ameliorates the degree of arterial stiffness. In conclusion, CAVI may be a promising marker for evaluating the effectiveness of immunosuppressive therapy in patients with aortitis syndrome.

Acacia(sen) SUPERGUM™ (Gum arabic): An evaluation of potential health benefits in human subjects

This study evaluated the cardiovascular and renal effects of dietary fibre supplementation with Acacia(sen) SUPERGUM™ (gum arabic) in normal individuals and a group of diabetic nephropaths. The normal diet was supplemented with 25 g of SUPERGUM™ daily for a period of 8–12 weeks. For the whole cohort dietary supplementation with SUPERGUM™ resulted in a fall in mean systolic blood pressure [SBP] (138.4 ± 18.9 mmHg to 132.83 ± 15.9 mmHg p = 0.01). Of note was a significant fall in SBP seen in normal individuals who neither had hypertension nor diabetes (129.1 ± 8.3 mmHg vs 123.6 ± 11.5 mmHg, n = 10 p = 0.02). Parameters of arterial stiffness were examined in patients with diabetic nephropathy and a fall in MAP. In this subgroup there was a significant fall in both central systolic and diastolic blood pressures, with no alterations in AI, AI @75 or PWV. This suggests that the beneficial effects of SUPERGUM™ on blood pressure are not the result of alterations in arterial stiffness. There were no effects of SUPERGUM™ on renal function and haemodynamics in patients with diabetic nephropathy. In contrast a reversible change in GFR (113.0 ml min vs 99.4 ml/min, p = 0.02) and ERPF (489.7 ml/min vs 463.0 ml/min, p = 0.04) was shown in the population of healthy volunteers. The key finding of this study is the a significant beneficial effect of dietary supplementation with SUPERGUM™ on blood pressure which is seen in both a patient group with diabetes and mild renal involvement as well as in a normal healthy normotensive cohort.

Arterial Stiffness Alterations During Hemodialysis

Arterial Stiffness Alterations During Hemodialysis

Associations of Plasma Natriuretic Peptide, Adrenomedullin, and Homocysteine Levels With Alterations in Arterial Stiffness

Increased arterial stiffness and higher plasma natriuretic peptide and homocysteine levels are associated with elevated risk for cardiovascular disease. Little is known about the relations of natriuretic peptides and homocysteine to arterial wall stiffness in the community. We assessed the relations of plasma N-terminal atrial natriuretic peptide, B-type natriuretic peptide, adrenomedullin, and homocysteine concentrations to arterial stiffness in participants in the Framingham Heart Study. Central pulse pressure, forward pressure wave, reflected pressure wave, carotid-femoral pulse wave velocity, and carotid-radial pulse wave velocity were assessed by tonometry in 1962 participants (mean age, 61 years; 56% women) in the Framingham Heart Study. Central systolic and diastolic blood pressures were 123/75 mm Hg in men and 119/66 mm Hg in women. After adjustment for age and clinical covariates, N-terminal atrial natriuretic peptide and B-type natriuretic peptide were associated with carotid-femoral pulse wave velocity (men: partial correlation, 0.069, P = 0.043 and r = 0.115, P < or = 0.001, respectively; women: r = -0.063, P = 0.037 and r = -0.062, P = 0.040), and carotid-radial pulse wave velocity (men: r = -0.090, P = 0.009 and r = -0.083, P < or = 0.015; women: r = -0.140, P < or = 0.001 and r = -0.104, P = 0.001, respectively). In men, N-terminal atrial natriuretic peptide and B-type natriuretic peptide also were associated with forward and reflected wave and carotid pulse pressure. In men, adrenomedullin was associated with mean arterial pressure (r = 0.089, P = 0.009), and homocysteine was associated with carotid-femoral pulse wave velocity (r = 0.072, P = 0.036), forward pressure (r = 0.079, P = 0.02), and central pulse pressure (r = 0.072, P = 0.035). Interaction tests indicated sex differences in the relations of several biomarkers to measures of arterial stiffness. Plasma natriuretic peptide, adrenomedullin, and homocysteine levels are associated with alterations in conduit vessel properties that differ in men and women.

Arterial Stiffness Alterations during Hemodialysis: The Role of Dialysate Calcium

Background/Aims: We investigated the way dialysate calcium (dCa) level can influence arterial stiffness (AS), measured by stiffness index (SI), a surrogate of pulse wave velocity, and reflection index (RI), a measure of the amount of pulse wave reflection, derived by digital volume pulse (DVP). Methods: Fourteen hemodialysis (HD) patients underwent two consecutive midweek 4-hour HD treatments in randomized order with a low dCa concentration of 1.25 mmol/l (LdCa) and a high dCa concentration of 1.75 mmol/l (HdCa), respectively. Before HD and at 1-hour intervals during the subsequent 4-hour HD sessions, SI and RI measurements were obtained from DVP contour analysis. Blood pressure (BP) and heart rate (HR) were measured after each measurement of AS. Ionized serum calcium (iCa) was measured before HD and at 120 and 240 min into the HD session. Results: iCa increased and decreased by 15.3 and 5.4% in the HdCa and LdCa groups, respectively, at the end of HD. SI and RI increased by 5.7 and 6% in the HdCa group, respectively, whereas they remained unchanged in the LdCa group. The treatment effect and the time × treatment effect were significant for both indices (ANOVA). BP and HR changes did not differ between treatments. Conclusion: Contrary to LdCa, HdCa treatment induced a BP-independent, significant increase in measured AS parameters. In the long run, HD with LdCa, by reducing the incidence of HD-induced hypercalcemia, may have a beneficial role in minimizing the cardiovascular risk related to the intermittent, intradialytic increase in AS, inherent in the chronic use of HdCa.

Acute effects of caffeine and tobacco on arterial function and wave travel

Caffeine and tobacco consumption are risk factors for heart failure, but their effects remain controversial. It has been hypothesized that they cause alterations in arterial stiffness and arterial wave travel which may increase ventricular loading. In this study the authors examined the influence of these widely used stimulants on wave intensity and arterial stiffness parameters using carotid wave intensity analysis. A new Doppler-based ultrasound method was used to measure the acute effects of caffeine and tobacco on wave intensity in the right common carotid artery. The measurements enabled changes in arterial stiffness parameters to be recorded. In 17 subjects compared with 10 controls, caffeine increased blood pressure, early systolic wave intensity and wave speed, but late-systolic wave intensity and mid-systolic reflections were unchanged. In 11 smokers studied before and after smoking one cigarette, blood pressure and arterial stiffness increased but wave intensity was unchanged. No changes were observed in the controls. Increased wave intensity during ejection after caffeine suggested sympathomimetic effects on the left ventricular function. Increased wave speed in the common carotid artery implied augmented central loading after caffeine, but the absence of measurable changes in local arterial stiffness in the carotid artery suggested more complex and regional effects. Cigarette smoking acutely increased local arterial stiffness in the common carotid artery. These changes can be detected using wave intensity analysis.

Increased Arterial Stiffness Following Repeated Valsalva Maneuvers

Resistance exercise (RE) increases arterial stiffness. Mechanisms underlying these modulations remain unknown. PURPOSE: To examine the role of blood pressure (BP) per se, as a stimulus contributing to alterations in arterial stiffness following RE. Specifically, we sought to compare a RE bout to a non-exercise control bout designed to alter BP in a similar pulsatile fashion. METHODS: Fourteen male participants completed, in a randomized fashion, a lower-body, unilateral RE bout and a repeated Valsalva Maneuver (VM) bout. Pulse wave velocity (PWV) was used to measure central and peripheral arterial stiffness. Augmentation index (AIx) was used as an index of central arterial pressure wave reflection. PWV and AIx were assessed before and 20-min after each perturbation. Beat-to-beat BP was assessed during bouts using finger plethysmography. RESULTS: Systolic BP, diastolic BP and pulse pressure were similar during both bouts. Central PWV increased following repeated VM (7. 1±0.3 m/s to 7.8±0.3 m/s) but not following RE (7.2±0.3 m/s to 7.2±0.3 m/s) (p = 0.032). There was no change in peripheral PWV following VM (8.9±0.3 m/s to 9.3±0.3 m/s) or RE (8.5±0.2 m/s to 8.4±0.2 m/s). There was also no significant change in AIx following VM (−7.3±2.7% to −3.3±5.0%) or RE (−7.7±2.9% to −6.4±3.3%). CONCLUSIONS: Repeated VM increased central artery stiffness without affecting central artery pressure wave reflection. Even though presented with a similar BP load, arterial stiffness did not increase following RE. Thus, alterations in BP may not be the underlying stimulus governing modulations in arterial wall properties following acute RE.