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Flavonoids exert vasculoprotective effects in humans, but interindividual variability in their action has also been reported. This study aims to identify genes that are associated with vascular health effects of flavonoids and whose polymorphisms could explain interindividual variability in response to their intake. Applying the predetermined literature search criteria, we identified five human intervention studies reporting positive effects of flavonoids on vascular function together with global genomic changes analyzed using microarray methods. Genes involved in vascular dysfunction were identified from genome-wide association studies (GWAS). By extracting data from the eligible human intervention studies, we obtained 5807 differentially expressed genes (DEGs). The number of identified upstream regulators (URs) varied across the studies, from 227 to 1407. The search of the GWAS Catalog revealed 493 genes associated with vascular dysfunction. An integrative analysis of transcriptomic data with GWAS genes identified 106 candidate DEGs and 42 candidate URs, while subsequent functional analyses and a search of the literature identified 20 top priority candidate genes: ALDH2, APOE, CAPZA1, CYP11B2, GNA13, IL6, IRF5, LDLR, LPL, LSP1, MKNK1, MMP3, MTHFR, MYO6, NCR3, PPARG, SARM1, TCF20, TCF7L2, and TNF. In conclusion, this integrated analysis identifies important genes to design future nutrigenetic studies for development of precision nutrition for polyphenols.

ABSTRACT Aim Materials and Methods Results Conclusions To investigate the effect of periodontitis on the long‐term changes of the cardio‐ankle vascular index (CAVI).A 10‐year retrospective cohort study of 3842 Thai participants (range 25–76 years) with normal CAVI at the study initiation was undertaken. Full‐mouth periodontal examination was performed by calibrated periodontists, and the extent and severity of periodontitis were determined at 5‐year intervals. Serial CAVI measurements were used to examine the incidence of high CAVI (≥ 9.0) and changes in CAVI over time (ΔCAVI).Participants with a higher extent or severity of periodontitis were found to have a significantly higher mean ΔCAVI. The incidence of high CAVI was also observed to be higher in those with periodontitis compared to those without it. The adjusted risk ratios for developing high CAVI were 1.309 and 1.513 for localized and generalized periodontitis, respectively. Participants with severe periodontitis had a 37% higher likelihood of developing CAVI ≥ 9.0 compared to individuals with no/mild periodontitis. This risk was consistent with a significant change in ΔCAVI of 0.054–0.140.Periodontitis, both in terms of extent and severity, was found to have a significant dose‐dependent effect on the risk of developing high CAVI over a 10‐year period, suggesting a causal relationship between these two parameters. [ABSTRACT FROM AUTHOR]

Objective: To compare maternal vascular indices and hemodynamic parameters at 35–37 weeks' gestation in pregnancies complicated by gestational diabetes mellitus (GDM), those with pre‐existing diabetes mellitus (DM) and those without GDM or pre‐existing DM. Methods: This was a prospective observational study in women with a singleton pregnancy attending for a routine hospital visit at 35 + 0 to 36 + 6 weeks' gestation. The visit included recording of maternal demographic characteristics and medical history, and measurement of vascular indices and hemodynamic parameters using a non‐invasive operator‐independent device. These included carotid‐to‐femoral pulse‐wave velocity, augmentation index, cardiac output, stroke volume, central systolic and diastolic blood pressure, total peripheral resistance and heart rate. The values in the GDM and pre‐existing DM groups were compared to those in the unaffected group. Results: We examined 6746 women, of whom 396 were excluded because they had chronic hypertension or developed pre‐eclampsia or gestational hypertension. The study population of 6350 pregnancies contained 99 (1.6%) with pre‐existing Type‐I or Type‐II DM and 617 (9.7%) that developed GDM, including 261 (42.3%) that were treated with diet alone, 239 (38.7%) treated with metformin alone and 117 (19.0%) treated with insulin with or without metformin. Among women with GDM and those with pre‐existing DM, compared to those without GDM or pre‐existing DM, there was a higher median cardiac output and heart rate, central systolic and diastolic blood pressure and pulse‐wave velocity, but there was no significant difference in stroke volume or total peripheral resistance. There were no significant differences within the GDM group according to treatment type, except for higher heart rate in women treated with metformin alone compared to the group treated with diet alone. Conclusion: Women with GDM and those with pre‐existing DM have evidence of early vascular disease in the third trimester, and this may contribute to their increased long‐term cardiovascular risk. © 2024 International Society of Ultrasound in Obstetrics and Gynecology. [ABSTRACT FROM AUTHOR]

Increased arterial stiffness is independently associated with cardiovascular risk. Obstructive sleep apnea (OSA) and sleep duration (SDUR) may contribute to increased arterial stiffness, but it is unclear whether this association is modulated by gender. We aimed to evaluate the potential impact of gender in modulating the association of OSA and SDUR with arterial stiffness. Participants from the ELSA-Brasil study performed sleep assessments with portable polygraph to define OSA severity and SDUR by 1-week wrist actigraphy. Pulse wave velocity (PWV) was measured using a standard technique without access to the sleep data. We studied 1863 participants (42.2% male, age: 49±8 years, respiratory disturbance index (RDI): 9.9 (4.5–19.4) events/h, SDUR: 6.5 (5.9–7.1) hours, mean PWV: 7.3 ± 1.2 m/s). We found that men had higher PWV, higher frequency of diabetes, and higher blood pressure when compared to women. The regression analysis showed an independent association between increased RDI and PWV in men (ß: 0.007; 95% CI: 0.001–0.012), but not in women. In contrast, an independent association between SDUR and increased arterial stiffness was observed only in women (ß: 0.068; 95% CI: 0.002–0.134). In conclusion, the association of sleep disorders with arterial stiffness showed a distinct gender pattern depending on the sleep variable studied. [ABSTRACT FROM AUTHOR]

Objectives: COVID-19 viral pneumonia can result in increased arterial stiffness, along with cardiac and systemic inflammatory responses. This study aimed to investigate the association between arterial stiffness, inflammation severity, and all-cause mortality in patients with COVID-19. Methods: In this study, anthropometric data, pneumonia infection severity, and blood tests were analyzed. Arterial stiffness was assessed using the non-invasive assessment indices, including arterial velocity pulse index (AVI) and central arterial pulse pressure (CAPP). Infection volumes and percentages for the whole lungs, most lobes, and most segments were extracted from CT images using artificial intelligence-based quantitative analysis software. The relationship between arterial stiffness, central hemodynamics, and all-cause mortality was investigated. Results: In multivariable Cox regression analysis, high CAPP was significantly associated with all-cause mortality (hazard ratio: 0.263, 95% CI, 0.073–0.945, p = 0.041). Whole lung infection percentages were independently associated with high CAPP, with an area under the curve (AUC) of 0.662 and a specificity of 89.09%. Conclusions: High CAPP, but not high AVI, demonstrated independent prognostic value for all-cause mortality in patients due to COVID-19 pneumonia infection. Evaluating this parameter could help in risk assessment and improve diagnostic and therapeutic strategies in viral pneumonia infections. [ABSTRACT FROM AUTHOR]

Objectives: This study examined the association between sarcopenic obesity and arterial stiffness using bioelectrical impedance analysis (BIA). Methods: This retrospective cross-sectional study included 20,601 Korean adults from January 2016 to December 2023. Sarcopenia was defined as height-adjusted appendicular skeletal muscle mass [(ASM/height2) <5.7 in women and <7.0 in men] using BIA. Obesity was defined by body mass index or waist circumference. Arterial stiffness was assessed by measuring brachial-ankle pulse wave velocity (baPWV). The participants were categorized into four groups: normal, sarcopenia, obesity, and sarcopenic obesity. The baPWV values were compared among the four groups to investigate the association between sarcopenic obesity and arterial stiffness using adjusted multivariate analyses. Results: The mean baPWV of the sarcopenic obesity group was higher (p < 0.001) than that of the other groups. The odds ratio for having high baPWV (>1800 cm/s) in the sarcopenic obesity group was 2.40 (95% CI, 1.07–5.38) after adjusting for age, sex, exercise, smoking, heavy alcohol consumption, hypertension, and dyslipidemia. Conclusions: Sarcopenic obesity was independently associated with increased arterial stiffness. [ABSTRACT FROM AUTHOR]

Vascular aging encompasses structural and functional changes in the vasculature, significantly contributing to cardiovascular diseases, which are the leading cause of death globally. The incidence and prevalence of these diseases increase with age, with most morbidity and mortality attributed to myocardial infarction and stroke. Diagnosing and intervening in vascular aging while understanding the mechanisms behind age-induced vascular phenotypic and pathophysiological alterations offers the potential for delaying and preventing cardiovascular mortality in an aging population. This review delves into various aspects of vascular aging by examining age-related changes in arterial health at the cellular level, including endothelial dysfunction, cellular senescence, and vascular smooth muscle cell transdifferentiation, as well as at the structural level, including arterial stiffness and changes in wall thickness and diameter. We also explore aging-related changes in perivascular adipose tissue deposition, arterial collateralization, and calcification, providing insights into the physiological and pathological implications. Overall, aging induces phenotypic changes that augment the vascular system's susceptibility to disease, even in the absence of traditional risk factors, such as hypertension, diabetes, obesity, and smoking. Overall, age-related modifications in cellular phenotype and molecular homeostasis increase the vulnerability of the arterial vasculature to structural and functional alterations, thereby accelerating cardiovascular risk. Increasing our understanding of these modifications is crucial for success in delaying or preventing cardiovascular diseases. Non-invasive techniques, such as measuring carotid intima-media thickness, pulse wave velocity, and flow-mediated dilation, as well as detecting vascular calcifications, can be used for the early detection of vascular aging. Targeting specific pathological mechanisms, such as cellular senescence and enhancing angiogenesis, holds promise for innovative therapeutic approaches. [ABSTRACT FROM AUTHOR]

Background: Arterial stiffness is a degenerative modification in the arterial wall that significantly affects normal aging. Arterial hypertension is a major risk factor for cerebrovascular impairment. Pulse wave velocity (PWV) is an established gold standard for measuring arterial stiffness. Studies demonstrated that individuals with elevated blood pressure (BP) and PWV are more likely to experience worse cognitive decline compared to those with either condition alone. The aim of this review is to explore the clinical importance of arterial stiffness for cognitive function in older adults with hypertension. Methods: The systematic review was reported following the PRISMA 2020 guidelines and Cochrane protocol and was registered in NIHR PROSPERO. PubMed, Embase, Web of Science, CINAHL, and Cochrane databases were searched for relevant publications up to December 2022. Articles were filtered by age and type of study and only those including a sample size of at least 500 individuals were selected. Screening of abstracts and full-text review of selected articles were carried out through Covidence. Results: The full-text review included a total of 434 articles. Twenty-eight prospective studies have met the inclusion criteria. Selected studies used PWV as the main measurement of stiffness: 24 used carotid-femoral, 2 used brachial-ankle, 1 used aortic PWV, and 11 compared different measures. Studies demonstrated a strong association between increased BP and PWV with brain damage and cognitive deterioration among older adults. One study did not find an interaction with hypertension, while another study found that PWV but not BP was associated with cognitive decline. Few studies showed that the association between stiffness and cognitive outcomes was not significant after adjustment for BP. Several authors suggested that cognitive decline induced by stiff vasculature and hypertension benefited from antihypertensive therapy. Conclusion: The results of this review demonstrated that arterial hypertension is an important factor linking arterial stiffness to cognitive health in older individuals. BP plays a crucial role in brain integrity, whereas PWV was shown to be a strong measure associated with cognitive decline. Together, they can lead to disabling cognitive outcomes. Early screening of stiffness, BP control, and compliance with treatment are essential for cerebrovascular disease prevention. Trial registration: NIHR PROSPERO registry ID: CRD42022379887. [ABSTRACT FROM AUTHOR]

This study aimed to evaluate the correlation between mental health status and arterial stiffness. A Symptom Checklist 90 (SCL-90) score was conducted for 10,688 employees of Kailuan Group Co., Ltd., of which 4936 participants received baPWV measurement. Of these, 4424 met the inclusion criteria. Based on the SCL-90 score, the study subjects were divided into normal mental health group (SCL-90 score < 160, 3993 cases) and abnormal mental health group (SCL-90 score ≥ 160, 431 cases). Statistical indicators include: General information, including levels of brachial-ankle pulse wave velocity (baPWV), age, gender, systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), body mass index (BMI), smoking and alcohol consumption, daily activity levels, nature of work and educational qualifications. The proportion of males, baPWV value, and abnormal proportion of baPWV in normal mental health group were higher than those in abnormal mental health group (P < 0.05). The Hs-CRP in normal mental health group were lower than that in abnormal mental health group (P < 0.05). There were significant differences in activity level and educational attainment between the two groups (P < 0.05). After adjusting for confounders, the results of the multiple linear regression analysis showed that, Age, MAP, HR, FBG, TG were positively correlated with baPWV; SCL-90 score, gender, BMI, educational qualification were negatively correlated with baPWV. When the SCL-90 score of the general population increased by one point, baPWV decreased by 0.246 cm/s. Each such increase corresponded with a decrease in baPWV of 0.299 cm/s for male participants in general (β = − 0.299, P = 0.007) and 0.412 cm/s for the male participants in the older-age group (β = − 0.412, P = 0.017). Although adverse psychological factors have a certain impact on arterial stiffness, it does not constitute an independent risk factor. [ABSTRACT FROM AUTHOR]

ABSTRACT The weight‐adjusted‐waist index (WWI) is an innovative measure of obesity that appears to surpass body mass index (BMI) in assessing lean body mass and fat mass. This study aimed to evaluate the relationship between WWI and AS in hypertensive adults in the United States. The study included 9753 adults diagnosed with hypertension from the National Health and Nutrition Examination Survey (NHANES), which spanned the years 2007–2016. WWI was calculated by dividing waist circumference (in cm) by the square root of body weight (in kg), and arterial stiffness (represented by estimated pulse wave velocity [ePWV]) was analyzed as the outcome. Weighted multiple linear regression and smooth curve fitting were used to test for linear and nonlinear associations. Threshold effects were determined using a two‐part linear regression model. Additionally, subgroup analyses and interaction tests were conducted to gain a more in‐depth understanding of the observed associations. The mean WWI of the participants was 11.32 ± 0.76. After multivariable adjustment, WWI showed a significant nonlinear association with ePWV, with a U‐shaped association observed between the two. Specifically, WWI below the threshold of 10.23 was negatively associated with arterial stiffness (β = −0.39, 95% CI: −0.54 to −0.25), while WWI above the threshold of 10.23 was positively associated with arterial stiffness (β = 0.04, 95% CI: 0.01–0.07). To conclude, the present findings imply that maintaining WWI within an optimal range could reduce AS in hypertensive individuals and potentially decrease cardiovascular risk. However, this observation needs to be confirmed in large clinical trials. [ABSTRACT FROM AUTHOR]

Arterial stiffness (AS) is a significant risk factor for cardiovascular diseases, which are the leading cause of death in developed countries. Based on the measurement of AS among residents supplied with soft drinking water (100 respondents) and hard water (100 respondents), a significant difference was found in the pulse wave velocity (PWVao), arterial age, and the difference between arterial and actual age (delta – Δ age). Among respondents consuming soft drinking water, PWVao was higher by 1.9 ms-1, arterial age was higher by 23 years, and Δ age was higher by 14.5 years. As an intervention, originally soft drinking water was treated to increase calcium (Ca) and magnesium (Mg) content by approximately 10–15 mg l-1 . After 18 months of consuming water with elevated Ca and Mg content, PWVao decreased by 0.93 m s-1, arterial age decreased by 10.42 years, and Δ age decreased by 11.79 years among respondents originally consuming soft drinking water. Thus, their risk of developing CVD was significantly reduced. [ABSTRACT FROM AUTHOR]

Simple Summary: Proteasome inhibitors, such as bortezomib and carfilzomib, are vital for treating relapsed or refractory multiple myeloma, but their potential link to cancer therapy-related cardiovascular dysfunction (CTRCD) raises concerns. Bortezomib, a reversible first-generation inhibitor, and carfilzomib, a second-generation irreversible inhibitor, have been associated with hypertension, heart failure, and arrhythmias. This study explored their impact on cardiac function, focusing on left ventricular ejection fraction (LVEF), and vascular function through arterial stiffness and vascular reactivity assessments. Twelve-week-old male mice were treated with either carfilzomib or bortezomib, with some receiving L-NAME to induce hypertension. Echocardiography was used to evaluate cardiac and vascular parameters at different time points, followed by ex vivo arterial stiffness and reactivity measurements. Results showed no significant changes in arterial stiffness at baseline pressures, but a steeper pressure-stiffness curve was noted in carfilzomib-treated normotensive and hypertensive mice. Carfilzomib also showed a trend toward reduced LVEF in hypertensive mice, with bortezomib showing similar trends. Vascular reactivity remained largely unchanged, but proteasome inhibition appeared to enhance endothelial-independent relaxation. Overall, short-term treatment with both drugs was deemed relatively safe under the tested conditions. Proteasome inhibitors such as bortezomib and carfilzomib induce apoptosis and are a cornerstone in the treatment of relapsed or refractory multiple myeloma. However, concerns have emerged concerning their link to cancer therapy-related cardiovascular dysfunction (CTRCD). Bortezomib, a reversible first-generation inhibitor, and carfilzomib, a second-generation irreversible inhibitor, are associated with hypertension, heart failure, and cardiac arrhythmias. The current study investigated the effects of bortezomib and carfilzomib on cardiac (left ventricular ejection fraction, LVEF) and vascular (arterial stiffness, vascular reactivity) function. Cardiac function assessment aimed to build upon existing evidence of proteasome inhibitors CTRCD, while arterial stiffness served as an early indicator of potential vascular remodeling. Groups of 12-week-old C57BL/6J male mice (n = 8 per group) were randomly assigned to receive vehicle, carfilzomib (8 mg/kg I.P.), or bortezomib (0.5 mg/kg I.P.). Additionally, proteasome inhibition was assessed in mice treated with L-NAME (0.5 mg/kg) to induce hypertension. Cardiac and vascular parameters were evaluated via echocardiography on days 0 and 3. On day 6, mice were sacrificed for ex vivo analysis of arterial stiffness and vascular reactivity. Overall, no changes in arterial stiffness were detected either in vivo or ex vivo at basal pressures. However, a steeper pressure–stiffness curve was observed for carfilzomib in normotensive (p < 0.01) and hypertensive (p < 0.0001) mice ex vivo. Additionally, in hypertensive mice, carfilzomib decreased LVEF (p = 0.06), with bortezomib exhibiting similar trends. Vascular reactivity remained largely unchanged, but proteasome inhibition tended to enhance endothelial-independent relaxations in both control and hypertensive mice. In conclusion, short-term treatment with carfilzomib and bortezomib is considered relatively safe for the protocols assessed in the study. [ABSTRACT FROM AUTHOR]

Background: Atherosclerosis, a leading cause of mortality, necessitates effective management of hypercholesterolemia, specifically elevated low‐density lipoprotein cholesterol (LDL‐C). The emergence of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) has revolutionised lipid‐lowering. PCSK9i demonstrates substantial LDL‐C reduction and cardiovascular benefits, particularly in statin‐intolerant or nonresponsive individuals. However, the potential pleiotropic effects of PCSK9i, especially on arterial stiffness, remain a subject of investigation. This systematic review and meta‐analysis seek to provide a nuanced understanding of the potential pleiotropic effects of PCSK9i, specifically on arterial health. The primary objective was to analyse the influence of PCSK9i on arterial stiffness, extending beyond traditional lipid‐lowering metrics and contributing to a more comprehensive approach to cardiovascular risk reduction. Methods: A systematic search was conducted across major databases, clinical trial registries and grey literature. Inclusion criteria comprised adults in prospective cohort studies undergoing PCSK9i augmentation in lipid‐lowering therapy, with a focus on arterial stiffness measured by pulse wave velocity (PWv). Random‐effects meta‐analyses, sensitivity analyses and meta‐regression models were employed to assess the pooled effect of adding PCSK9i to lipid‐lowering interventions on arterial stiffness. Results: Five studies (158 participants) met the inclusion criteria, demonstrating a significant reduction in PWv (mean difference: −2.61 m/s [95% CI: −3.70, −1.52]; ES: −1.62 [95% CI: −2.53, −.71]) upon adding PCSK9i to lipid‐lowering interventions. Subgroup analysis and meta‐regression models suggested potential sex‐based and baseline PWv‐dependent variations, emphasising patient‐specific characteristics. Conclusion: The meta‐analysis provides robust evidence that adding PCSK9i to lipid‐lowering interventions significantly improves arterial stiffness, indicating broader vascular benefits beyond LDL‐C reduction. [ABSTRACT FROM AUTHOR]

This study investigated the long-term cardiovascular effects of coronavirus disease (COVID-19) in elite male athletes by comparing the heart rate variability (HRV), arterial stiffness, and other cardiovascular parameters between those with and without prior COVID-19 infection. Methods: This cross-sectional study evaluated 120 elite male athletes (60 post COVID-19, 60 controls) using anthropometric measurements, body composition analysis, pulmonary function tests, HRV analysis, arterial stiffness assessments, hemodynamic monitoring, and microcirculatory function tests. Results: Athletes post COVID-19 showed significantly higher lean mass (p = 0.007), forced vital capacity (p = 0.001), and forced expiratory volume in 1 s (p = 0.007) than controls. HRV parameters did not significantly differ between the groups. Post-COVID-19 athletes exhibited peripheral vascular resistance (p = 0.048) and reflection index (p = 0.038). No significant differences were observed in the blood pressure, cardiac output, oxygen saturation, or microcirculatory oxygen absorption. Conclusions: Elite male athletes showed notable cardiovascular resilience after COVID-19, with only minor differences in vascular function. The maintained cardiac autonomic function and improved lung parameters in post-COVID-19 athletes suggests an adaptive response. These findings support the cardiovascular health of elite athletes following COVID-19 but emphasize the importance of continued monitoring. [ABSTRACT FROM AUTHOR]

Physical activity and regular exercise are well known to reduce the risks of cerebrovascular and cardiovascular diseases, leading the American College of Sports Medicine to endorse the concept that "exercise is medicine". However, a single bout of exercise temporarily raises arterial blood pressure (BP) to meet the metabolic demands of working muscle, and this BP response is particularly exaggerated in older adults and patients with cardiovascular conditions, such as hypertension, resulting in an exaggerated BP response during exercise. This presents a paradox: while regular exercise is crucial for preventing these diseases, excessively high BP responses during exercise could increase the risk of vascular damage. The mechanisms underlying this exaggerated BP response during exercise remain unclear, and effective exercise regimens for these populations have yet to be established. Currently, low-intensity exercise is recommended; however, its efficacy in disease prevention is uncertain. Notably, even among healthy individuals, there is significant variation in the BP response to exercise. Some healthy individuals, despite having normal resting BP, exhibit an exaggerated BP response during physical activity. Importantly, these individuals are often unaware that their BP becomes excessively elevated during physical activity. Repeated exposure to these heightened BP responses through regular physical activity may increase their long-term risk of cardiovascular disease. How can we prevent disease development in these individuals while still ensuring the effectiveness of exercise? Some studies have shown that individuals with a family history of hypertension may experience this phenomenon even in children and adolescents. Additionally, left ventricular hypertrophy contributes to an exaggerated BP response to exercise, suggesting a possible genetic influence. Conversely, other reports indicate that factors such as arterial stiffness, obesity, and low exercise capacity also contribute to this exaggerated response. Our recent preliminary data suggest that the cognitive benefits of exercise may be diminished in individuals who exhibit an exaggerated BP response during exercise. This implies that individuals with an exaggerated BP response, despite having normal resting BP, may not fully benefit from exercise. In this perspective paper, we review the physiological aspects of this phenomenon and explore strategies to address it. Additionally, we discuss BP responses in athletes within this content. Our goal is to prevent disease while maximizing the benefits of exercise for healthy individuals with an exaggerated BP response, as well as for elderly and cardiovascular patients. [ABSTRACT FROM AUTHOR]

Background. Cardiovascular (CV) diseases are the most common causes of morbidity and mortality in hemodialysis (HD) patients. We studied the effect of high visit-to-visit ultrafiltration (UF) variability on CV abnormalities in HD patients. Methods. Twenty-nine consecutive patients (age: 65.6 ± 10.4 years) were recruited. Samples for routine lab tests were drawn pre-HD for syndecan-1 (SDC-1) and endothelin-1 (ET-1) measurements pre-, mid- and post-HD. Applanation tonometry was performed pre-, mid- and post-HD. Visit-to-visit ultrafiltration volume variability (UVSD) was calculated as the standard deviation of the UF volume/dialysis session in the preceding 12 months. Echocardiography was performed post-HD. Results. Patients were divided into two groups based on the median of UVSD (500 mL). The average UF volume/HD was not different between the groups. Blood pressure (BP) values were similar. Pre-HD cfPWV (10.75 m/s) was lower in the high UVSD group (14.1 m/s, p = 0.03). In the high UVSD group, post-HD cfPWV (13.9 m/s) was higher than the pre-HD cfPWV (p < 0.05). Pre-HD ET-1 was lower in the high UVSD group (8.6 ± 3.9 vs. 10.8 ± 2.7 pg/mL, p < 0.05). Left ventricular end-diastolic diameter (LVEDD) and left ventricular mass index (LVMI) were higher in the high UVSD group (55.7 ± 7.3 vs. 51.0 ± 5.4 mm and 449.9 ± 180.5 vs. 350.3 ± 85.9 g/m², p < 0.005, respectively). Left ventricular ejection fraction (LVEF) was lower in the high UVSD group (53.5 vs. 60, p < 0.05). Conclusions. High UVSD was associated with increased left ventricular hypertrophy and dysfunction and decreased LVEF compared to low visit-to-visit UV variability despite similar UF volumes temporarily compensated by more elastic arteries. The observed abnormalities may increase CV risk. [ABSTRACT FROM AUTHOR]

The present cross-sectional study aimed to compare climacteric symptoms and arterial stiffness indices between perimenopausal and postmenopausal women. The study sample comprised 70 healthy female participants, including 27 perimenopausal (49.8 ± 3.8 years) and 43 postmenopausal (55.7 ± 4 years) individuals. Validated methods were used to assess physical activity level, quality of life, climacteric symptoms, and anthropometric data. Arterial stiffness parameters were measured using Mobil-O-Graph. Pulse wave velocity (PWV) had a higher mean in the postmenopausal group than in the perimenopause group [8.04 m/s (SD 0.79) vs 7.01 m/s (SD 0.78), p <.001). PWV was strongly correlated with peripheral (r = 0.619) and central (r = 0.632) Systolic Blood Pressure (SBP) in postmenopausal group and an even stronger correlation was observed in perimenopausal group (r = 0.779 pSBP and 0.782 cSBP). BMI was a risk predictor in the perimenopausal group contributing positively to increase Pulse Pressure Amplification (PPA) (0.458, p <.05). In postmenopausal women, heart rate (HR) was a stronger predictor for central SBP, cardiac output, and total vascular resistance, whereas perimenopausal women HR influenced central diastolic blood pressure and PPA. Vascular changes initiating during perimenopause may contribute to the development of cardiovascular pathologies in the postmenopausal period. Further research with larger, representative samples is warranted to corroborate these findings. [ABSTRACT FROM AUTHOR]

Excess sodium consumption contributes to arterial dysfunction in humans. The C57BL/6 strain of mice has been used to identify mechanisms by which arterial dysfunction occurs after excess sodium consumption. However, there are concerns that C57BL/6 mice have strain-specific resistance to high-sodium (HS) diet-induced hypertension. To address this concern, we performed a meta-analysis to determine if excess sodium consumption in C57BL/6 mice induces arterial dysfunction. Databases were searched for HS versus standard diet studies that measured arterial function [i.e., systolic blood pressure (BP), endothelium-dependent dilation (EDD), and central arterial stiffness] in C57BL/6 mice. A total of 39 studies were included, demonstrating that the HS condition resulted in higher systolic BP than control mice with a mean difference of 9.8 mmHg (95% confidence interval [CI] = [5.6, 14], P < 0.001). Subgroup analysis indicated that the systolic BP was higher in HS compared with the control condition when measured during night compared with daytime with telemetry (P < 0.001). We also identified that the difference in systolic BP between HS and control was ∼2.5-fold higher when administered through drinking water than through food (P < 0.001). A total of 12 studies were included, demonstrating that the HS condition resulted in lower EDD than control with a weighted mean difference of −12.0% (95% CI = [−20.0, −4.1], P = 0.003). It should be noted that there was considerable variability across studies with more than half of the studies showing no effect of the HS condition on systolic BP or EDD. In summary, excess sodium consumption elevates systolic BP and impairs EDD in C57BL/6 mice. NEW & NOTEWORTHY: C57BL/6 mice are perceived as resistant to high-sodium diet-induced arterial dysfunction. This meta-analysis demonstrates that excess sodium consumption elevates blood pressure and impairs endothelium-dependent dilation in C57BL/6 mice. Nighttime measurements show more pronounced blood pressure elevation. In addition, sodium administration via drinking water, compared with food, induces a greater blood pressure elevation. These findings may be influenced by outlier studies, as the majority of studies showed no adverse effect of excess sodium consumption on arterial function. [ABSTRACT FROM AUTHOR]

Independently, both prolonged uninterrupted sitting and the onset of menopause negatively impact markers of cardiovascular risk. Whether their combination augment these responses additively remains unknown. This study assessed whether prolonged uninterrupted sitting causes greater central and peripheral cardiovascular dysfunction in post-menopausal women compared to pre-menopausal women. To address this, 23 healthy women (13 pre-menopausal [43.77 ± 4.30 years] and 10 post-menopausal [57.20 ± 8.55 years]) sat uninterrupted for 2-h. Carotid-femoral pulse wave velocity (cf-PWV), pulse wave analysis (PWA), lower limb venous pooling (HHb), and calf circumference were assessed pre-and post-sitting using general linear mixed models, with age as a covariate. Changes in MAP over time (both between and within groups) was assessed using a two-way repeated-measures-ANOVA. There were no significant interactions for any outcome measures. However, for cf-PWV, there was a significant main effect of group (Δ = 0.854 ± 0.354 m s−1; p = 0.026, ηp2 = 0.707). For PWA, only heart rate (HR) and pressure forwards (Pf) showed significant main effects 13 of time [Δ = 6 ± 1 bts-min−1, p < 0.001, ηp2 = 0.861] and group [Δ = 3.893 ± 1.450 mmHg, p = 0.016, ηp2 = 0.271], respectively. Both HHb (Δ = 2.737 ± 0.952, p = 0.009, ηp2 = 0.742) and calf circumference (Δ = 0.812 ± 0.128 cm, p < 0.001, ηp2 = 0.863) significantly increased over time. Whilst post-menopausal women demonstrated greater overall arterial stiffness (increased cf-PWV at baseline), there was no difference in cardiovascular response (central or peripheral) to 2-h of prolonged sitting between the pre- and post-menopausal women. [ABSTRACT FROM AUTHOR]

Background: The association between arterial stiffness and alcohol consumption is still controversial. We investigated this relationship by performing continuous analysis in men drinking only beer/cider, and women drinking only red wine. Methods: This cross‐sectional study involved participants aged 40–69 years consisting of 9029 men who drank only beer/cider, and 6989 women drinking only red wine. Alcohol consumption was captured by self‐reported questionnaire and reported as units per week, where one unit is equal 10 mL pure ethanol. Arterial stiffness index (ASI) was estimated using photoplethysmography. Results: In men consuming a mean 17.8 (5th and 95th percentiles, 2.6–76.7) units/week, ASI increased by heptiles (sevenths) of alcohol captured from beer/cider consumption and after adjusting for age (9.14, 9.40, 9.51, 9.53, 9.80, 9.80, 10.00 m/s; p‐trend < 0.001) and after full adjustment (9.29, 9.46. 9.55, 9.55, 9.73, 9.73, 9.75 m/s; p‐trend = 0.013). Similarly, in women consuming a mean 8.1 (1.6–29.3) units/week, ASI increased by heptiles of alcohol captured from red wine consumption and after adjusting for age (8.05, 8.05, 8.05, 8.11, 8.17, 8.30, 8.45 m/s; p‐trend = 0.012) and borderline significant after full adjustment (8.05, 8.07, 8.05, 8.07, 8.11, 8.22, 8.43 m/s; p‐trend = 0.055). These associations were confirmed in multivariable‐adjusted regression analysis in all men, men younger and older than 50 years, and when consuming more than 14 units per week. Similarly, these associations were confirmed in all women, women older than 50 years, and in those consuming more than 14 units per week. Conclusions: Positive linear relationships exist between arterial stiffness and alcohol, irrespective of whether captured from beer/cider consumption in men or red wine consumption in women. No evidence existed to support the notion that our arteries benefit from any level of alcohol consumption. [ABSTRACT FROM AUTHOR]

Objective: To compare maternal vascular indices and hemodynamic parameters at 35–37 weeks' gestation in pregnancies complicated by delivery of a small‐for‐gestational‐age (SGA) or growth‐restricted (FGR) neonate. Methods: This was a prospective observational study of women with a singleton pregnancy attending for a routine hospital visit at 35 + 0 to 36 + 6 weeks' gestation. The visit included recording of maternal demographic characteristics, medical history, vascular indices and hemodynamic parameters, which were obtained using a non‐invasive operator‐independent device and included pulse‐wave velocity, augmentation index, cardiac output, stroke volume, central systolic and diastolic blood pressure, total peripheral resistance and heart rate. Women with hypertensive disorders of pregnancy were excluded. SGA was diagnosed if birth weight was < 10th percentile. FGR was diagnosed if, in addition to birth weight < 10th percentile, at the 35–37‐week scan, uterine artery or umbilical artery pulsatility index (PI) was > 95th percentile or fetal middle cerebral artery PI was < 5th percentile. Results: Among the 6413 women included in the study, there were 605 (9.4%) cases of SGA, 133 (2.1%) cases of FGR and 5675 (88.5%) cases that were unaffected by SGA or FGR. Women with SGA or FGR, compared to unaffected pregnancies, had increased peripheral vascular resistance and reduced cardiac output. Central systolic and diastolic blood pressure were increased in the FGR group compared with the unaffected group. Aortic stiffness, as assessed by pulse‐wave velocity, and augmentation index did not differ between affected and unaffected pregnancies. In the FGR group, compared with the SGA group, central systolic and diastolic blood pressure were higher, whereas heart rate was lower. Conclusions: SGA and FGR pregnancies exhibit deranged maternal hemodynamic responses compared with unaffected pregnancies. Pregnancies with FGR have higher central blood pressure compared to those with SGA, but it remains unclear whether these differences are driven by the size of the fetus or pathological fetal growth. © 2024 International Society of Ultrasound in Obstetrics and Gynecology. [ABSTRACT FROM AUTHOR]

Familial Mediterranean fever (FMF) is an autoinflammatory disease which may cause endothelial dysfunction and arterial stiffness. In this study, we evaluated patients with FMF in terms of arterial stiffness indicators and investigated whether there was any difference according to colchicine response. This is a single-center, prospective, case-control study conducted on pediatric patients with FMF. Patients were categorized into 2 groups: patients on colchicine monotherapy (group 1) and patients who used anti-interleukin-1 (IL-1) plus colchicine (group 2). Patient age, mutations in the MEFV gene, overall duration of treatments, and general characteristics of symptoms were recorded. Laboratory values in an attack-free period were noted. Pulse wave velocity (PWV) was measured in all patients. Erythrocyte sedimentation rate and C-reactive protein, nocturnal hypertension, and PWV were higher in group 2. Arterial stiffness develops due to subclinical inflammation in patients with FMF. It is more pronounced in colchicine-resistant patients. [ABSTRACT FROM AUTHOR]

Preeclampsia is a hypertensive disorder of pregnancy marked by vascular dysfunction, large artery stiffness, and excess oxidized low-density lipoprotein (oxLDL). oxLDL activates oxidative stress pathways which contribute to arterial stiffness through interaction with the lectin-like oxLDL receptor 1 (LOX-1). Increased vascular stiffness is associated with higher pulse wave velocity and downstream microvasculature damage. Here we evaluated the ability of LOX-1 inhibition (LOX-1i) to prevent large artery structural and microvascular structural and functional changes via assessment of the descending thoracic aorta (DTAo) and posterior cerebral arteries (PCA) in a high cholesterol model of preeclampsia. Adult female Sprague Dawley normal late-pregnant (LP) and experimentally preeclamptic (ePE, high cholesterol diet d7-19) animals underwent intraperitoneal (i.p.) implantation of a mini-osmotic pump at d12 containing LOX-1 neutralizing antibodies (ePE + LOX-1i, n = 7) or goat IgG as vehicle control (LP + IgG, n = 8 and ePE + IgG, n = 8). Animals were studied at d19. DTAos and PCAs were removed for histologic assessment and isolated vessel experiments, respectively. Fetuses and placentas were weighed individually. Plasma was analyzed for markers of oxidative stress. ePE + IgG DTAo elastin content (an indirect metric of stiffness) was not significantly different from the LP + IgG group. Nonetheless, trending elastin break and sinuosity data (higher number of breaks and lower sinuosity in the ePE + IgG group compared to LP + IgG) suggested increased stiffness in this high cholesterol PE model. LOX-1i appeared to prevent a decrease in elastin. PCAs showed no structural changes with ePE or LOX-1i. ePE PCAs had increased reactivity to the nitric oxide donor sodium nitroprusside and decreased tone that was unaffected by LOX-1i. ePE animals had increased plasma oxLDL and 3-nitrotyrosine that was unaffected by LOX-1i. Taken together, LOX-1i may improve large artery stiffness without mitigation of the oxidative stress or cerebral microvascular dysfunction seen in ePE. Understanding these mechanisms is important in abating the long-term risks of preeclampsia. [ABSTRACT FROM AUTHOR]

Introduction: Multiple sclerosis (MS) is an immune-mediated, neurodegenerative disease of the central nervous system. Fatigue represents one of the most prevalent and limiting symptoms of MS, and is associated with vascular dysfunction, notably increased arterial stiffness. Objective: This study examined the relationship between arterial stiffness and perceived fatigue in persons with MS. Methods: The sample of 52 persons with MS (71.2% Female; Age: 46.7 ± 12.3 yrs.) completed arterial stiffness and fatigue assessments as baseline for an exercise training intervention. Applanation tonometry measured arterial stiffness, pulsatility and waveform characteristics, and yielded the following outcomes: carotid-femoral pulse wave velocity (cfPWV), carotid pulse-pressure (cPP), and aortic augmentation pressure (AP). Perceived fatigue was measured using the Fatigue Severity Scale (FSS). Results: The mean (SD) scores for cfPWV, cPP, and AP were 7.0 ± 1.8 m/s, 35.7 ± 8.8 mmHg, 8.2 ± 6.2 mmHg, respectively. The mean (SD) FSS score was 4.6 ± 1.4 and indicated elevated fatigue. There were statistically significant (p <.05) inverse correlations between cfPWV (r = –.32), cPP (r = –.37) and AP (r = –.32) with FSS scores, and the correlations remained significant even after controlling for disability, body mass index, age, and sex. Conclusion: Our results indicate a consistent pattern of inverse relationships between arterial stiffness, pulsatility, and waveforms with fatigue independent of disability, body mass index, age, and sex in MS. This could be explained by lower sympathetic activation linking higher arterial stiffness, pulsatility and augmentation pressure with lower fatigue in persons with MS. [ABSTRACT FROM AUTHOR]

To investigate the association between cardiovascular risk estimated using the Framingham Risk Score (FRS) and carotid stiffening determined using ultrafast pulse wave velocity (ufPWV) measurements in apparently healthy individuals. We enrolled 1034 apparently healthy participants without known cardiovascular disease who underwent ufPWV measurements. Clinical and laboratory findings, carotid intima–media thickness (cIMT), pulse wave velocity at the beginning of systole (PWV-BS), and pulse wave velocity at the end of systole (PWV-ES) were assessed. In FRS assessments based on major cardiovascular risk factors (CVRFs), participants were assigned into three risk categories: low risk (<10%, n = 679), intermediate risk (10–20%, n = 191), and high risk (>20%, n = 164); the low-risk category was further subdivided into three subcategories: < 1% (n = 58), 1%− 5% (n = 374) and > 5% (n = 247). Multivariate logistic regression analyses with crude and adjusted odds ratios (ORs) were used to evaluate the association of carotid stiffening and FRS-based risk stratification. Carotid stiffening indicated by PWV-BS and PWV-ES differed notably between the FRS-estimated low-risk vs. intermediate-risk and high-risk categories, but only PWV-ES differed notably among the low-risk subcategories (all p < 0.010), and correlated notably with the FRS-estimated risk most obviously in low-risk participants (r = 0.517). In participants with cIMT < 0.050 cm, only PWV-ES differed significantly among the FRS-estimated risk categories (all p < 0.001). Increased PWV-BS (adjusted OR: 1.49; p = 0.003) and PWV-ES (adjusted OR: 1.29; p = 0.007) were both associated with FRS categories independent of conventional CVRFs in low- vs. intermediate-risk categories, but not in low- vs. high-risk categories (all p > 0.050). In vivo imaging of carotid stiffening by ufPWV measurements is independently linked to FRS categories, and ufPWV indices may help stratify differing levels of cardiovascular risk in apparently healthy young people. Data generated or analyzed during the study are available from the corresponding author by reasonable request. • Carotid stiffening quantified by ufPWV measurements differed notably among FRS-estimated risk categories and low-risk subcategories. • ufPWV indices correlated notably with FRS-estimated risk and major CVRFs. • PWV-ES increased steeply with higher FRS categories, even with normal cIMT. • ufPWV indices were associated with cardiovascular risk stratification independently in low- vs. intermediate-risk populations. • ufPWV may be a promising quantitative predictor for cardiovascular risk stratification in apparently healthy young people. [ABSTRACT FROM AUTHOR]

Background: Arterial stiffness is a crucial factor in the pathogenesis of cardiovascular disease, often associated with aging. However, the impact of smoking on arterial stiffness is frequently underestimated. This study aims to investigate the intricate relationship between smoking and arterial stiffness to advance our understanding of and therapeutic approaches to cardiovascular health. Methods: A prospective analysis was conducted from January to July 2024, focusing on arterial stiffness parameters in a cohort of students from the Carol Davila University of Medicine and Pharmacy. Participants were categorized as smokers or non-smokers based on self-reported smoking status. The study endpoints included correlations between high pulse wave velocity, elevated peripheral and central systolic blood pressure, increased peripheral and central pulse pressure, and smoking status. These markers were assessed using an arteriograph device measuring the time difference between the initial forward pulse wave and the reflected pulse wave in the brachial artery to indirectly estimate the PWV using oscillometric pulsations. Results: Our investigation, involving 102 young individuals aged 20 to 26 (69 females, 33 males), revealed that smokers exhibited significantly higher average values of arterial stiffness indicators compared to non-smokers. Current smokers had higher mean systolic blood pressure (130.65 vs. 123.05 mmHg), higher mean peripheral pulse pressure (53.19 vs. 45.64 mmHg), higher mean central pulse pressure (33.66 vs. 29.69 mmHg), and higher mean pulse wave velocity (5.27 vs. 5.03 m/s). Conclusions: The utilization of arterial stiffness markers as predictive tools offers opportunities for personalized treatment strategies, potentially enhancing cardiovascular health outcomes. [ABSTRACT FROM AUTHOR]

BACKGROUND Myostatin is a protein compound, structurally related to the transforming growth factor-beta protein, which plays a pivotal role in regulating muscle growth and extracellular matrix production. It exerts both profibrotic and antihypertrophic effects on vascular smooth muscle cells. Aim of the study was to explore the potential association between serum myostatin levels (sMSTN) and carotid-femoral pulse wave velocity (cf-PWV), carotid-radial pulse wave velocity (cr-PWV), and their ratio (PWVr), in a cohort of healthy adolescents. METHODS A cohort of 128 healthy subjects (mean age 17 ± 2 years, 59% male) was randomly selected from participants to the MACISTE (Metabolic And Cardiovascular Investigation at School, TErni) study. sMSTN was assessed utilizing an enzyme-linked immunosorbent assay. PWVs were measured in the supine position using high-fidelity applanation tonometry. RESULTS The mean cf-PWV was 5.1 ± 0.9 m/s, cr-PWV was 6.9 ± 0.9 m/s, and PWVr was 0.75 ± 0.12. PWVr exhibited a linear increase across increasing quartiles of sMSTN (0.71 ± 0.1, 0.74 ± 0.1, 0.7 ± 0.1, 0.77 ± 0.1, P for trend = 0.03), whereas the association between sMSTN and each single component of PWVr (cf-PWV, cr-PWV) did not attain statistical significance. Quartiles of sMSTN displayed a positive trend with serum HDL-cholesterol (P  = 0.01) and a negative one with LDL-cholesterol (P  = 0.01). In a multivariate linear model, the association between PWVr and sMSTN was independent of SBP values, age, sex, heart rate, BMI, HDL-cholesterol, and HOMA Index CONCLUSIONS In healthy adolescents, sMSTN showed independent associations with PWVr, a measure of central-to-peripheral arterial stiffness gradient. sMSTN may exert differential effects on the structural and functional properties of the arterial wall. [ABSTRACT FROM AUTHOR]

BACKGROUND We evaluated whether chronic coffee consumption affects arterial stiffness, assessed by cardio-ankle vascular index (CAVI). METHODS In 514 subjects, aged 66.6 ± 9.9 years (mean ± SD), recruited in the 3rd follow-up of the PAMELA study, subdivided into 3 groups according to the daily intake of regular coffee (0, 1–2, and ≥3 cups/day), we measured CAVI and clinic, ambulatory blood pressure (BP), and other variables. RESULTS The 3 groups displayed similar age, gender, metabolic, and renal profile. Clinic and ambulatory BPs were similar in the 3 groups, this being the case for CAVI (0 cup: 9.1 ± 1.8, 1–2 cups: 9.5 ± 2.3, and ≥3 cups: 9.2 ± 2.1 m/s, P  = NS). No significant gender difference in CAVI and in participants under antihypertensive treatment was detected. CONCLUSIONS Our data show that chronic coffee consumption leaves unaffected arterial stiffness in the general population, this being the case in subgroups. The neutral vascular impact of coffee may favor the absence of any significant BP effect of habitual coffee intake. [ABSTRACT FROM AUTHOR]

Background: Hyperglycemia-induced oxidative stress is a well-established pathological mediator of vascular complications in diabetes. We assessed plasma oxidant and antioxidant levels in response to acute and chronic hyperglycemia in relation to vascular stiffness and varying degrees of kidney disease in type 1 diabetes individuals. Methods: The acute hyperglycemia study included 22 type 1 diabetic individuals with normal albumin excretion rate (AER) and 13 non-diabetic controls. These individuals received an acute glucose challenge during a 120-minute hyperglycemic clamp. The chronic hyperglycemia study included 118 type 1 diabetic individuals with chronically low (n = 60) or high (n = 58) HbA1c concentrations and varying degrees of diabetic kidney disease (DKD) classified as normal, moderate, or severe albuminuria (AER). Levels of malondialdehyde (MDA), reactive oxygen metabolites (ROMs), total antioxidant capacity (TAC), biological antioxidant potential (BAP) and superoxide dismutase (SOD) were measured from plasma or serum samples in the FinnDiane study. Results: Levels of MDA (p < 0.01) and ROMs (p < 0.01) were elevated in type 1 diabetes individuals compared to non-diabetic controls at baseline. Acute hyperglycemia further increased MDA levels (p < 0.05) and sustained the elevation of ROMs in type 1 diabetes individuals. Acute hyperglycemic challenge impaired TAC in both non-diabetic (p < 0.05) and type 1 diabetes (p < 0.01) individuals compared to baseline whereas BAP was increased (p < 0.05) with no difference observed in non-diabetic controls. There was a positive association between high circulating MDA and AIx (r2 = 0.611, p = 0.05), and between delta ROMs and delta AIx (r2 = 0.955, p = 0.014) in combined analysis of individuals with type 1 diabetes and non-diabetic controls. Type 1 diabetes individuals with varying status of DKD, showed elevated levels of ROMs in those with high HbA1c compared to their counterpart with low HbA1c (p < 0.05). Individuals with severe albuminuria showed elevated ROM levels (p < 0.01) and depressed antioxidant capacity (p < 0.01) compared to those with normal AER of comparable HbA1c concentrations. Conclusions: Biomarkers of oxidative stress are associated with vascular stiffness and DKD following acute and chronic hyperglycemic exposure and may provide added value to HbA1c in understanding disease pathology, predicting risk and assessing the status of secondary complications of type 1 diabetes. [ABSTRACT FROM AUTHOR]

Background: Postmenopausal women are at an increased risk of arterial stiffness, which can be assessed using estimated pulse wave velocity (ePWV). This study aimed to investigate the relationship between serum klotho levels and ePWV in postmenopausal women. Methods: This cross-sectional study used data from postmenopausal women who participated in the National Health and Nutrition Examination Survey (NHANES) between 2007 and 2016. Participants were divided into two groups based on the presence of hypertension. Weighted multivariate linear regression was used to analyze the relationship between serum Klotho levels and ePWV in each group. Restricted cubic spline models with multivariable adjustments were employed to examine nonlinear associations within each group. Results: Our analysis included 4,468 postmenopausal women from the NHANES database, with 1,671 in the non-hypertensive group and 2,797 in the hypertensive group. In all regression models, serum Klotho (lntransformed) levels were significantly and independently negatively correlated with ePWV in the non-hypertensive group. After fully adjusting for confounders, a 1-unit increase in ln(Klotho) was associated with a 0.13 m/s decrease in ePWV (b = -0.13, 95% CI -0.23 to -0.03; p = 0.008). Additionally, in the fully adjusted model, participants in the highest quartile of ln(Klotho) had an ePWV value 0.14 m/s lower than those in the lowest quartile (p for trend = 0.017; 95% CI -0.23 to -0.05; p = 0.002). This negative correlation was consistent across subgroups and was particularly significant among women aged < 60 years, nonsmokers, and non-Hispanic Black women. However, no association was observed between serum Klotho levels and ePWV in the hypertensive group. Conclusion: Hypertension may affect the relationship between serum Klotho level and ePWV in postmenopausal women. Increased serum Klotho levels may reduce arterial stiffness in postmenopausal women. Further studies are required to confirm these findings. [ABSTRACT FROM AUTHOR]

Background/Objectives: This study compares the power of the radiofrequency (RF) signal reflected from the media layer (media power) of the common carotid artery (CCA) and the CCA stiffness between individuals with and without type 2 diabetes mellitus (T2DM). It also evaluates the associations of CCA media power with plasma glucose and lipid levels, as well as carotid stiffness. Methods: A total of 540 individuals, 115 with and 425 without T2DM (273 males, mean age = 64 ± 8 years) were studied using RF-based tracking of the right CCA. The following parameters were measured: CCA media thickness, luminal diameter, wall tensile stress (WTS), local pulse wave velocity (PWV), and media power. Results: Compared to the non-diabetic individuals, the T2DM patients had significantly higher CCA media thickness (652 ± 122 vs. 721 ± 138 microns, p < 0.005), luminal diameter (6.12 ± 0.78 vs. 6.86 ± 0.96 mm, p < 0.0005), media power (36.1 ± 4.8 vs. 39.3 ± 4.6, p < 0.0001), and PWV (7.65 ± 1.32 vs. 8.40 ± 1.89 m/s; p < 0.01), but comparable WTS (32.7 ± 10.4 vs. 33.1 ± 10.7 kPa; p = 0.25). In the entire population, CCA media power was independently associated with male sex, pulse pressure, current smoking, and T2DM; when T2DM was not included in the model, triglycerides emerged as an independent determinant of media power. The CCA PWV was independently associated with age, pulse pressure, media power, and T2DM. Conclusions: Our findings suggest the presence of structural changes in the arterial media of T2DM patients, leading to carotid stiffening and remodeling, aiming to preserve WTS. T2DM-related changes in arterial wall composition may be driven by high plasma triglyceride levels, which have previously been associated with both arterial stiffening and the incidence of CV events. [ABSTRACT FROM AUTHOR]

Background: Sleep regularity has been linked to a risk of arterial stiffness (AS). However, the association between sleep regularity indicators, which reflect 24-hour sleep variability, and AS has not yet been examined. Methods: We analyzed data from 516 adults, aged 40–65 years (the median age of 51 years), from the 'Follow-up Study of Sleep Characteristics and Chronic Diseases in the Middle-aged and Elderly Population in Guizhou Province'. Participants underwent assessments of AS (OMRON HBP-8000, baPWV ≥ 1400 cm/s) and sleep (wrist smart band (Honor band 5i) for ≥ 7 days). Logistic regression was utilized to evaluate the odds ratio (OR) and 95% confidence interval (CI) of the association between sleep regularity and AS. Results: A total of 516 people were included in this study, of which 279 (54.07%) were in the AS group. The univariate results showed that the AS group (Median 71.18) had lower SRI compared to the No-AS group (Median 75.00) (p < 0.001). The multifactorial results showed participants with higher SRI scores were more likely to have a lower risk of AS compared to those with lower SRI scores (ORQ4 VS. Q1=0.46, 95%CI: 0.25–0.85, p = 0.013). The SRI effect was more pronounced in male (ORQ4 VS. Q1=0.28, 95%CI: 0.12–0.69, p = 0.005), snoring populations (ORQ4 VS. Q1=0.13, 95%CI: 0.04–0.48, p = 0.002), and non-retired populations (ORQ4 VS. Q1=0.45, 95%CI: 0.22–0.92, p = 0.028). Conclusions: The present findings indicated that the effect between SRI and AS may be more sensitive than the standard deviation of sleep duration as well as the standard deviation of sleep onset. [ABSTRACT FROM AUTHOR]

This study aimed to assess the effect of a combination of aerobic exercise training (ET) and Chlorella (CH) intake on arterial nitric oxide (NO) production and arterial stiffness in obese rats. Twenty-week-old obese male rats were randomly grouped into four (n = 6): OBESE-SED (sedentary control), OBESE-ET (treadmill 25 m/min, 1 h, 5 d/week), OBESE-CH (0.5% Chlorella powder in normal diet), and OBESE-ET+CH (combination of ET and CH intake) groups. The carotid–femoral pulse wave velocity (cfPWV), an index of arterial stiffness, was significantly lesser in the OBESE-ET, OBESE-CH, and OBESE-ET+CH groups than in the OBESE-SED group, and in the OBESE-ET+CH group significantly further enhanced these effects compared with the OBESE-ET and OBESE-CH groups. Additionally, arterial nitrate/nitrite (NOx) levels were significantly greater in the OBESE-ET, OBESE-CH, and OBESE-ET+CH groups than in the OBESE-SED group, and the OBESE-ET+CH group compared with the OBESE-ET and OBESE-CH groups. Furthermore, arterial NOx levels were positively correlated with arterial endothelial NO synthase phosphorylation levels (r = 0.489, p < 0.05) and negatively correlated with cfPWV (r = −0.568, p < 0.05). In conclusion, a combination of ET and CH intake may reduce arterial stiffness via an enhancement of the arterial NO signaling pathway in obese rats. [ABSTRACT FROM AUTHOR]

Background/Objectives: The present study examined the effect of 12-week combined exercise training in normobaric hypoxia on arterial stiffness, inflammatory biomarkers, and red blood cell (RBC) hemorheological function in 24 obese older women (mean age: 67.96 ± 0.96 years). Methods: Subjects were randomly divided into two groups (normoxia (NMX; n = 12) and hypoxia (HPX; n = 12)). Both groups performed aerobic and resistance exercise training programs three times per week for 12 weeks, and the HPX group performed exercise programs in hypoxic environment chambers during the intervention period. Body composition was estimated using bioelectrical impedance analysis equipment. Arterial stiffness was measured using an automatic waveform analyzer. Biomarkers of inflammation and oxygen transport (tumor necrosis factor alpha, interleukin 6 (IL-6), erythropoietin (EPO), and vascular endothelial growth factor (VEGF)), and RBC hemorheological parameters (RBC deformability and aggregation) were analyzed. Results: All variables showed significantly more beneficial changes in the HPX group than in the NMX group during the intervention. The combined exercise training in normobaric hypoxia significantly reduced blood pressure (systolic blood pressure: p < 0.001, diastolic blood pressure: p < 0.001, mean arterial pressure: p < 0.001, pulse pressure: p < 0.05) and brachial–ankle pulse wave velocity (p < 0.001). IL-6 was significantly lower in the HPX group than in the NMX group post-test (p < 0.001). Also, EPO (p < 0.01) and VEGF (p < 0.01) were significantly higher in the HPX group than in the NMX group post-test. Both groups showed significantly improved RBC deformability (RBC EI_3Pa) (p < 0.001) and aggregation (RBC AI_3Pa) (p < 0.001). Conclusions: The present study suggests that combined exercise training in normobaric hypoxia can improve inflammatory biomarkers and RBC hemorheological parameters in obese older women and may help prevent cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Objective Patients with Behçet's disease (BD) may experience long-term morbidity caused by various forms of cardiovascular disease. This study aimed to assess the risk for cardiovascular comorbidity in paediatric BD patients with and without vascular involvement, independent of the contribution of traditional risk factors. Methods Paediatric patients classified as having BD according to the 2015 Peadiatric BD (PEDBD) criteria were included in the study. Twenty-four-hour ambulatory blood pressure monitoring (ABPM), transthoracic echocardiography, and carotid intima-media thickness (cIMT) measurements were performed. Patients with an active disease or those who have other known risk factors for cardiovascular disease were not included in the study. Results Thirty-one children and adolescents with paediatric BD (16 female, 51.6%; F/M: 1.06) were enrolled in the study. Among the BD patients, 10 patients (34.4%) had abnormal ABPM. Carotid IMT values, mean arterial pressure, systolic and diastolic blood pressure by ABPM and the prevalence of abnormal ABPM, non-dipping, and ambulatory hypertension were similar between patients with and without vascular involvement. The echocardiography measurements showed that BD patients with vascular involvement had a significantly higher velocity and velocity time integral of the left ventricle outflow tract, which may indicate increased stiffness of the aorta. Conclusion Paediatric BD patients with vascular involvement may tend to have more cardiovascular risk factors. However, cardiovascular assessment should be considered in all BD patients, regardless of the involved systems. We suggest that ABPM may accurately define hypertension and cardiovascular risk in BD. [ABSTRACT FROM AUTHOR]

Background and Aims Methods Results Conclusion Cardiovascular disease is the leading cause of death in patients with chronic kidney disease (CKD) and has been associated with abnormalities of mineral metabolism and vascular calcification. Vitamin D influences parathyroid hormone values and calcium and phosphate metabolism, and may play a role in vascular function and bone health. We aimed to test our hypothesis that vitamin D deficiency is associated with arterial stiffness, aortic calcification and lower bone mineral density (BMD) in patients with CKD.A cross‐sectional analysis was performed using baseline data from the IMpact of Phosphate Reduction On Vascular Endpoints in CKD (IMPROVE‐CKD) study cohort. Clinical and laboratory parameters were compared between those with and without vitamin D deficiency, defined as 25‐hydroxyvitamin D (25(OH)D) <50 nmol/L. Univariable and multivariable linear regression analyses were performed to assess associations between serum 25(OH)D levels and pulse wave velocity (PWV), augmentation index (AIx), abdominal aortic calcification (measured by the Agatston score) and lumbar spine BMD.Baseline 25(OHD) values were available in 208 out of 278 IMPROVE‐CKD study participants, with a mean value of 70.1 ± 30.7 nmol/L. Of these, 57 (27%) patients had vitamin D deficiency. Those with 25(OH)D deficiency were more likely to have diabetes (56% vs 38%), cardiovascular disease (54% vs 36%) and lower serum calcium (2.29 ± 0.13 vs 2.34 ± 0.13 mmol/L). On univariable and multivariable regression analyses, baseline 25(OH)D values were not associated with PWV, the AIx, Agatston score or BMD.Baseline 25(OH)D levels were not associated with intermediate markers of vascular function and BMD in patients with CKD stages 3b and 4. [ABSTRACT FROM AUTHOR]

Cardio‐ankle vascular index (CAVI) is an innovative indicator of large‐artery stiffness, which is evaluated by the pulse wave velocity (PWV) measurement. Mortality and morbidity due to cardiovascular diseases among the general public with high‐risk conditions such as hypertension are usually associated with arterial stiffness. CAVI modelizes the hazard of future cardiovascular events with standard risk factors. Additionally, the "European Society of Hypertension and Cardiology" included the aortic PWV assessment in managing hypertension in their updated guidelines in 2007. We conducted this systematic review to collect, summarize, and evaluate the evidence from relevant reported studies. A literature search of four databases was conducted comprehensively until February 2024. Cardiovascular events are the primary outcome of interest in this study, cardiovascular events that have been defined as major adverse cardiac events include "heart failure", "stroke", "myocardial infarction", "cardiovascular deaths", "stable angina pectoris", "coronary revascularization", and "unstable angina pectoris". We included five studies with a 11 698 sample size in this systematic review. All five prospective studies investigated composite cardiovascular events as an outcome. Three of them revealed a statistically significant prediction ability of CAVI to assess Cardiovascular disease (CVD) risk. Further analysis is required. Current evidence is insufficient to confirm the predictive power of CAVI in the assessment of cardiovascular risk in hypertensive patients. CAVI is modestly associated with incidents of CVD risk. It is necessary to conduct further studies to assess CAVI concerning CVD predictor measures in the masses and nations other than Asia. [ABSTRACT FROM AUTHOR]

Introduction: High-intensity interval exercise (HIIE) has demonstrated positive effects on cardiovascular function improvement. However, research on HIIE's effects on vascular function often lacks focus on women despite known variations in arterial stiffness improvement across different menstrual stages. Consequently, the effects of HIIE performed during various menstrual phases on vascular function in women remains unclear. Therefore, this study aimed to examine the acute effects of HIIE on cardiovascular function in healthy young women across different menstrual phases to elucidate its cardiovascular benefits. Methods: We recruited 13 regularly exercising female college students and determined their menstrual cycle status through a questionnaire. One week before formal HIIE, we measured the participants' peak heart rate (HRpeak). Next, HIIE sessions were conducted during the follicular and luteal phases within the same menstrual cycle. Each session consisted of 10 one-minute bouts of exercise at 90% HRpeak intensity, followed by one minute of rest. Blood pressure and finger-toe pulse wave velocity (ftPWV) were measured at rest, immediately postexercise (T0), and at 15-minute intervals up to 60 minutes post-exercise (T15, T30, T45, T60). The statistical analysis used two-way repeated measures ANOVA. The trapezoidal rule was used to calculate the incremental area under the curve (iAUC) for ftPWV, systolic blood pressure (SBP), and diastolic blood pressure (DBP) from rest to T0, with differences analyzed using a paired samples ttest. Results: ftPWV was significantly lower in the luteal phase group than in the follicular phase group at rest, T0, T15, and T30 (p < 0.05). SBP was significantly lower in the luteal phase group at rest (p < 0.05) and in the follicular phase group at T30, T45, and T60 compared to rest (p < 0.05). DBP was significantly lower in the luteal phase group at rest, T30, T45, and T60 (p < 0.05). The iAUC for ftPWV, SBP, and DBP were significantly lower in the luteal phase group than in the follicular phase group during the rest-T0 period (p < 0.05). Conclusion: Healthy young women can achieve optimal cardiovascular stimulation by engaging in HIIE during the follicular phase, while exercising during the luteal phase may help reduce the adverse effects on vascular function. [ABSTRACT FROM AUTHOR]

The objective of our study was to evaluate the changes in cardiovascular parameters in patients with hypertension who completed a 3-month physical exercise program. 229 subjects with high normal values of blood pressure and stage 1 hypertension (group 1) and 120 patients with stage 2 hypertension (group 2) followed a 3-month physical exercise program. The following parameters were measured: systolic blood pressure, diastolic blood pressure, pulse pressure, heart rate, pulse wave velocity. For group 1 there were statistically significant differences for all the tested parameters after the 3-month program (decreased systolic blood pressure, heart rate, pulse pressure and pulse wave velocity, p< 0.0001; lower diastolic blood pressure, p=0.018)). In group 2 all the tested parameters had decreased values after the 3-month rehabilitation program. However, only for the pulse wave velocity there was recorded a statistically significant reduction after the exercise program (p< 0.001). There were significant direct correlations between total cholesterol and pulse wave velocity for group 1 at both initial (p=0.024) and final assessments (p=0.03), and for group 2 patients at the 3-month assessment (p=0.001). A medium-term physical exercise program improved the cardiovascular parameters (blood pressure, arterial stiffness) in hypertensive patients. [ABSTRACT FROM AUTHOR]

Vascular aging, marked by alterations in the structure and function of blood vessels, including heightened arterial stiffness and impaired endothelial function, is linked to a higher likelihood of developing cardiovascular and age-associated pathological conditions. Oxidative stress and inflammation are key stimulation factors in vascular aging. Engaging in healthy dietary habits could enhance the functioning of blood vessels. The aim of this study was to conduct a literature review of the evidence regarding the relationship between food regimens, nutraceuticals, and dietary supplements and vascular health. A search of electronic databases, including PubMed, Scopus, and Web of Science Core Collection, was performed. Experimental and observational studies evaluating the association between food groups, nutraceuticals, supplements, and endothelial function and/or arterial stiffness were deemed eligible for this narrative review. Based on the current body of the included studies, food groups, nutraceuticals, and dietary supplements may not demonstrate superiority over placebos in enhancing markers of vascular health. To obtain more reliable evidence on the effectiveness of interventions in vascular health, additional RCTs with larger sample sizes, extended follow-up periods, and multi-center participation are necessary. Enhancing the credibility of these RCTs requires better control of dietary variables and more precise measurement of vascular health markers. [ABSTRACT FROM AUTHOR]

This study evaluated the relationship of non-invasive arterial stiffness parameters with an individual 10-year risk of fatal and non-fatal atherosclerotic cardiovascular disease (ASCVD) events in the cohort post-coronavirus disease 2019 (COVID-19). The study group included 203 convalescents aged 60.0 (55.0–63.0) and 115 (56.7%) women. The ASCVD risk was assessed as low to moderate to very high based on medical history (for 62 participants with pre-existing ASCVD/diabetes/chronic kidney disease in the entire cohort) or calculated in percentages using the Systemic Coronary Risk Evaluation 2 (SCORE2) algorithm based on age, sex, smoking status, systolic blood pressure (BP), and non-high-density lipoprotein cholesterol (for 141 healthy participants). The stiffness index (SI) and reflection index (RI) measured by photoplethysmography, as well as pulse pressure (PP), calculated as the difference between systolic and diastolic BP, were markers of arterial stiffness. Stiffness parameters increased significantly with the increase in ASCVD risk in the entire cohort. In 30 (14.8%) patients in the low- to moderate-risk group, the median SI was 8.07 m/s (7.10–8.73), RI 51.40% (39.40–65.60), and PP 45.50 mmHg (40.00–57.00); in 111 (54.7%) patients in the high-risk group, the median SI was 8.70 m/s (7.40–10.03), RI 57.20% (43.65–68.40), and PP 54.00 mmHg (46.00–60.75); and in 62 (30.5%) patients in the very-high-risk group, the median was SI 9.27 m/s (7.57–10.44), RI 59.00% (50.40–72.40), and PP 60.00 mmHg (51.00–67.00). In healthy participants, the SI ≤ 9.0 m/s (sensitivity of 92.31%, area under the curve [AUC] 0.686, p < 0.001) based on the receiver operating characteristics was the most sensitive variable for discriminating low to moderate risk, and PP > 56.0 mmHg (sensitivity of 74.36%, AUC 0.736, p < 0.001) was used for discriminating very high risk. In multivariate logistic regression, younger age, female sex, PP ≤ 50 mmHg, SI ≤ 9.0 m/s, and triglycerides < 150 mg/dL had the best relationship with low to moderate SCORE2 risk. In turn, older age, currently smoking, PP > 56.0 mmHg, RI > 68.6%, and diastolic BP ≥ 90 mmHg were related to very high SCORE2 risk. In conclusion, arterial stiffness is significantly related to ASCVD risk in post-COVID-19 patients and can be helpful as a single risk marker in everyday practice. Cut-off points for arterial stiffness parameters determined based on SCORE2 may help make individual decisions about implementing lifestyle changes or pharmacological treatment of ASCVD risk factors [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the potential association between endothelial glycocalyx damage, as well as arterial stiffness, and the retinal changes on optical coherence tomography (OCT) and OCT-angiography (OCT-A) in patients with type 2 diabetes mellitus (DM). Methods: Participants in this cross-sectional study were 65 patients with DM type 2 and 42 age- and gender-matched controls without DM. The demographic and clinical characteristics of the participants were recorded. All patients underwent a thorough ophthalmological examination and multimodal imaging, including fundus photography, OCT, and OCT-A. In addition, evaluation of the endothelial glycocalyx thickness by measuring the perfused boundary region (PBR5-25) of the sublingual microvessel, as well as of the arterial stiffness, by measuring the carotid–femoral pulse wave velocity (PWV), the central aortic pressures and the augmentation index (Aix) was performed. Univariate and multivariate logistic regression analysis was performed for the examination of the potential association between the eye imaging variables and the cardiovascular-related variables. The odds ratios (OR) with the respective 95% confidence intervals (CI) were calculated. A p-value < 0.05 was considered statistically significant. Results: Patients with DM presented significantly higher PBR5-25 compared to controls without DM (p = 0.023). At the univariate analysis, increased PBR5-25 (≥2.19 μm vs. <2.19 μm) was associated with decreased peripapillary VD at the superior quadrant (univariate OR (95% CI) = 0.34 (0.12–0.93), p = 0.037). Multivariate logistic regression analysis showed that increased PWV (≥13.7 m/s vs. <13.7 m/s) was associated with an increased foveal avascular zone (FAZ) area on OCT-A (p = 0.044) and increased FAZ perimeter (p = 0.048). Moreover, increased Aix (≥14.745% vs. <14.745%) was associated with diabetic macular edema (DME) presence (p = 0.050) and increased perifoveal and parafoveal superior and temporal thickness on OCT (p < 0.05 for all associations). Conclusions: Markers of endothelial damage and arterial stiffness were associated with structural and microvascular retinal alterations in patients with DM, pointing out that OCT-A could be a useful biomarker for detecting potential cardiovascular risk in such patients. [ABSTRACT FROM AUTHOR]

Background and Aim: Several reports show a significant association between metabolic dysfunction‐associated steatotic liver disease (MASLD) and arterial stiffness (estimated pulse wave velocity [ePWV]) as a surrogate marker of vascular age. We investigate whether ePWV as arterial stiffness in MASLD is associated with all‐cause/cause‐specific mortality. Methods: This cohort study was based on the third National Health and Nutrition Examination Survey (NHANES, 1988–1994) and NHANES 2007–2014 and linked mortality datasets through 2019. Cox regression models assessed the association between ePWV categorized by quartile and all‐cause/cause‐specific mortality among individuals with MASLD. Results: During the follow‐up of a median of 26.3 years (interquartile range: 19.9–27.9), higher levels of ePWV among individuals with MASLD were associated with increased all‐cause mortality, which remained significant after adjusting for demographic, lifestyle, clinical, and metabolic risk factors. Furthermore, higher ePWV in MASLD was associated with higher cardiovascular mortality. There was a 44% (hazard ratio: 1.44, 95% confidence interval: 1.32–1.58) increase in all‐cause mortality and a 53% (hazard ratio: 1.53, 95% confidence interval: 1.32–1.77) increase in cardiovascular mortality for every 1 m/s increase in ePWV in MASLD. However, there was no significant association between ePWV and cancer‐related mortality. Sensitivity analyses using the NHANES 2007–2014 dataset showed results identical to the original analysis. Conclusion: Higher ePWV in MASLD was associated with a higher risk of all‐cause and cardiovascular mortality beyond traditional cardiovascular risk factors. Screening for ePWV in individuals with MASLD may be an effective and beneficial approach to reducing all‐cause and cardiovascular mortality. [ABSTRACT FROM AUTHOR]

Background: The cardiac toxicity of chemotherapy for breast cancer is not uncommon and has been associated with elevated morbidity and mortality. In the present study, we assessed the impact of chemotherapy on cardiovascular function by assessing the cardio–ankle vascular index (CAVI), global longitudinal strain (GLS) and ventricular–arterial coupling (VAC: CAVI/GLS ratio) in chemotherapy-treated women. Methods: This prospective study enrolled 78 women with breast cancer who were receiving anthracycline-based chemotherapy +/− anti-HER2 therapy (trastuzumab +/− pertuzumab). Forty-one age-matched healthy women served as controls. We comparatively evaluated left ventricular ejection fraction (LVEF), CAVI, GLS and VAC, between the chemotherapy and control groups. We also assessed their changes over time (baseline, 3-month and 6-month time point) and their independent association with the incidence of cancer therapy-related cardiovascular dysfunction (CTRCD) in the chemotherapy group. Results: In comparison to healthy controls, women receiving chemotherapy presented with significantly higher GLS (from −21.02 ± 2.09% to −19.01 ± 2.81%, p < 0.001) and VAC (−0.36 ± 0.06 to −0.41 ± 0.11, p < 0.001). The presence of CTRCD was associated with a further increase in GLS and CAVI and a significant decline in LVEF and VAC compared to CTRCD-free women (p < 0.001). Baseline, CAVI, GLS and VAC were independently associated with CTRCD development during follow-up. Conclusion: Women with breast cancer undergoing chemotherapy displayed abnormal levels of CAVI, VAC and GLS, compared to healthy individuals. Those effects on VAC and CAVI were more exaggerated among women with CTRCD, implicating their potential use to refine screening and therapeutic strategies for this specific population. [ABSTRACT FROM AUTHOR]

Aim: Central retinal artery occlusion (CRAO) leads to significant, non-painful loss of sight due to retinal infarction. Most CRAO patients have atherosclerotic risk factors. Pulse wave velocity (PWV) and Flow-mediated dilatation (FMD) can provide insights into the onset and development of atherosclerosis. This research aims to assess arterial stiffness measures and identify endothelial dysfunction in individuals with CRAO. Materials and Methods: 33 consecutive CRAO patients (63 ± 7 years, 21 men (63.6%)) were recruited in the study. 35 age/sex-matched participants were included as a control group. FMD and PWV were measured from the brachial artery, as indicators of endothelial dysfunction and atherosclerosis in the arterial wall, respectively. Additionally, the transthoracic echocardiographic parameters of the patients were investigated. Results: CRAO patients had significantly higher frequencies of hypertension, hyperlipidemia, and smoking status. Furthermore, the frequency of diabetes was also higher in the CRAO group, but this difference did not reach statistical significance. CRAO patients showed markedly elevated PWV and reduced FMD. However, no notable differences were observed between groups in terms of left ventricle systolic and diastolic functions. Conclusion: Our study showed that CRAO patients may have increased arterial stiffness and endothelial dysfunction. Systemic endothelial dysfunction and atherosclerosis may be linked to the development of CRAO. [ABSTRACT FROM AUTHOR]

Severe acute coronavirus‐2 (SARS‐CoV‐2) infection has been associated with endothelial damage, and impaired nitric oxide production, which results in arterial stiffness and increased risk of cardiovascular disease. Long COVID is a term used to describe the persistence or the development of new symptoms that can occur after an acute infection. Little is known about the association between arterial stiffness and Long COVID. An observational, cross‐sectional study in which arterial stiffness was measured with pulse wave velocity (PWV) was carried out in 74 participants between 19 and 40 years old (53 with Long COVID, 21 age and gender‐matched controls). Data was collected from participants between 1 and 9 months after acute COVID‐19 infection using the Complior analyze unit protocol. The Long COVID group had higher carotid‐radial‐PWV (crPWV) than controls (10 m/s interquartile range [IQR] 8.5–11.2 m/s) versus 8.8 m/s (IQR 7.7–9.2 m/s) as was their carotid‐radial‐arterial stiffness index (crASI) (2.26 cm/ms (IQR 1.9–2.56 cm/ms) vs. 2.01 cm/ms (IQR 1.82–2.27 cm/ms); p < 0.05) in both. They also had more type‐A waveforms, indicating increased arterial stiffening. Peripheral arterial stiffness was higher in adults with Long COVID than in controls who were never infected with SARS‐CoV‐2 as noted by the elevated levels of crPWV and crASI among adults with Long COVID. [ABSTRACT FROM AUTHOR]

Hypertension, a disease with known sexual dimorphism, accelerates aging-associated arterial stiffening, partly because of the activation of matrix remodeling caused by increased biomechanical load. In this study, we tested the effect of biological sex and the role of the matrix remodeling enzyme lysyl oxidase-like 2 (LOXL2) in hypertension-induced arterial stiffening. Hypertension was induced by angiotensin II (ANG II) infusion via osmotic minipumps in 12- to 14-wk-old male and female mice. Blood pressure and pulse wave velocity (PWV) were measured noninvasively. Wire myography and uniaxial tensile testing were used to test aortic vasoreactivity and mechanical properties. Aortic wall composition was examined by histology and Western blotting. Uniaxial stretch of cultured cells was used to evaluate the effect of biomechanical strain. LOXL2's catalytic function was examined using knockout and inhibition. ANG II infusion-induced hypertension in both genotypes and sexes. Wild-type (WT) males exhibited arterial stiffening in vivo and ex vivo. Aortic remodeling with increased wall thickness, intralamellar distance, higher LOXL2, and collagen I and IV content was noted in WT males. Female mice did not exhibit increased PWV despite the onset of hypertension. LOXL2 depletion improved vascular reactivity and mechanics in hypertensive males. LOXL2 depletion improved aortic mechanics but worsened hypercontractility in females. Hypertensive cyclic strain contributed to LOXL2 upregulation in the cell-derived matrix in vascular smooth muscle cells (VSMCs) but not endothelial cells. LOXL2's catalytic function facilitated VSMC alignment in response to biomechanical strain. In conclusion, in males, arterial stiffening in hypertension is driven both by VSMC response and matrix remodeling. Females are protected from PWV elevation in hypertension. LOXL2 depletion is protective in males with improved mechanical and functional aortic properties. VSMCs are the primary source of LOXL2 in the aorta, and hypertension increases LOXL2 processing and shifts to collagen I accumulation. Overall, LOXL2 depletion offers protection in young hypertensive males and females. NEW & NOTEWORTHY: We examined the effect of sex on the evolution of angiotensin II (ANG II)-induced hypertension and the role of lysyl oxidase-like 2 (LOXL2), an enzyme that catalyzes matrix cross linking. While ANG II led to hypertension and worsening vascular reactivity in both sexes, aortic remodeling and stiffening occurred only in males. LOXL2 depletion improved outcomes in males but not females. Thus males and females exhibit a distinct etiology of hypertension and LOXL2 is an effective target in males. [ABSTRACT FROM AUTHOR]

Purpose: Postmenopausal women experience augmented aortic hemodynamic responses to isometric handgrip (IHG) exercise and metaboreflex activation post-exercise muscle ischemia (PEMI). Relationships between endothelial function brachial artery flow-mediated dilation (FMD) and aortic stiffness carotid-femoral pulse wave velocity (cfPWV) with aortic pulsatile hemodynamics during IHG and PEMI have not been determined. The relationships between aortic hemodynamic responses to PEMI were evaluated. Methods: Aortic blood pressure (BP), wave reflection, and pressure of forward (Pf) and backward (Pb) waves were measured using arterial tonometry at rest, IHG at 30% maximal force, and PEMI in 30 (15/group) postmenopausal women with low (≤ 4.5%) and normal (≥ 5.5%) FMD. Hemodynamic responses were analyzed as the change (Δ) from rest to the last minute of IHG and PEMI. Results: Brachial and aortic systolic BP (SBP) responses to IHG were higher in the low vs normal FMD group (P < 0.05). Aortic SBP (Δ20 ± 8 vs Δ11 ± 7 mmHg), pulse pressure (PP) (Δ12 ± 8 vs Δ6 ± 4 mmHg), augmented pressure (AP) (Δ5 ± 3 vs Δ2 ± 2 mmHg), and Pb (Δ6 ± 4 vs Δ3 ± 2 mmHg) responses to PEMI were greater (P < 0.05) in women with low vs. normal FMD. FMD was negatively correlated with aortic SBP, PP, AP, and Pb (P < 0.05) responses to PEMI. cfPWV was not correlated with responses to PEMI. Conclusion: Endothelial dysfunction relates to augmented aortic pulsatile load during metaboreflex activation, which may increase cardiovascular risk in postmenopausal women. [ABSTRACT FROM AUTHOR]

Rest-activity rhythm is an essential behavior for human health. However, the association between rest-activity rhythm and atherosclerotic cardiovascular disease (ASCVD) risk remains unclear. Therefore, this study aimed to elucidate the association. This study included 87,039 participants from the UK Biobank who had 7-day accelerometry data and were free of ASCVD at baseline. Relative amplitude was calculated as the difference between the most active continuous 10-h period (M10) and the least active continuous 5-h period (L5) in 24 h, and lower relative amplitude indicated the disruption of rest-activity rhythm. Cox proportional hazard model was used to examine the association of relative amplitude with ASCVD. Further, the linear association between relative amplitude and arterial stiffness measurements, including arterial stiffness index (ASI) and carotid intima-media thickness (cIMT), was examined. During a mean follow-up period of 6.80 ± 1.10 years, 2798 ASCVD cases were identified. A dose-response relationship was observed between relative amplitude and ASCVD risk (P for trend<0.001). The adjusted hazard ratio, for the highest vs the lowest quintile of relative amplitude, was 1.54 (95 % confidence interval: 1.31, 1.79). Further, we found significant association of lower relative amplitude with ASI and cIMT. The onset timing of M10 at ≤06:00, 09:00, 10:00, or ≥11:00, as opposed to the reference time of 07:00, was associated with higher ASCVD risk. Low rest-activity rhythm amplitude was associated with a higher risk of ASCVD. Rest-activity rhythm amplitude may provide a method to identify individuals at risk of ASCVD in public health and clinical practice. • Rest-activity rhythm is an essential behavior for human health. • Low rest-activity rhythm amplitude was associated with higher ASCVD risk. • Early or late onset timing of 10h activity was associated with higher ASCVD risk. • Low rest-activity rhythm amplitude was associated with increased arterial stiffness. • Rest-activity rhythm amplitude could be a novel risk factor for ASCVD. [ABSTRACT FROM AUTHOR]

Chronic pain is associated with development of cardiovascular disease. We investigated the association between how widespread chronic pain is and the development of cardiovascular dysfunction. We analysed data from participants enrolled in the UK Biobank study who underwent examinations at baseline, plus first follow-up and two imaging visits. Pain sites (including hip, knee, back, neck/shoulder, or 'all over the body') and pain duration were recorded at each visit. Chronic pain was defined as pain lasting for ≥3 months. Participants were categorised into six groups: no chronic pain, chronic pain in one, two, three, or four sites, or 'all over the body'. Arterial stiffness index was measured at each time point. Carotid intima-media thickness, cardiac index, and left ventricular ejection fraction (LVEF) were measured using ultrasound and heart MRI at two additional imaging visits in a subset of participants. Mixed-effect linear regression models were used for the analyses. The number of chronic pain sites was directly related to increased arterial stiffness index (n =159,360; β=0.06 per one site increase, 95% confidence interval 0.04 to 0.08). In 23,899 participants, lower LVEF was associated with widespread chronic pain (β=–0.17 per one site increase, 95% confidence interval –0.27 to –0.07). The number of chronic pain sites was not associated with carotid intima-media thickness (n =30,628) or cardiac index (n =23,899). A greater number of chronic pain sites is associated with increased arterial stiffness and poorer cardiac function, suggesting that widespread chronic pain is an important contributor to cardiovascular dysfunction. [ABSTRACT FROM AUTHOR]