Elevated Arterial Stiffness Research Articles

The modified 6-chromanol SUL-238 protects against accelerated vascular aging in vascular smooth muscle Ercc1-deficient mice

Introduction: Vascular aging is marked by increased mitochondrial reactive oxygen species (ROS) production, which leads to decreased nitric oxide (NO)-mediated vasodilation. Loss of NO can be partially compensated by endothelium-derived hyperpolarization (EDH), which partly relies on increased mitochondrial Ca2+ release to maintain vascular dilation. Thus, intervention in mitochondria may target both NO and EDH signaling to alleviate aging-related vascular dysfunction. DNA damage by mitochondrial ROS is an important cause of organismal aging. Previous work showed that local vascular Ercc1 knockout dramatically accelerates vascular aging. The aim of the study was to investigate the effect of chronic treatment with the modified 6-chromanol, SUL-238, an inhibitor of mitochondrial reverse electron flux and ROS, in a mouse model of accelerated vascular smooth muscle aging induced by DNA repair endonuclease Ercc1 knockout (SMC-KO). Aim: The aim of the study was to investigate the effect of chronic treatment with the modified 6-chromanol, SUL-238, an inhibitor of mitochondrial reverse electron flux and ROS, in a mouse model of accelerated vascular smooth muscle aging induced by DNA repair endonuclease Ercc1 knockout (SMC-KO). Methods: SMC-KO mice and healthy wild-type littermates received SUL-238 (90 mg/kg/day) in drinking water from 12 to 22 weeks of age. At the age of 21 weeks, arterial stiffness was measured in vivo with echography and they were euthanized at the age of 22 weeks. Ex vivo vascular function was assessed in wire myography setups and mitochondrial function of the thoracic aorta was assessed using a seahorse assay. Results: SMC-KO mice showed reduced EDH-mediated vasodilation, elevated arterial stiffness, and increased elastin breaks at 22 weeks of age compared to their wild-type littermates. SUL-238 improved EDH, thus restoring aortic and mesenteric relaxation in SMC-KO mice. Furthermore, the number of elastin breaks was reduced and arterial stiffness normalized after treating SMC-KO mice with SUL-238. Mitochondrial respiration measured in the aorta was not different between the groups. Conclusion: Chronic treatment with SUL-238 alleviates features of vascular aging, including decreased vasodilation and increased arterial stiffness. SUL-238 seems to have a more general effect on aging rather than involving a direct coupling between mitochondrial function and vascular signaling. SUL-238 is the first small-molecule drug reported to increase EDH after chronic treatment.

Resistive index of central retinal artery, aortic arterial stiffness and OCTA correlated parameters in the early stage of fabry disease

This study aimed to evaluate the impact of Fabry disease (FD) on retinal microvasculature using optical coherence tomography angiography (OCTA), arterial stiffness, and the resistive index (RI) of the central retinal artery (CRA) in early disease stages. Twenty-nine genetically confirmed FD patients and twenty-six healthy controls were enrolled. Vessel density (VD) values of the superficial, deep, and choriocapillaris plexuses (SCP, DCP, and CC) were measured via OCTA. CRA RI was studied using color Doppler and grayscale sonography, and aortic pulse wave velocity (PWV) was assessed with the Complior method. CRA RI was significantly lower in the control group compared to the Fabry group (p < 0.001). Central VD was found to be significantly higher in the control group compared to the Fabry group in all the retinal layers (SCP (p < 0.001), DCP (p < 0.005), CC (p < 0.001)). PWV was significantly higher in the Fabry group than in the control group (p = 0.03). Fabry disease patients demonstrate elevated arterial stiffness, increased CRA RI, and diminished retinal microvascular density compared to healthy controls, indicating early ocular damage. Continuous monitoring and targeted screening for organ impairment are crucial in FD management. Identifying biomarkers for assessing ocular vascular involvement and treatment response is imperative. Further research is needed.

Blood eosinophil count is associated with early atherosclerotic artery changes in asthma

ObjectiveAsthma is linked to atherosclerosis, yet the underlying mediators remain elusive. Eosinophils may contribute to both asthmatic and atherosclerotic inflammation. Hence, this study aimed to explore the potential associations of eosinophils with artery changes among patients with asthma.MethodsWe assessed strain values of the common carotid arteries (CCAs) via vascular speckle tracking and compared asthma patients with low (< 300/µl) and high (≥ 300/µl) blood eosinophil counts (BEC).ResultsWe enrolled 100 patients, 42 with a BEC of < 300 and 58 with a BEC of ≥ 300 n/µl. Patients with high BEC exhibited more severe disease, characterized, e.g., by a higher frequency of acute exacerbations (1.3 ± 2.1 vs. 2.6 ± 2.4 n/year, p = 0.005). Both groups presented similar profiles in terms of conventional cardiovascular risk. The high BEC group demonstrated elevated arterial stiffness, reflected by reduced radial strain (mean radial strain of the right CCA: 2.7 ± 1.4% for BEC ≥ 300 n/µl vs. 3.5 ± 1.7% for BEC < 300 n/µl, p = 0.008; left CCA: 2.6 ± 1.4% vs. 4.1 ± 2.2%, p < 0.001). A weak yet statistically significant negative correlation was observed between BEC and radial strain for the right CCA (R2 = 0.131, b=-0.001, p = 0.001) and left CCA (R2 = 0.086, b=-0.001, p = 0.015). However, the prevalence of cerebrovascular disease was similar in both groups (31,0% vs. 50,0%, p = 0.057).ConclusionWe identified a correlation between BEC and vascular stiffness, which supports the hypothesis that eosinophils may promote atherosclerosis.Clinical trial numberDue to the exploratory and predominantly retrospective nature of the study, trial registration was not conducted. The only prospective procedure conducted was the angiological sonography to evaluate the current state. No ensuing health-related interventions were performed specifically for this study.

Lactoferrin in Pediatric Chronic Kidney Disease and Its Relationship with Cardiovascular Risk.

Pediatric CKD is associated with a high risk of cardiovascular disease (CVD). Early detection of subclinical CVD in childhood CKD can be achieved through various cardiovascular (CV) assessments, including carotid intima-media thickness (cIMT), ambulatory blood pressure monitoring (ABPM), and arterial stiffness indices. Lactoferrin (LF), a key functional glycoprotein found in breast milk, has been linked to several diseases and has potential as a biomarker. In our study of 102 children with CKD stages G1-G4, we explored the relationship between LF and CV risk markers. We found that LF concentration was not related to the severity or underlying causes of childhood CKD, but was positively correlated with overweight/obesity. Lower LF levels were correlated with increased cIMT and elevated arterial stiffness indices. Notably, abnormalities in ABPM profiles were observed in up to 60% of the children with CKD, with low LF levels linked to nighttime hypertension, nocturnal non-dipping, and ABPM abnormalities. In conclusion, LF shows promise as a biomarker for detecting subclinical CVD in children with CKD. Its potential utility in early detection could be instrumental in guiding timely interventions and improving long-term CV outcomes, although further research is needed to clarify the underlying mechanisms.

Association between Mixed Heavy Metal Exposure and Arterial Stiffness, with Alkaline Phosphatase Identified as a Mediator.

Elevated arterial stiffness has been associated with exposure to heavy metals such as lead (Pb) and cadmium (Cd). However, the collective impact of multiple metals and the underlying mechanisms are not fully elucidated. The purpose of this study was to assess the combined effects of exposure to nine heavy metals on arterial stiffness and explore whether serum alkaline phosphatase (ALP) acts as a mediator in this relationship. In the retrospective analysis, data from 8,700 participants were retrieved from the National Health and Nutrition Examination Survey (NHANES) spanning from 1999 to 2018. Arterial stiffness was measured by estimated pulse wave velocity (ePWV). The cumulative impact of exposure to multiple metals was examined using adaptive elastic-net, environmental risk score, weighted quantile sum regression, and quantile g-computation. Additionally, mediation analysis was conducted to explore the potential mediating role of serum ALP. We found that combined exposure to multiple metals was consistently associated with elevated ePWV, with Ba, Pb, and Sb exhibiting the greatest contributions. Notably, serum ALP partially mediated the associations between individual (Pb, Sb) and mixed metal exposure with ePWV, with mediation proportions at 10.76% for Pb, 18.22% for Sb, and 11.07% for mixed metal exposure. In conclusion, this study demonstrates a clear association between exposure to heavy metals, either individually or in combination, and heightened arterial stiffness. Furthermore, the findings suggest that serum ALP activity may act as a mediator in these relationships.

Arterial stiffness and genetic polymorphism of some cytokines in normotensive patients with ankylosing spondylitis

Aim of the study was to identify the incidence of arterial stiffness in normotensive patients with ankylosing spondylitis (AS) in the Trans-Baikal region, to study polymorphism of genes for some cytokines and prognostic factors for increased arterial stiffness in this disease. Material and methods. We examined 100 patients with AS, natives of the Transbaikal region, HLA-В27 positive and 100 healthy controls, HLA-B27 negative; all included in the study were Caucasian. Arterial hypertension was an exclusion criterion. Determination of single nucleotide polymorphisms of the genes IL1B (‒31T/C, rs1143627), IL10 (‒592C/A, rs1800872), IL10 (‒819C/T, rs1800871), TNF (‒308G/A, rs1800629) was carried out in all patients with AS and healthy individuals. 74 patients with AS and 40 patients in the control group underwent applanation tonometry using SphygmoCor (AtCor Medical, Australia). Results. Pulse wave velocity on the carotid-femoral segment in patients with AS was 6.5 [4.1; 11.7] m/s, in the control group – 5.2 [3.9; 7.0] m/s (p = 0.0001). In 18 patients with AS (24.32 %) it was more than the age norm, these patients made up the group with elevated arterial stiffness. In patients with AS, carriage of the homozygous AA genotype of the IL10 gene (rs1800872, ‒592C/A) was 2.18 times more common, the homozygous GG genotype of the TNF gene (rs1800629, ‒308G/A) was 1.23 times more common, and the heterozygous ST genotype of the IL10 gene (rs1800871, ‒819C/T) was 1.5 times more common than in the control group. Prognostic factors for increased arterial stiffness in patients with AS were carriage of the IL10 rs1800871 polymorphism, age, and the radiological stage of changes in the sacroiliac joints. Conclusions. Increased arterial stiffness was detected in 24.3 % of normotensive patients with AS. The CT genotype of the IL10 gene (rs1800871, ‒819C/T), AA genotype of the of the IL10 gene (rs1800872, ‒592C/A), the G allele and the GG genotype of the TNF gene (rs1800629, позиция ‒308G/A) are associated with the development of AS in Caucasians. Multivariate regression analysis identified clinical and genetic factors that predict an increase in arterial stiffness in patients with AS, natives of the Trans-Baikal Territory.

Effect of low-dose terazosin on arterial stiffness improvement: A pilot study.

Arterial stiffness, a prominent hallmark of ageing arteries, is a predictor of all-cause mortality. Strategies for promoting healthy vascular ageing are encouraged. Here we conducted a pilot study to evaluate the potential effects of low-dose Terazosin on arterial stiffness. We enrolled patients aged over 40 with elevated arterial stiffness, defined as a brachial-ankle pulse wave velocity (baPWV) ≥1400 cm/s, who were administered Terazosin (0.5 and 1.0 mg/day) from December 2020 to June 2023. Treatment responses were assessed every 3 months. Linear regression analysis was used to characterise the improvement. We matched cases who took Terazosin for 1 year with Terazosin-free controls using propensity score matching (PSM). Our findings demonstrate that Terazosin administration significantly affected arterial stiffness. (1) Arterial stiffness significantly improved (at least a 5% reduction in baPWV) in 50.0% of patients at 3 months, 48.6% at 6 months, 59.3% at 9 months, and 54.4% at 12 months, respectively. (2) Those with higher baseline baPWV and hypertension exhibited a significantly reduced risk of non-response. (3) Terazosin was associated with a reduction of baPWV at 1-year follow-up (linear regression: β = -165.16, p < 0.001). This pilot study offers valuable insights into the potential significance of Terazosin in improving arterial stiffness and paves the way for future randomised clinical trials in combating vascular ageing.

Associations of coal mine dust exposure with arterial stiffness and atherosclerotic cardiovascular disease risk in chinese coal miners.

Whether coal mine dust exposure increases cardiovascular diseases (CVDs) risk was rarely explored. Our objective was to examine the association between coal mine dust exposure and cardiovascular risk. We estimated cumulative coal mine dust exposure (CDE) for 1327 coal miners by combining data on workplace dust concentrations and work history. We used brachial-ankle pulse wave velocity (baPWV, a representative indicator of arterial stiffness) and ten-year atherosclerotic cardiovascular disease (ASCVD) risk to assess potential CVD risk, exploring their associations with CDE. Positive dose-response relationships of CDE with baPWV and ten-year ASCVD risk were observed after adjusting for covariates. Specifically, each 1 standard deviation (SD) increase in CDE was related to a 0.27m/s (95% CI: 0.21, 0.34) increase in baPWV and a 1.29 (95% CI: 1.14, 1.46) elevation in OR(odds ratio) of risk of abnormal baPWV. Moreover, each 1 SD increase in CDE was associated with a 0.74% (95% CI: 0.63%, 0.85%) increase in scores of ten-year ASCVD and a 1.91 (95% CI: 1.62, 2.26) increase in OR of risk of ten-year ASCVD. When compared with groups unexposed to coal mine dust, significant increase in the risk of arterial stiffness and ten-year ASCVD in the highest CDE groups were detected. The study suggested that cumulative exposure to coal mine dust was associated with elevated arterial stiffness and ten-year ASCVD risk in a dose-response manner. These findings contribute valuable insights for cardiovascular risk associated with coal mine dust.

A cost-effective, machine learning-driven approach for screening arterial functional aging in a large-scale Chinese population.

An easily accessible and cost-free machine learning model based on prior probabilities of vascular aging enables an application to pinpoint high-risk populations before physical checks and optimize healthcare investment. A dataset containing questionnaire responses and physical measurement parameters from 77,134 adults was extracted from the electronic records of the Health Management Center at the Third Xiangya Hospital. The least absolute shrinkage and selection operator and recursive feature elimination-Lightweight Gradient Elevator were employed to select features from a pool of potential covariates. The participants were randomly divided into training (70%) and test cohorts (30%). Four machine learning algorithms were applied to build the screening models for elevated arterial stiffness (EAS), and the performance of models was evaluated by calculating the area under the receiver operating characteristic curve (AUC), sensitivity, specificity, and accuracy. Fourteen easily accessible features were selected to construct the model, including "systolic blood pressure" (SBP), "age," "waist circumference," "history of hypertension," "sex," "exercise," "awareness of normal blood pressure," "eat fruit," "work intensity," "drink milk," "eat bean products," "smoking," "alcohol consumption," and "Irritableness." The extreme gradient boosting (XGBoost) model outperformed the other three models, achieving AUC values of 0.8722 and 0.8710 in the training and test sets, respectively. The most important five features are SBP, age, waist, history of hypertension, and sex. The XGBoost model ideally assesses the prior probability of the current EAS in the general population. The integration of the model into primary care facilities has the potential to lower medical expenses and enhance the management of arterial aging.

Arterial Stiffness and Obesity as Predictors of Diabetes: Longitudinal Cohort Study.

Previous studies have confirmed the separate effect of arterial stiffness and obesity on type 2 diabetes; however, the joint effect of arterial stiffness and obesity on diabetes onset remains unclear. This study aimed to propose the concept of arterial stiffness obesity phenotype and explore the risk stratification capacity for diabetes. This longitudinal cohort study used baseline data of 12,298 participants from Beijing Xiaotangshan Examination Center between 2008 and 2013 and then annually followed them until incident diabetes or 2019. BMI (waist circumference) and brachial-ankle pulse wave velocity were measured to define arterial stiffness abdominal obesity phenotype. The Cox proportional hazard model was used to estimate the hazard ratio (HR) and 95% CI. Of the 12,298 participants, the mean baseline age was 51.2 (SD 13.6) years, and 8448 (68.7%) were male. After a median follow-up of 5.0 (IQR 2.0-8.0) years, 1240 (10.1%) participants developed diabetes. Compared with the ideal vascular function and nonobese group, the highest risk of diabetes was observed in the elevated arterial stiffness and obese group (HR 1.94, 95% CI 1.60-2.35). Those with exclusive arterial stiffness or obesity exhibited a similar risk of diabetes, and the adjusted HRs were 1.63 (95% CI 1.37-1.94) and 1.64 (95% CI 1.32-2.04), respectively. Consistent results were observed in multiple sensitivity analyses, among subgroups of age and fasting glucose level, and alternatively using arterial stiffness abdominal obesity phenotype. This study proposed the concept of arterial stiffness abdominal obesity phenotype, which could improve the risk stratification and management of diabetes. The clinical significance of arterial stiffness abdominal obesity phenotype needs further validation for other cardiometabolic disorders.

The association between time-restricted eating and arterial stiffness status in community-dwelling elderly Chinese individuals

Background and aimsEmerging studies indicate that time-restricted eating (TRE) may protect against cardiovascular disease (CVD); however, studies performed in elderly adults are limited. This study aimed to analyze the association of TRE with arterial stiffness (AS) in community-dwelling elderly Chinese individuals. Methods and resultsThis cross-sectional study recruited 3487 participants aged ≥60 y from Shanghai, China. TRE was determined by calculating the end time of the last meal minus the start time of the first meal of the average day. Participants were then categorized into those with a time-restricted window lasting ≤11 h (TRE) and >11 h (non-TRE). The mean age of the sample was 71.78 ± 5.75 y, and 41.2 % were men. Having a TRE pattern was 72.2 %. In the logistic analysis, TRE was associated with borderline arterial stiffness (OR = 1.419; 95 % CI = 1.077–1.869) and elevated arterial stiffness (OR = 1.699; 95 % CI = 1.276–2.263). In a subgroup analysis, the significance remained in the group at risk of malnutrition (with borderline arterial stiffness: OR = 2.270; 95 % CI = 1.229–4.190; with elevated arterial stiffness: OR = 2.459; 95 % CI = 1.287–4.700), while in well-nourished participants, the association only remained with elevated arterial stiffness (OR = 1.530; 95 % CI = 1.107–2.115) and not with borderline arterial stiffness. ConclusionsTRE is a risk factor for both borderline and elevated arterial stiffness in community-dwelling Chinese individuals and varies by nutritional status. (Protocol code 2019-WJWXM-04-310108196508064467.)

Arterial Stiffness and Heart Failure With Preserved Ejection Fraction.

Heart failure with preserved ejection fraction (HFpEF) is prevalent and associated with a poor prognosis, imposing a significant burden on society. Arterial stiffness is increasingly recognized as a crucial factor in the pathophysiology of HFpEF, affecting diagnosis, management, and prognosis. As a hallmark of vascular aging, arterial stiffness contributes to increased afterload on the left ventricle (LV), leading to diastolic dysfunction, a key feature of HFpEF. Elevated arterial stiffness is linked with common cardiovascular risk factors in HFpEF, such as hypertension, diabetes and obesity, exacerbating the progression of disease. Studies have demonstrated that patients with HFpEF exhibit significantly higher levels of arterial stiffness compared to those without HFpEF, highlighting the value of arterial stiffness measurements as both diagnostic and prognostic tools. Moreover, interventions aimed at reducing arterial stiffness, whether through pharmacological therapies or lifestyle modifications, have shown potential in improving LV diastolic function and patient outcomes. Despite these advancements, the precise mechanisms by which arterial stiffness contributes to HFpEF are still not fully understood, necessitating the need for further research.

Associations Between Arterial Stiffness and Metabolic Target in Children and Adolescents With Type 1 Diabetes Treated in a Modern Setting

Objective: To investigate the prevalence of elevated arterial stiffness and associations to known and potentially novel risk factors in a modern European technology‐based cohort of children and adolescents with type 1 diabetes.Research Design and Methods: Cross‐sectional study, including 127 children recruited from Pediatric Diabetes Departments across Eastern Denmark between May 2022 and January 2024. Arterial stiffness was assessed as carotid–femoral pulse‐wave‐velocity (cfPWV) using the Sphygmocor XCEL system. Unadjusted and adjusted linear regression models explored associations between cfPWV and other risk factors. Adjustments included age, sex, diabetes duration, time‐in‐range, hemoglobin A1c (HbA1c), body mass index (BMI) z‐score, low‐density lipoprotein (LDL)‐cholesterol, and mean arterial pressure (MAP).Results: Median (interquartile range [IQR]) age was 14.2 years (12.0, 16.4), diabetes duration was 4.7 years (2.7, 8.4), HbA1c level was 7.0% (6.5, 7.9), (53 mmol/l: 48–63), time‐in‐range was 63% (53–75), and 52% were male. The majority were treated with continuous‐subcutaneous‐insulin‐infusion (82%), and all (except two) used continuous‐glucose‐monitors. The prevalence of elevated arterial stiffness (cfPWV z‐score over the 90th percentile) was 16%. Unadjusted analyses demonstrated higher cfPWV was associated with longer diabetes duration, higher age, HbA1c, MAP, and liver stiffness, and lower time‐in‐range and insulin sensitivity. Higher cfPWV remained associated with higher age (standardized β (confidence interval (CI) 95%): 0.38 (0.27, 0.48); p &lt; 0.001) and lower time‐in‐range (−0.15 ((−0.26), (−0.03)); p &lt; 0.011) after adjustment.Conclusions: Despite modern treatment technology and better overall metabolic control, children and adolescents with type 1 diabetes present with a high prevalence of elevated arterial stiffness. Higher arterial stiffness was associated with higher age and lower time‐in‐range, independent of other risk factors, including HbA1c.

Abstract 13113: Associations of Cerebrovascular Regulation and Arterial Stiffness With Cerebral Small Vessel Disease: A Systematic Review and Meta-Analysis

Background: The global incidence of ischemic stroke is projected to increase ~20% by 2030, with one-fifth of these cases attributed to cerebral small vessel disease (cSVD). Stiffening of central arteries potentiates small vessel injury in the brain, which may precede or develop in parallel with disruption of local regulatory mechanisms such as cerebrovascular reactivity. However, evidence of these vascular etiologies of cSVD remains inconclusive. To address this, we conducted separate systematic meta-analyses to characterize the relationship between cerebrovascular reactivity or arterial stiffness and cSVD. Methods: MEDLINE and Web of Science were searched for studies reporting odds ratios (OR) using arterial stiffness or cerebrovascular reactivity as continuous predictors for the presence of cSVD. Data were extracted using predefined tables and random-effects meta-analyses were performed to determine pooled OR and 95% confidence intervals. Results: Four cross-sectional studies were included in the analysis between cerebrovascular reactivity and cSVD, including 294 participants (38.1% women). Decrements in cerebrovascular reactivity were associated with a greater cSVD burden (OR = 1.93, 95% CI: 1.15-3.24, p = 0.01, I 2 = 97.4%). For arterial stiffness, 34 cross-sectional studies comprising of 26,541 participants (52.9% women) were included. Increases in indices of arterial stiffness were associated with a greater burden of cSVD (OR = 1.13, 95% CI: 1.07-1.20, p &lt; 0.0001, I 2 = 60.2%). Conclusion: Impaired cerebrovascular reactivity and elevated arterial stiffness were both associated with an increased incidence of cSVD. While investigation of a link between cerebrovascular reactivity and arterial stiffness is a growing field, our findings suggest that the two measures have either individual or overlapping relationships with cSVD. This highlights the need for monitoring of both local and global cardiovascular regulation in high-risk individuals.

Associations Between Urine Sodium and Potassium Level, Elevated Arterial Stiffness, and Hypertension in a Population-Based Study: A Mediation Analysis

Associations Between Urine Sodium and Potassium Level, Elevated Arterial Stiffness, and Hypertension in a Population-Based Study: A Mediation Analysis

Post-Doc Competition (Knowledge Generation) ID 1985177

Background Heart Disease is the leading cause of death after spinal cord injury (SCI). Individuals with paraplegia develop hypertension and elevated arterial stiffness prior to their age matched peers. Overground exoskeleton training is becoming an increasingly prevalent form of exercise. In the general population, exercise training has been shown to reduce arterial stiffness. Recent RCT failed to show changes in arterial stiffness with arm ergometry or body weight supported treadmill training. Objectives The aim of this project is to determine the effect of Exoskeleton Exercise on changing arterial stiffness. Study Design The study setting will take place at a rehabilitation facility. The study will involve 34 sessions over the span of approximately 18-20 weeks. The key intervention utilized in the investigation will be an Overground EksoNR gait and balance training program. The primary outcome measure will be carotid-femoral pulse wave velocity (cfPWV) and secondary measures will include heart rate (HR), blood pressure (BP), waist circumference (WC), and oxygen saturation (SpO2). Statistical Analysis will involve mean changes at baseline, midway, and end of study. Methods The 34-session (2x/week for ∼18 weeks) rehabilitation protocol will focus on using the EksoNR for overground gait and balance activities. For measurement of cfPWV, two transcutaneous Doppler flowmeters will be used at the common carotid and femoral artery. To calculate cfPWV, the distance travelled by the pulse is divided by the average pulse transit time (PTT). Hypothesis The 18-week Exoskeleton Program would improve arterial stiffness (cfPWV) in individuals with chronic incomplete SCI/D.

Association Between Progression of Arterial Stiffness and Left Ventricular Remodeling in a Community-Based Cohort

BackgroundCross sectionally measured, elevated arterial stiffness is associated with unfavorable left ventricular (LV) remodeling, suggesting its important role in the pathophysiology of heart failure. However, data linking the degree of arterial stiffness progression with LV remodeling are scarce. ObjectivesThe purpose of this study was to investigate the association between longitudinal change in arterial stiffness and changes in LV remodeling. MethodsSerial measurements of arterial stiffness by cardio-ankle vascular index (CAVI) were performed in 317 participants without cardiovascular disease and with normal arterial stiffness. LV size, mass, and function were assessed by transthoracic echocardiography and including LV global longitudinal strain (LVGLS) by speckle-tracking and tissue Doppler velocity (e’) of the mitral annulus (diastolic function). ResultsDuring a median follow-up of 26.8 mo, there was a significant increase in CAVI (P < 0.001). Generalized estimating equation analyses showed that longitudinal increase in CAVI was associated with impaired LVGLS (estimate 0.46, 95% CI: 0.11-0.82; P = 0.010) after adjustment for demographics and baseline cardiovascular factors, but not with changes of LV mass index and e’ velocity. When controlling for longitudinal change of covariates, CAVI progression remained associated with change in LVGLS (estimate 0.50, 95% CI: 0.16-0.85; P = 0.004). In sex stratified analysis, progression of CAVI was significantly associated with LVGLS deterioration only in women (estimate 0.92, 95% CI: 0.27-1.58; P = 0.006). ConclusionsLongitudinal increase in arterial stiffness is associated with deterioration in LVGLS. Vascular-ventricular coupling plays an important role in the progressive decline in ventricular function even at an early, subclinical stage.

CARDIOVASCULAR HAEMODYNAMICS IN TWO GROUPS OF HYPERTENSION: RESISTANT HYPERTENSION AND MALIGNANT HYPERTENSION

Objective: Patients with malignant and resistant hypertension have poor prognosis and high rate of complications. Understanding the pathophysiological mechanisms underlying the severe forms of hypertension and their relationship to cardiac haemodynamics and vascular function is crucial to the management of blood pressure (BP). Design and method: In a cross-sectional comparison, of age and sex matched groups, we assessed left ventricle (LV) strain function using speckle tracking echocardiography (STE), (Figure 1), endothelial function using flow mediated dilation (FMD) and arterial stiffness using pulse wave velocity (PWV) in patients with confirmed RH (n = 23), treated malignant hypertension (MHT) (n = 54) and normotensive control (NC) (n = 23). Results: Characteristics pf study population are provided in table 1. Both hypertension groups showed markedly reduced global longitudinal strain (GLS) vs. NC (MHT -15.6% {-17 – -15}, RH -17.7% {-20 – -16} vs. NC -25% {-28 – -22]}, all p &lt; 0.001) with GLS being lower in MHT vs. RH (p &lt; 0.05). Both hypertensive groups also showed preserved but lower global circumferential strain (GCS) vs. NC (MHT -30.7% ± 4.7, RH -30.0% ± 4.3 vs. NC -34.3% ± 4.5, p = 0.004 and p = 0.03, respectively). FMD was markedly attenuated in both hypertensive groups (RH: 5.5 % ±2.6 and MHT: 5.9 % ± 2.6 vs. NC: 9.9 % ± 2.5%, p &lt; 0.001). Carotid-femoral pulse wave velocity (cfPWV) was increased in both hypertensives compared to NC (p &lt; 0.05). Subendocardial viability ratio (SEVR) and total peripheral resistance (TPR) were decreased in MHT compared to NC (p = 0.01 and p = 0.002, respectively). After adjustment for potential confounders (presence of hypertension, duration of hypertension, age, BMI, and eGFR), presence of MHT (p &lt; 0.001), presence of RH (p &lt; 0.001) and age (p = 0.01) showed significant negative association with GLS, whereas eGFR showed significant positive association with GLS (p = 0.03), (Table 2). Conclusions: This is the first cardio-vascular assessment of two extreme phenotypes of hypertension. Patients with MHT and RH had persistent impaired cardiac remodelling independent of preserved EF, impaired endothelial function and elevated arterial stiffness. Early cardiac remodelling marker, GLS was more impaired in MHT patients.

Carotid pulse wave velocity measured using a fast single‐slice oblique‐sagittal phase‐contrast MRI is associated with cognitive impairment

AbstractBackgroundArterial stiffness is one of the earliest markers of vascular dysfunction1. Elevated arterial stiffness leads to the transmission of excessive pulsations into the downstream microvasculature, which may be linked to cognitive impairment in aged individuals. Pulse wave velocity (PWV) is an established surrogate of arterial stiffness. To date, PWV measurement at carotid arteries or above has been still limited. Previous work has introduced a fast MRI method to measure carotid PWV (cPWV) using single‐slice oblique‐sagittal phase‐contrast MRI (OS PC‐MRI)3. In this study, we evaluated the association between cPWV and cognitive impairment in an aged group.MethodThe MRI experiments were conducted on Siemens Prisma 3T MRI scanner. A 2min TOF MRI was performed to localize carotid arteries including CCA and ICA. The 3D MR angiogram was reformatted to determine an oblique slice to maximally cover both CCA and ICA (Figure 1a). A single‐slice retrospectively gated 2D OS PC‐MRI with a single in‐plane velocity encoding (CCA to ICA) (Venc = 80cm/s, temporal resolution = 14.22ms) was performed to simultaneously acquire blood velocity waveforms at each location along the CCA‐ICA segment. cPWV was calculated as the inverse slope of the line fitted to the transit time versus distance along the vessel (Figure 1b). 15 elderly participants (age: 71.4 ± 8.5 years) were enrolled in this study. Each participant underwent cognitive assessments including CDR and 13 out of 15 were conducted the MoCA.ResultThere was a significant difference (p = 0.0496) in cPWV between the participants with normal cognition (CDR = 0) and cognition impairment (CDR&gt; = 0.5). Figure 3 shows the scatter plot of cPWV vs. MoCA. Overall, cPWV increased with lower MoCA. However, there was no significance (r = ‐0.5294, p = 0.0767) obtained between cPWV and MoCA given a small sample size and the presence of a suspicious data point indicated by a green circle in Figure 3. After excluding this potential outlier, a significant negative correlation between cPWV and MoCA was obtained (r = ‐0.8113, p = 0.0014).ConclusionThe pilot study demonstrates that increased cPWV is associated with cognitive impairment, suggesting cPWV measured using 2D OS PC‐MRI could be an imaging marker for cognitive impairment.

Carotid arterial stiffness and cerebral blood flow variability in individuals with mild cognitive impairment

Background: It is unclear whether cerebral blood flow variability is a sign of impaired vascular function or an adaptation to chronic cerebral hypoperfusion in individuals with cognitive dysfunction. Elevated arterial stiffness increases transmission of pulsatile pressure to the brain, but the relationship between arterial stiffness, the magnitude of cerebral blood flow variability, and cognitive dysfunction is unknown. In this pilot study, we hypothesized that carotid artery stiffness would be higher in individuals with mild cognitive impairment (MCI) compared with individuals with normal cognition (NC), resulting in higher cerebral blood flow variability. Methods: In individuals with MCI (N=5) or NC (N=7), R-wave to common carotid artery (CCA) pulse wave velocity (PWV) was assessed as an index of arterial stiffness (via tonometry). CCA velocity (CCAv) and middle cerebral artery velocity (MCAv) were measured via transcranial Doppler ultrasound, with concurrent measurements of mean arterial pressure (MAP) via finger photoplethysmography. The amplitude of MAP, CCAv, and MCAv oscillations in the low frequency range (LF; 0.07-0.15 Hz) were assessed via fast Fourier transformation, and normalized to total power (0.04-0.4 Hz) for each participant to account for high inter-individual variability. Relationships between R-wave-carotid PWV and LF variability in CCAv and MCAv were assessed via correlational analyses. Results: There were no between-group differences for R-wave-carotid PWV (MCI: 0.91±0.16 m/s vs. NC: 0.87±0.07 m/s; P=0.70), mean CCAv (MCI: 31.8±8.8 cm/s vs. NC: 29.7±2.0 cm/s; P=0.54), mean MCAv (MCI: 50.9±6.5 cm/s vs. NC: 47.9±12.7 cm/s; P=0.63), or MAP (MCI: 102.1±10.2 mmHg vs. 104.7±13.8 mmHg; P=0.73). While there was also no difference between groups for nLF power of CCAv (MCI: 0.28±0.03 au vs. NC: 0.33±0.10 au; P=0.41), nLF power for MCAv was lower in the MCI group (MCI: 0.26±0.07 au vs. 0.43±0.12; P=0.02). Overall, there was a strong positive correlation between R-wave-carotid PWV and CCAv nLF power (R=0.81, P=0.005), but a weaker relationship for MCAv nLF power (R=0.56, P=0.09). While sub-group correlational analyses are limited based on the small sample sizes, relationships between R-wave-carotid PWV and CCAv nLF power were high for both MCI (R=0.98, P=0.02) and NC (R=0.79, P=0.06) groups, but were lower for MCAv nLF power (MCI: R=-0.12, P=0.88; NC: R=0.69, P=0.13). Conclusion: Contrary to our hypothesis, there were no differences in R-wave-carotid PWV between groups, and blood flow variability was either similar between groups (for CCAv), or lower in the MCI group (for MCAv). Overall, there was a strong positive relationship between R-wave-carotid PWV and blood flow variability in the CCA, which was also observed in sub-analysis of the MCI and NC groups. Future investigations with a larger sample size are needed to definitively determine the role of arterial stiffness on cerebral blood flow variability with cognitive dysfunction. R56AG068630, NIH National Institute for Aging (NIA), “Hemodynamic Mechanisms Linking Aortic Arch Stiffness with Brain Insult in Older Adults” This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.