Increase In Arterial Stiffness Research Articles

Anticancer Therapy-Related Increases in Arterial Stiffness: A Systematic Review and Meta-Analysis.

BackgroundCardio‐oncology is a clinical discipline focused primarily on the early detection of anticancer therapy–related cardiomyopathy. However, there is growing evidence that the direct adverse consequences extend beyond the myocardium to affect the vasculature, but this evidence remains limited. In addition, there remains a paucity of clinically based strategies for monitoring vascular toxicity in these patients. Importantly, arterial stiffness is increasingly recognized as a surrogate end point for cardiovascular disease and may be an important vascular outcome to consider. Therefore, the aim of this systematic review and meta‐analysis was to summarize evidence of increased arterial stiffening with anticancer therapy and evaluate the effect of treatment modifiers.Methods and ResultsA total of 19 longitudinal and cross‐sectional studies that evaluated arterial stiffness both during and following anticancer therapy were identified using multiple databases. Two separate analyses were performed: baseline to follow‐up (12 studies) and control versus patient groups (10 studies). Subgroup analysis evaluated whether stiffness differed as a function of treatment type and follow‐up time. Standard mean differences and mean differences were calculated using random effect models. Significant increases in arterial stiffness were identified from baseline to follow‐up (standard mean difference, 0.890; 95% CI, 0.448–1.332; P<0.0001; mean difference, 1.505; 95% CI, 0.789–2.221; P≤0.0001) and in patient versus control groups (standard mean difference, 0.860; 95% CI, 0.402–1.318; P=0.0002; mean difference, 1.437; 95% CI, 0.426–2.448; P=0.0052). Subgroup analysis indicated differences in arterial stiffness between anthracycline‐based and non‐anthracycline‐based therapies (standard mean difference, 0.20; 95% CI, 0.001–0.41; P=0.048), but not follow‐up time.ConclusionsSignificant arterial stiffening occurs following anticancer therapy. Our findings support the use of arterial stiffness as part of a targeted vascular imaging strategy for the identification of early cardiovascular injury during treatment and for the detection of long‐term cardiovascular injury into survivorship.

The risk of developing chronic heart failure in patients with hypertension depending on the actual arterial stiffness

Objective. To determine the risk of developing chronic heart failure (CHF) in patients with hypertension (HTN) depending on the actual arterial stiffness.Material and Methods. The study included 175 patients with HTN without a verified diagnosis of heart failure. The average age was 48.5 ± 6.8 years. Patients underwent general clinical examination, volume sphygmoplethysmography assessments of cardio-ankle vascular index (CAVI), echocardiography study (left ventricular (LV) ejection fraction, LV diastolic function, LV myocardial mass index, indexed LV volume by echocardiography), and tests for serum N-terminal pro-B-type natriuretic peptide (NT-proBNP). Patients were divided into two groups depending on CAVI. Group 1 included 141 (80.6%) patients with CAVI &lt; 9; group 2 included 34 (19.4%) patients with CAVI &gt; 9.Results. In patients of group 1, the level of NT-proBNP was 0.008 [0.006; 5.770], which was significantly lower than the corresponding value in group 2, where the level of NT-proBNP was 13.08 [0.01; 350.65] ng/mL (p = 0.041). Indicators of odds ratio (OR) and relative risk (RR) were also significant. The chance of developing CHF with CAVI &gt; 9 increased by almost 7 times (OR = 6.9; 95% CI = 2.8–16.8), and OR of CHF onset was 4.1 (95% CI = 2.2–7.6). Sensitivity and specificity rates were 55.9% and 84.4%, respectively. Correlation analysis revealed a medium degree of dependence and direct relationships between NT-proBNP level and CAVI values (r = 0.35; p &lt;0.05).Conclusion. Serum level of NT-proBNP depended on the actual arterial stiffness. Patients with CAVI &gt; 9 indicative of an increase in true arterial stiffness had a greater risk of developing heart failure assessed based on the level of NT-proBNP in the blood. Further studies are required to assess the effects of arterial stiffness, registered within the intermediate values of CAVI index, on the risk of heart failure onset.

Physical Activity, Autonomic Function And Cerebral Pulsatility In Young Women

Cerebral pulsatility increases stress on the microvasculature of the brain causing damage. Age-related increases in arterial stiffness augment cerebral pulsatility via effects on large artery buffering capacity. Autonomic nervous system function also affect cerebral pulsatility by altering vascular tone. Physical activity (PA) may have a favorable effect on both vascular and autonomic function, and in turn, cerebral pulsatility. PURPOSE: 1) Determine the relationship between aortic stiffness and autonomic function with cerebral pulsatility index (PI) in young women. 2) Explore the role of PA as a potential correlate. METHODS: Eighty-two women (21±4 years) participated in this study. Moderate-to-vigorous physical activity (MVPA) was measured for 7 days using an accelerometer. Body composition was assessed using air displacement plethysmography. Middle cerebral artery PI was determined via transcranial Doppler. Aortic stiffness was measured via carotid-femoral pulse wave velocity (cf-PWV) using applanation tonometry. Autonomic function was assessed via heart rate variability (HRV). Low frequency (LF) power of HRV was used as a measure of sympathetic activity, while high frequency (HF) power of HRV was used as a measure of parasympathetic activity. RESULTS: PI was not significantly correlated with cf-PWV (r=-0.03, p=0.82) or lnHF (r=0.25, p=0.06). There was a significant, positive association between lnLF and PI (r=0.39, p=0.002). MVPA was not associated with cf-PWV (r=-0.18, p=0.13), lnLF (r=0.01, p=0.95) or PI (r=-0.04, p=0.79). CONCLUSION: Sympathetic activity is a more prominent correlate of cerebral pulsatility than large artery stiffness in young women. Sympathetic tone may increase vasoconstriction of the cerebral vasculature resulting in augmentation of cerebral pulsatility. Physical activity was not associated with vascular or autonomic correlates of cerebral pulsatility in young women. Supported by NIH Grant 1R03MD011306-01A1

Racial Differences In Cardiovascular Responses Following Acute Bouts Of Anaerobic Exercise

Despite the growing popularity of high-intensity anaerobic exercise, few studies have examined the acute effects of this form of exercise on cardiovascular hemodynamics, or potential racial differences in these responses. In addition, post exercise hypotension may be absent in African Americans (AA) following aerobic exercise, consistent with their higher risk for hypertension. It is unknown whether AA and Caucasian Americans (CA) would exhibit different blood pressures following acute bouts of anaerobic exercise. PURPOSE: To assess hemodynamic changes in healthy, young AA and CA women following repeated bouts (two) of maximal anaerobic exercise. METHODS: Eight young, healthy AA women and 9 CA women completed this study. Vascular and hemodynamic measurements were taken at rest, and 5 (P5-1st), 15 (P15-1st), and 30 minutes (P30-1st) following a maximal anaerobic exercise test on cycle ergometer, and 5 (P5-2nd), 15 (P15-2nd), and 30 (P30-2nd) minutes following the second maximal anaerobic exercise test. Brachial systolic (SBP), diastolic (DBP) blood pressures, central aortic SBP, DBP and mean arterial blood pressure (aortic MAP) were measured. Carotid arterial stiffness (beta-stiffness index) were obtained using ultrasonography. RESULTS: Data were presented in Table 1 as mean ± standard error. Resting DBP and aortic DBP were significantly different between AA and CA (§ p<0.05). There was a significant race by time interaction for aortic MAP (* p<0.05). And there was a trend towards significance in race by time interaction for beta stiffness index (p=0.06). CONCLUSION: Acute bouts of anaerobic exercise increase aortic MAP in young AA but not in CA, and it may be related to increases in arterial stiffness in AA. The heightened BP and vascular responses to exercise stimulus may play a role in the pathogenesis of hypertension in AA. Supported by New England ACSM New Investigator Award to HY.Table 1: Hemodynamic responses to two acute bouts of maximal anaerobic exercise.

Reproducibility Of The Impact Of Menstrual Phase On Arterial Stiffness Over Two Consecutive Menstrual Cycles

Chronic increases in arterial stiffness are associated with increased risk of cardiovascular disease. Estrogen (E2), the primary female sex hormone, has been found to have cardioprotective effects, with several but not all, studies reporting a reduction in arterial stiffness in the late follicular (high E2; LF) phase compared to the early follicular (low E2; EF) phase of the menstrual cycle. Individual heterogeneity in the impact of phase on arterial stiffness and the consistency of these responses across consecutive cycles has yet to be explored. PURPOSE: to determine the impact of menstrual phase E2 fluctuations on arterial stiffness over two consecutive cycles. METHODS: 13 premenopausal women completed 4 experimental visits over 2 menstrual cycles (EFvisit 1, LFvisit 2, EFvisit 3, LFvisit 4). Central (CF) and peripheral (FF) PWV were measured twice during each visit using arterial tonometry. Participants were classified as positive, negative or non-responders, wherein positive responders experienced a reduction in PWV from EF to LF and negative responders experienced an increase in PWV from EF to LF that was greater than 2*typical error. RESULTS: At the group level, CF PWV did not differ between phases (p=0.11) or cycles (p=0.18; EFvisit 1=5.8±0.8, LFvisit 2=5.6±0.5, EFvisit 3=5.9±0.6, LFvisit 4=5.8±0.7). Likewise, FF PWV did not differ between phases (p=0.979) or cycles (p=0.58; EFvisit 1=8.1±1.0, LFvisit 2=8.1±1.1, EFvisit 3=7.9±1.4, LFvisit 4=8.0±1.3). Phase changes in E2 were not associated with phase changes in PWV in cycle 1 (CF: r=0.38, p=0.20; FF: r=0.11, p=0.73) or cycle 2 (FF: r=0.38, p=0.36). Classification of individuals as responders or non-responders revealed that no participants were consistently positive or negative responders for both cycles. CONCLUSION: At the group level, arterial stiffness was not impacted by menstrual phase over two cycles. Individual changes in arterial stiffness were inconsistent, with phase changes in cycle 1 not reflecting phase changes in cycle 2. Variability in phase changes in arterial stiffness does not appear to be driven by inter-individual differences in E2 fluctuation across phase. Future research is needed to investigate the mechanisms resulting in inter-individual variability in arterial stiffness and inconsistency between cycles. Funded by NSERC

Prospective evaluation of vascular changes in acute respiratory infections in children with cystic fibrosis

Background/aim Acute exacerbations and chronic inflammation are risk factors for cardiovascular disease (CVD) in cystic fibrosis (CF) patients. The aim of this study was to investigate the effects of acute exacerbation therapy on arterial stiffness in children with CF.Materials and methods Augmentation index (Aix) and pulse wave velocity (PWV) were measured before and after treatment and 1 month after the end of treatment in patients with acute exacerbation. The relationship between hemodynamic measurements and c-reactive protein (CRP) and pulmonary function tests (PFTs) was investigated.Results Measurements before and after treatment were evaluated in 27 patients and were repeated in 21 patients who were clinically stable 1 month following acute exacerbation. There was a significant decrease in CRP and an increase in spirometry parameters after treatment. While no significant difference was found between PWV (P = 0.33), a significant difference for Aix before (41.95 ± 12.96%) and after (30.95 ± 11.47%) treatment and before treatment and stable clinical condition (34.19 ± 14.36%) was obtained (P =0.00, and P =0.01, respectively). No significant difference in heart rate and other hemodynamic measurements was found. Pretreatment Aix is associated with poor clinical condition (PFTs, BMI, and clinical score) and systemic inflammation (CRP) (P <0.05).Conclusion The decrease of arterial stiffness (Aix) with acute exacerbation treatment in children with CF has been demonstrated. This result shows that systemic inflammation in CF may cause an increase in arterial stiffness and recurrent exacerbations may increase the risk of CVD.

Role of Changes in State of Bound Water and Tissue Stiffness in Development of Age-Related Diseases.

An essential effect of environmental stiffness on biological processes in cells at present is generally accepted. An increase in arterial stiffness with advanced age has been reported in many publications. The aim of the present review is to summarize current information about possible chemical reactions and physical processes that lead to tissue stiffening and result in age-related diseases in order to find methods that can prevent or retard time-dependent tissue stiffening. The analysis of published data shows that bound water acts as a plasticizer of biological tissues, a decrease in bound water content results in an increase in biological tissue stiffness, and increased tissue stiffness leads to NF-kB activation and triggered actin polymerization—NF-kB activation is associated with age-related diseases. It can be suggested that changes in bound water content through changing tissue stiffness can affect cellular processes and the development of pathologies related to aging. Both age-related diseases and COVID-19 may be associated with tight-junction disruption and increased tissue stiffness and permeability.

Cerebrovascular reactivity: a new frontier for measuring cognitive health in models of accelerated ageing?

Cerebrovascular reactivity: a new frontier for measuring cognitive health in models of accelerated ageing?

Correlation of arterial stiffness parameters with indicators of carotid atherosclerosis in patients with Metabolic Syndrome

Background: Many studies have shown that metabolic syndrome is accompanied by an increase in arterial stiffness. In connection therewith, early detection of an increase in arterial stiffness in patients with metabolic syndrome can help to prevent cardiovascular complications. Aim: To determine the relationship between arterial stiffness parameters such as cfPWV and CAVI with carotid atherosclerosis indicators (intima-media thickness, carotid plaque presence) in patients with metabolic syndrome. Material and methods: The study included 100 patients at the age of 40-70 years: 45 men and 55 women (56.54±8.98 years). Subjects were divided into 2 groups: 1st - 42 patients with metabolic syndrome; 2nd - 58 patients without metabolic syndrome. The arterial stiffness parameters such as CAVI and cfPWV were calculated. In the analysis we used threshold values recommended by manufacturers and European expert consensus document on arterial stiffness: for CAVI – <8, for cfPWV – ≤10 m/c). Duplex scanning carotid arteries was performed to evaluate the “intima-media thickness” and carotid plaque presence. Results: In the group with metabolic syndrome the CAVI is significantly associated with the indicators of carotid atherosclerosis: intima-media thickness (OR=4.94 95%; CI: 1.49-3.80; p=0.047), carotid plaque presence (OR=3.06; 95% CI: 1.42-2.28; p=0.065). But statistically significant associations of cfPWV with indicators of carotid atherosclerosis were not obtained (p>0.05). In the group without metabolic syndrome none of the arterial stiffness parameters (CAVI, cfPWV) statistically significantly correlated with any of the carotid atherosclerosis indicators (p>0.05). Conclusion: The CAVI parameter, in contrast to the cfPWV, statistically significantly correlated with indicators of carotid atherosclerosis in patients with metabolic syndrome. In this connection, this parameter can be used to identify signs of not only increased arterial stiffness but also to determine subclinical signs of carotid atherosclerosis in patients with metabolic syndrome.

Adverse Childhood Experiences (ACEs) Predict Increased Arterial Stiffness from Childhood to Early Adulthood: Pilot Analysis of the Niagara Longitudinal Heart Study.

An association among adults between adverse childhood experiences (ACEs) and arterial stiffness and between arterial stiffness and cardiovascular disease has been established. Recent cross-sectional evidence suggests that ACEs is linked to the development and progression of arterial stiffness, but it remains unclear when these changes begin to manifest. We examine the relationship between ACEs and changes in arterial stiffness from childhood into adulthood using population-based longitudinal data. The Niagara Longitudinal Heart Study (NLHS) pilot data included 76 young adults (females = 44), with an average age of 21years (SD = 1), and had a follow-up period of 9years. Mixed effects modeling was used to examine the effect of ACEs on changes in arterial stiffness over time adjusting for sex, changes in heart rate, systolic blood pressure, body mass index, and physical activity. Individuals with four or more ACEs have a greater increase in arterial stiffness over time from childhood into young adulthood. This increase was similar for both males and females and independent of the effects of change in heart rate, systolic blood pressure, body mass index, and physical activity. Exposure to ACEs is associated with greater increase in arterial stiffness, a marker for cardiovascular disease among adults. This suggests that interventions targeted at individuals with high exposure to ACEs early on in life could lower the risk of arterial stiffness and in turn the cascade of events leading to cardiovascular disease.

Antioxidant cocktail following a high-sodium meal does not affect vascular function in young, healthy adult humans: a randomized controlled crossover trial

Chronic high sodium intake is a risk factor for cardiovascular disease as it impairs vascular function through an increase in oxidative stress. The objective of this study was to investigate the acute effects of a high-sodium meal (HSM) and antioxidant (AO) cocktail on vascular function. We hypothesized that a HSM would impair endothelial function, and increase arterial stiffness and wave reflection, while ingestion of the AO cocktail would mitigate this response. Healthy adults ingested either an AO cocktail (vitamin C, E, alpha-lipoic acid) or placebo (PLA) followed by a HSM (1500 mg) in a randomized crossover blinded design. Blood pressure (BP), endothelial function (flow-mediated dilation; FMD) and measures of arterial stiffness (pulse wave velocity; PWV) and wave reflection (augmentation index; AIx) were made at baseline and 30, 60, 90, and 120 min after meal consumption. Forty-one participants (20M/21W; 24 ± 1 years; BMI 23.4 ± 0.4 kg/m2) completed the study. Mean BP increased at 120 min relative to 60 min (60 min: 79 ± 1; 120 min: 81 ± 1 mmHg; time effect P = .01) but was not different between treatments (treatment × time interaction P = .32). AIx decreased from baseline (time effect P < .001) but was not different between treatments (treatment × time interaction P = .31). PWV (treatment × time interaction, P = .91) and FMD (treatment × time interaction P = .65) were also not different between treatments. In conclusion, a HSM does not acutely impair vascular function suggesting young healthy adults can withstand the acute impact of sodium on the vasculature and therefore, the AO cocktail is not necessary to mitigate the response.

Increased Arterial Stiffness Measured By Carotid Femoral (Aortic) Pulse Wave Velocity In Patients with Inactive Behçet's Disease.

Introduction Behçet's disease (BD) is a chronic, multisystemic disease characterised by vascular involvement. Acute and chronic inflammatory processes associated with BD may cause endothelial dysfunction, which can then lead to a subsequent increase of arterial stiffness and altered pressure wave reflections. The aim of this study was to evaluate the pulse wave velocity (PWV) measurements in patients with inactive BD and control subjects.Methods We studied 50 patients with inactive BD and 49 healthy control subjects without known cardiovascular disease. Carotid-femoral PWV was determined in all subjects by the same expert research clinician using Complior device (Colson, Paris, France).Results Mean disease duration was 3.23±2.31 years. Patients with BD (mean age 36.04±9.94 years) had significantly higher PWV levels compared to controls (9.57±1.88 vs. 8.47±1.13 m / s; p=0,003). PWV was found to be positively correlated with age, systolic, diastolic, mean blood pressure, waist, and waist / hip ratio.Conclusion In our study we demonstrated that patients with BD exhibit significantly increased arterial stiffness assessed by increased carotid-femoral PWV compared to healthy control subjects.

Adults With Type 2 Diabetes Mellitus Exhibit a Greater Exercise-Induced Increase in Arterial Stiffness and Vessel Hemodynamics.

Individuals with type 2 diabetes mellitus (T2DM) have a greater blood pressure (BP) response to acute maximal exercise compared to those without T2DM; however, whether they exhibit a different arterial stiffness response to maximal exercise has yet to be explored. Adults with (n=66) and without T2DM (n=61) underwent an arterial stress test: at rest and immediately postexercise, carotid-femoral pulse wave velocity, the gold standard measure of arterial stiffness, brachial BP, heart rate, and other hemodynamic measurements were assessed. Linear regression models were used to evaluate between-group differences at rest, and the response to exercise (postexercise value), adjusting for covariates including BP and heart rate when relevant, and the corresponding baseline value of each parameter. All participants (mean±SD: age 59.3±10.6 years; body mass index 31.2±3.9 kg/m2) had hypertension (mean BP 130±14/80±9 mm Hg). At rest, participants with T2DM had significantly higher carotid-femoral pulse wave velocity (10.3±2.7 versus 9.1±1.9 m/s), heart rate (69±11 versus 66±10 beats/min), and lower diastolic BP (79±9 versus 83±9 mm Hg), but systolic BP (129±15 versus 131±13 mm Hg) was similar. In response to exercise, participants with T2DM showed greater increases in carotid-femoral pulse wave velocity (1.6 [95% CI, 0.4-2.9 m/s]) and systolic BP (9 [95% CI, 1-17 mm Hg]) than participants without T2DM. A greater proportion of participants with T2DM had a hypertensive response to exercise compared to participants without T2DM (n=23, 35% versus n=11, 18%; P=0.033). By incorporating exercise as a vascular stressor, we provide evidence of a greater increase in arterial stiffness in individuals with T2DM, independently of resting arterial stiffness, and the BP postexercise.

Impact of Vitamin E supplementation on vascular function in haptoglobin genotype stratified diabetes patients (EVAS Trial): a randomised controlled trial

AimsVitamin E (Vit-E) may preferentially improve cardiovascular risk in haptoglobin 2-2 (Hp2-2) genotype diabetes individuals. We studied the impact of Vit-E supplementation on vascular function in diabetes individuals stratified by haptoglobin genotype in Singapore.MethodsIn this 24-week, double blind, placebo-controlled RCT, we recruited 187 subjects (101 Hp2-2, 86 non-Hp2-2). Intervention: alpha-tocopherol-400 IU. Primary Outcome: Change in EndoPAT-derived reactive-hyperaemia index (RHI) and augmentation index (AIx); Secondary Outcomes: Pulse-Wave velocity (Sphygmocor-PWV), carotid intima media thickness (CIMT), inflammation (hsCRP), derivatives of reactive-oxygen metabolites (dROMs), biological antioxidant-potential (BAPs), HbA1c, LDL-C, HDL-C and oxidised LDL-C (ox-LDL).ResultsOverall, with Vit-E supplementation no significant change in RHI, PWV, CIMT, hsCRP, dROMS, BAPs, HDL-C and HbA1c was observed (p > 0.05); an increase in LDL-C with concomitant decrease in ox-LDL, and incidentally increase in eGFR was observed (p < 0.05). No interaction effect with haptoglobin genotype was seen for all outcomes (p > 0.05). Subgroup analysis: In the non-Hp-2-2 group, Vit-E supplementation led to a higher EndoPAT-derived AIx, accompanied by higher LDL and ox-LDL concentrations (p < 0.05); Hp2-2 group: Vit-E supplementation led to higher eGFR when compared to the non-Hp2-2 group (exploratory) (p < 0.05). We observed an interaction effect for baseline haptoglobin concentration (threshold > 119 mg/dl) with intervention in terms of increased EndoPAT-derived AIx in the Hp > 119 mg/dl group whereas no change in the group with Hp ≤ 119 mg/dl.ConclusionVit-E supplementation did not show any preferential benefit or deleterious effect on vascular function in Hp2-2 diabetes subjects in Singapore. A possible deleterious effect of an increase in arterial stiffness in individuals with Hp > 119 mg/dl was observed. Future studies should consider personalisation based on baseline Hp concentrations in patients with T2DM rather than just Hp2-2 genotype to evaluate impact on the detailed lipid pathways, cardiac and renal physiology. The impact of ethnic differences needs to be explored in greater details.

Ethnicity and Arterial Stiffness.

Early vascular aging reflects increased arterial stiffness of central blood vessels at young chronological ages and powerfully predicts cardiovascular events and mortality, independent of routine brachial blood pressure and other risk factors. Since ethnic disparities exist in routine blood pressure, in hypertension and cardiovascular outcomes, this review evaluates major studies comparing arterial stiffness through the life course between different ethnic groups or races (which have no biological definition)-in children, adolescents, young, and middle-aged adults and the very elderly. Most report that compared with white European-origin samples, populations of black African descent have increased central arterial stiffness throughout different life stages, as well as a more rapid increase in arterial stiffness at young ages. Exceptions may include African Caribbean origin people in Europe. Differences in vascular structure and function are clearest, where obesity, socioeconomic, and psychosocial factors are most marked. Few studies evaluate a wider spectrum of ethnic groups or factors contributing to these ethnic disparities. Genetic effects are not obvious; maternal risk and intergenerational studies are scarce. Nevertheless, across all ethnic groups, for given levels of blood pressure and age, some people have stiffer central arteries than others. These individuals are most at risk of vascular events and mortality and, therefore, may benefit from early, as yet untested, preventive action and treatment.

Age‐Related Increase in Extra‐Media Thickness is Associated with Arterial Stiffening and Carotid Blood Pressure

Older age is a primary risk factor associated with future cardiovascular disease (CVD) related events. Age‐related changes in perivascular adipose tissue (PVAT) and vascular remodeling both contribute to arterial stiffening and increased blood pressure which are established CVD risk factors. The non‐invasively measured extra‐media thickness (EMT) is a novel and composite measure, which includes PVAT, arterial adventitia, and the jugular vein that may provide translational insight for these factors contributing to age‐related arterial stiffening and higher blood pressure. However, it is unknown if aging increases EMT and is associated with arterial stiffness and blood pressure. We hypothesized that age‐related increases in EMT will be associated with higher arterial stiffness and blood pressure. Forty participants (young: 8M/12F, 23.2 ± 1.1 yrs and middle‐aged/older: 7M/13F, 60.7 ± 9.4 yrs) underwent measures of blood pressure (brachial; carotid), arterial stiffness (carotid b‐stiffness), EMT via ultrasonography and body composition with dual x‐ray absorptiometry. All measurements were taken in the supine position. Group mean differences between young and middle‐aged/older participants were analyzed with unpaired t‐tests and Pearson correlations were used to assess relations between EMT and arterial stiffness and blood pressure endpoints. Compared to younger participants, middle‐aged/older participants had higher EMT (0.80 ± 0.03 vs. 0.69 ± 0.02 mm), carotid beta stiffness (3.24 ± 0.08 vs. 2.60 ± 0.04), carotid SBP (116.5 ± 4.9 vs. 99.1 ± 2.3 mmHg), and carotid PP (44.6 ± 4.2 vs. 34.8 ± 1.5 mmHg) (all, p&lt;0.05). Brachial SBP was not different between groups (p&gt;0.05). Carotid beta stiffness (r= 0.410), carotid SBP (r= 0.501), and carotid PP (r= 0.5037) were all positively correlated with EMT for the entire cohort (all, p&lt;0.05). Our findings indicate that there is an age‐related increase in EMT that is associated with both carotid arterial stiffness and pressure. These data suggest that increases in arterial stiffness and blood pressure with advancing age may be attributable, in part, to increases in EMT, which may be due to changes in PVAT and arterial adventitial remodeling. Therefore, EMT, a potential surrogate for PVAT and arterial remodeling, may provide novel insight into age‐related arterial stiffening, higher blood pressure and increased CVD risk with aging.

Effect of Anti‐hypertensive Treatment Lisinopril on Central Arterial Stiffness and Cognitive Functions in Adult Hypertensive Dahl Salt‐Sensitive Rats

Effect of Anti‐hypertensive Treatment Lisinopril on Central Arterial Stiffness and Cognitive Functions in Adult Hypertensive Dahl Salt‐Sensitive Rats

Two Distinct Classes of Heart Failure with Preserved Ejection Fraction Emerge from Analysis of Standard Clinical Measures using Mechanistic Models of the Cardiovascular System

Diagnosis and treatment of heart failure are determined through the analysis of echocardiography (EC) and right heart catheterization (RHC) measures made in the clinic. To uncover the underlying causes of heart failure with reduced ejection fraction (HFrEF, ejection fraction &lt; 50%) and heart failure with preserved ejection fraction (HFpEF, ejection fraction &gt; 50%), thirty‐one patient records (ten HFrEF, twenty‐one HFpEF) have been obtained from the Cardiovascular Health Improvement Project (CHIP) database at the University of Michigan. Using these patient specific EC and RHC measures, we identify key parameters representing mechanical and hemodynamic function including systemic arterial stiffness, contractility of the right and left ventricle, diastolic relaxation as well as ventricular filling in a closed loop model of the cardiovascular system. Model simulations were tuned to match RHC and EC measures of systolic and diastolic pressures in the right ventricle, pulmonary artery, and aorta, along with cardiac output, pulmonary capillary wedge pressure, and left ventricular volumes in each patient with average error between data and model of 6.0 ± 2.3%. The underlying physiological parameters of these thirty‐one tuned models were then plotted against model‐based norms (blue dotted line in Figure 1 below) and compared between the HFrEF and HFpEF groups. Our results confirm that the main parameter driving HFrEF is reduced left ventricular contractility, while for HFpEF there is an evident increase in systemic arterial stiffness and left ventricle elastance, and a reduced relaxation during diastolic filling. Conducting a Principal Component Analysis (PCA) of both clinical measures and optimized model parameters shows a distinct group of HFpEF patients sharing strong patterns with our HFrEF cohort. However, only the analysis of our optimized parameters give us an understanding of the mechanistic differences between the two HFpEF groups. The optimized parameter PCA indicates significant differences (p‐value&lt;. 05) in left ventricular active contractility, left ventricular relaxation, right ventricular relaxation and systemic arterial stiffness when comparing our classical HFpEF patients to those grouped as similar to HFrEF. These results as well as the wide range of parameter values in HFpEF supports the observed clinical heterogeneity and suggests that cardiovascular system modeling of standard clinical data is able to phenotype and group HFpEF as different sub diagnoses, elucidating patient specific treatment strategies for these patients.Support or Funding InformationThis work is supported by grants from the National Institute of Health HL139813, R01 HL139813, U01 HL122199, T32GM008322, F31HL149214Normalized model parameters from analysis of clinical measures. A: Ejection fraction from patient data records. Panels B, C and D: Left ventricular active contractility, systemic arterial stiffness and left ventricular passive stiffness, respectively. Model parameters are normalized to a value representing normal cardiovascular function. Gray dashed line is average, light dotted is standard deviation and the grey box contains the middle 50% of the parameter values.Figure 1

Central and peripheral blood pressures and arterial stiffness increase in hypoparathyroidism.

Objective The aim of the present study was to evaluate whether arterial stiffness is affected in the patients with hypoparathyroidism through pulse wave analysis (PWA). Subjects and methods Sixty-three patients diagnosed with hypoparathyroidism and sixty volunteers were evaluated for the study. When 21 patients were excluded in the hypoparathyroidism group due to exclusion criteria, the research continued with 42 patients and 60 volunteers who are similar to the patients in terms of age, gender and body mass index (BMI). Fasting plasma glucose after 10 hours of fasting, creatinine, thyroid stimulating hormone (TSH), free thyroxine (fT4), albumin, calcium, phosphorus, magnesium, 25-OH vitamin D, parathormone (PTH) and urine calcium results in 24-hour urine for the patients in the hypoparathyroidism group were recorded. Evaluation of arterial stiffness was performed by Mobil-O-Graph 24h PWA device. Results Systolic blood pressure (SBP) (p = 0.01), diastolic blood pressure (DBP) (p = 0.005), mean blood pressure (p = 0.009), central SBP (p = 0.004), central DBP (p = 0.01) and pulse wave velocity (PWV) (p = 0.02) were found higher in the hypoparathyroidism group. A positive correlation was detected between phosphorus level and SBP [(p = 0.03. r = 0.327)], central SBP [(p = 0.04, r = 0.324)] and PWV [(p = 0.003, r = 0.449)]. We detected that age and serum phosphorus levels were independent predictor variables for PWV (B = 0.014, p < 0.001 and B = 0.035, p < 0.001, respectively). Conclusion We detected that hypoparathyroidism causes an increase in blood pressure and arterial stiffness. The most significant determinant factors were detected as advanced age and hyperphosphatemia. The patients diagnosed with hypoparathyroidism should be closely monitored and treatment planning should include to prevent the patients from hyperphosphatemia.

Clinical and diagnostical value of 24-hour arterial stiffness monitoring in patients with bronchial asthma

To evaluate 24-hour dynamics of the arterial stiffness main indicators in patients with bronchial asthma of various severity and control. The study included 119 patients with bronchial asthma, who formed main groups: the first group 48 patients with mild and moderate asthma, the second 71 patients with severe asthma. All patients underwent the vascular stiffness parameters study using a multifunctional complex for the 24-hour monitoring and office measurements of blood pressure and vessels condition. At the same time vascular stiffness indicators were examined: PWVao pulse wave velocity in the aorta (m/s); Aix augmentation index (%); ASI the arterial stiffness index (mmHg). When comparing the 24-hour arterial stiffness dynamics indicators, changes were found in patients with severe asthma and non-control. Thus, a statistically significant increase in the pulse wave velocity in the aorta and augmentation index in second group compared to patients of the 1st group and control subjects. In patients with severe asthma Aix at night is significantly higher than daytime, which indicates an increase in arterial stiffness at night. Patients with severe bronchial asthma have increased arterial stiffness in comparison with controls and mild and moderate asthma. Also, in patients with severe asthma arterial stiffness parameters were higher at night-time in comparison with daytime.