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Background and Aims: Arterial function (specifically arterial stiffness) is an important cardiovascular risk factor. Pulse wave velocity (PWV) and augmentation index (Alx $x$) are established indicators of arterial function. The present study aimed to evaluate the repeatability and reproducibility of PWV and Alx $x$ in healthy individuals. Methods: Forty healthy participants (age 33 ± 11 years, 17 females) underwent resting supine PWV and Alx $x$ assessments. Measurements were made in triplicate and repeated 1 week apart. Alx $x$ was measured by brachial occlusion and PWV was measured from the carotid artery to the femoral artery via the tonometer‐oscillometric method. Repeatability and reproducibility were assessed using the intraclass correlation coefficient (ICC). Interoperator reproducibility was performed on 10 participants. Results: The average values for week‐to‐week visits for PWV and Alx $x$ were 6.20 ± 0.91 versus 6.13 ± 0.91 ms−1 and 14.0 ± 11.8 versus 16.3 ± 12.2% respectively. For same‐day measurements, both PWV and Alx $x$ showed excellent repeatability (PWV: ICC = 0.96, 95% CI: 0.92–0.98, p < 0.01; Alx $x$: ICC = 0.90, 95% CI: 0.84–0.94, p < 0.01) and interoperator reproducibility (PWV: ICC = 0.98, 95% CI: 0.93–1.00, p < 0.01; Alx $x$: ICC = 0.93, 95% CI: 0.69–0.98, p < 0.01). Measurements were repeated 1 week apart and showed good reproducibility (PWV: ICC = 0.77, 95% CI: 0.61–0.87, p ≤ 0.01; Alx $x$: ICC = 0.73, 95% CI: 0.73–0.86, p < 0.01). Conclusion: PWV and Alx $x$ demonstrate excellent repeatability and good reproducibility. Considering these variables are noninvasive and easy‐to‐measure, arterial function assessment may have a role in routine clinical practice to facilitate risk stratification in cardiovascular diseases. Summary: PWV and Alx $x$ are repeatable and reproducible measures of arterial functionPWV is more repeatable and reproducible than Alx $x$ but requires training before operation [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the long-term effect of body composition, physical activity, and cardiorespiratory fitness (CRF) from puberty on arterial health in late adolescent males. Methods: The cumulative burden of physical activity (measured with accelerometer), CRF (VO2peak0.82), and body composition (body mass index, fat mass, and fat percentage) from puberty to late adolescence (sum of 4 time points from 12 to 18 y) was assessed in 102 males. Additional analysis on the first (T1) and last (T4) time points was performed. Intima-media thickness (IMT), carotid-femoral pulse wave velocity, and augmentation index adjusted to heart rate of 75 beats per minute (bpm) as dependent variables were measured at T4 and analyzed in multivariable regression models adjusted for known risk factors including maturation, blood pressure, and smoking habits. Results: T1 and cumulative body composition measures were independently associated with IMT, while cumulative (β = −0.011, P =.036) and T4 (β = −0.0.031, P =.001) CRF revealed independent associations with IMT. Individuals with moderate to vigorous physical activity >60 minutes per day at T1 showed relationship (β = −1.091, P =.026) with IMT independently of late adolescent physical activity. No significant relationship was present for arterial function. Conclusion: Arterial structure in adolescent males is associated with physical activity at 12 years while relationship with CRF can be seen in late adolescence and cumulatively from puberty to late adolescence. [ABSTRACT FROM AUTHOR]

Abstract A collective tribute to a colleague, friend, and mentor from those that have known him through his journey of the meanderings of the arterial pulse in health and disease; a journey that extended beyond borders and confines, with far-reaching personal and global impact. The Editorial Board of the Artery Research Journal and the Executive Committee of the Artery Society extend their due respects to Prof. Michael O’Rourke.

A collective tribute to a colleague, friend, and mentor from those that have known him through his journey of the meanderings of the arterial pulse in health and disease; a journey that extended beyond borders and confines, with far-reaching personal and global impact. The Editorial Board of the Artery Research Journal and the Executive Committee of the Artery Society extend their due respects to Prof. Michael O'Rourke. [ABSTRACT FROM AUTHOR]

The metabolic network's primary sources of free fatty acids (FFAs) are long- and medium-chain fatty acids of triglyceride origin and short-chain fatty acids produced by intestinal microorganisms through dietary fibre fermentation. Recent studies have demonstrated that FFAs not only serve as an energy source for the body's metabolism but also participate in regulating arterial function. Excess FFAs have been shown to lead to endothelial dysfunction, vascular hypertrophy, and vessel wall stiffness, which are important triggers of arterial hypertension and atherosclerosis. Nevertheless, free fatty acid receptors (FFARs) are involved in the regulation of arterial functions, including the proliferation, differentiation, migration, apoptosis, inflammation, and angiogenesis of vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs). They actively regulate hypertension, endothelial dysfunction, and atherosclerosis. The objective of this review is to examine the roles and heterogeneity of FFAs and FFARs in the regulation of arterial function, with a view to identifying the points of intersection between their actions and providing new insights into the prevention and treatment of diseases associated with arterial dysfunction, as well as the development of targeted drugs. [ABSTRACT FROM AUTHOR]

Abstract Background and Aims Arterial function (specifically arterial stiffness) is an important cardiovascular risk factor. Pulse wave velocity (PWV) and augmentation index (Alx) are established indicators of arterial function. The present study aimed to evaluate the repeatability and reproducibility of PWV and Alx in healthy individuals. Methods Forty healthy participants (age 33 ± 11 years, 17 females) underwent resting supine PWV and Alx assessments. Measurements were made in triplicate and repeated 1 week apart. Alx was measured by brachial occlusion and PWV was measured from the carotid artery to the femoral artery via the tonometer‐oscillometric method. Repeatability and reproducibility were assessed using the intraclass correlation coefficient (ICC). Interoperator reproducibility was performed on 10 participants. Results The average values for week‐to‐week visits for PWV and Alx were 6.20 ± 0.91 versus 6.13 ± 0.91 ms−1 and 14.0 ± 11.8 versus 16.3 ± 12.2% respectively. For same‐day measurements, both PWV and Alx showed excellent repeatability (PWV: ICC = 0.96, 95% CI: 0.92–0.98, p

Background Our aim was to assess the relationships of cardiovascular health metrics, cardiorespiratory fitness, lean mass, and fat percentage with arterial structure and function from childhood to adolescence. Methods and Results Five hundred four children aged 6 to 9 years were examined in the PANIC (Physical Activity and Nutrition in Children) study at baseline, 2 and 8 years later. The associations of adjusted American Heart Association cardiovascular health metrics (smoking status, body mass index—SD score, moderate‐to‐vigorous physical activity, diet quality, plasma total cholesterol, systolic blood pressure, plasma glucose categorized into poor, intermediate, and ideal), the American Heart Association cardiovascular health score, cardiorespiratory fitness measured by maximal oxygen uptake in a bicycle exercise test, lean mass and fat percentage with carotid intima–media thickness (cIMT) and pulse wave velocity (PWV) were analyzed cross‐sectionally and longitudinally in 277 participants at age 15 to 17 years. Higher American Heart Association cardiovascular health score at baseline was associated with lower PWV at 8‐year follow‐up (ß, −0.19 [95% CI, –0.32 to −0.05]). Higher body mass index—SD score and systolic blood pressure were associated with higher cIMT (ß, 0.18 [95% CI, 0.05–0.31]); and (ß, 0.13 [95% CI, 0.00–0.25]; respectively) and PWV (ß, 0.20 [95% CI, 0.07–0.34]) and (ß, 0.13 [95% CI, 0.00–0.26]; respectively) at 8‐year follow‐up. Higher moderate‐to‐vigorous physical activity was associated with higher cIMT (ß, 0.25 [95% CI, 0.07–0.43]); yet lower PWV (ß, −0.25 [95% CI, ‐0.44 to ‐0.06]) at 8‐year follow‐up. Better cardiorespiratory fitness (ß, 0.29 [95% CI, 0.08–0.51]) and higher lean mass (ß, 0.51 [95% CI, 0.03–0.98]) were associated with higher cIMT after accounting for American Heart Association cardiovascular health score at 8‐year follow‐up. Conclusions While our results suggest that higher cardiometabolic risk factors in childhood may exert unfavorable effects on arterial health during adolescence, we demonstrated the complexity of relationships between cardiovascular health metrics and arterial health indicators in childhood and adolescence. We found different associations of cardiovascular health metrics with cIMT and PWV in childhood and adolescence, calling for caution when interpreting the results of various cardiovascular risk factors with measures of arterial health, particularly in youth. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT01803776.

This study examined the relationship between childhood diet quality and arterial stiffness and thickness during adolescence/early adulthood. Participants were from the Avon Longitudinal Study of Parents and Children (ALSPAC) with dietary data at ages 7, 10 and 13 years and pulse wave velocity (PWV) and carotid intima-media thickness (cIMT) at ages 17 and/or 24 years. Diet quality (DQ) was assessed using five scores: a children's Mediterranean-style diet (C-rMED) Z -score, a children's Dietary Inflammatory Z -score (C-DIS), a DASH diet Z -score, a children's Eatwell Guide (C-EWG) Z -score reflecting UK dietary guidelines and a data-driven obesogenic Z -score. Adjusted regression models examined the associations between DQ scores at 7–13 years and PWV and cIMT at 17 and 24 years. In adjusted models, a high v. low Obesogenic Z -score at 7 and 10 years was associated with higher PWV at 17: β 0.07 (95 % CI 0.01, 0.13) and β 0.10 (95 % CI 0.04, 0.16), respectively. A high v. low C-rMED Z -score at 7 years was associated with lower PWV at 17 (β −0.07; 95 % CI −0.14, −0.01). A high (more anti-inflammatory) vs low C-DIS Z -score at 10 years was associated with a lower PWV at 17 years: β −0.06 (95 % CI −0.12, −0.01). No other associations were observed. In conclusion, an Obesogenic dietary pattern in childhood (7–10 years) was related to increased arterial stiffness, while Mediterranean-style and anti-inflammatory diets were related to decreased arterial stiffness in adolescence. This highlights the importance of establishing healthy dietary habits early in life to protect against vascular damage. [ABSTRACT FROM AUTHOR]

Acute mental stress can impair arterial function (e.g., arterial stiffness and endothelial function) transiently. Repeated exposures to stress-induced transient vascular dysfunction in daily life potentially leads to persistent vascular dysfunction, which increases the risk of cardiovascular disease. Therefore, it is important to devise an effective strategy to protect the vasculatures from daily stress, and exercise is one of the possible solutions. This review briefly outlines the detrimental impacts of acute mental stress on arterial function and introduces our recent research regarding exercise as a countermeasure.

Anthracyclines, chemotherapeutic agents used to treat common forms of cancer, increase cardiovascular (CV) complications, thereby necessitating research regarding interventions to improve the health of cancer survivors. Vascular dysfunction, which is induced by anthracycline chemotherapy, is an established antecedent to overt CV diseases. Potential treatment options for ameliorating vascular dysfunction have largely been understudied. Furthermore, patients treated with anthracyclines have impaired cognitive function and vascular dysfunction is an independent risk factor for the development of mild cognitive impairment. Here, we will focus on: anthracycline chemotherapy associated CV diseases risk; how targeting mechanisms underlying vascular dysfunction may be a means to improve both CV and cognitive health; and research gaps and potential future directions for the field of cardio-oncology. [ABSTRACT FROM AUTHOR]

We explored global myocardial work index (GWI), a novel measure of myocardial function that integrates left ventricular (LV) hemodynamic load, in relation to sex and increased body mass index (BMI). We used data from 467 individuals (61% women, average age 47 ± 9 years and BMI 31.2 kg/m2) without known cardiac disease. Central arterial function was analysed by applanation tonometry. GWI was calculated from global longitudinal strain (GLS) and post-echocardiography supine blood pressure (BP). Covariables of GWI were identified in linear regression analyses. Women had higher BMI, aortic augmentation pressure (12 ± 7 vs. 8 ± 6 mmHg), LV GLS (20.0 ± 2.8 vs. 18.8 ± 2.8%), and GWI (2126 ± 385 vs. 2047 ± 389 mmHg%) than men (all p < 0.05). In univariable analyses, higher GWI was associated with female sex, higher age, systolic BP, LV wall stress, LV ejection fraction, left atrial size, LV ejection time, and with lower waist circumference (all p < 0.05). In multivariable analysis, adjusting for these correlates, female sex remained independently associated with higher GWI (β = 0.13, p = 0.007). After additional adjustment for aortic augmentation pressure or central pulse pressure, this association became non-significant. In conclusion, the higher GWI in women compared to men was mainly explained by increased LV workload due to higher aortic augmentation pressure in women. [ABSTRACT FROM AUTHOR]

Advanced age is accompanied by arterial dysfunction, as well as a diminished glycocalyx, which may be linked to reduced high molecular weight–hyaluronan (HMW-HA) synthesis. However, the impact of glycocalyx deterioration in age-related arterial dysfunction is unknown. We sought to determine if manipulations in glycocalyx properties would alter arterial function. Tamoxifen-induced hyaluronan synthase 2 (Has2) reduction was used to decrease glycocalyx properties. Three weeks post-tamoxifen treatment, glycocalyx thickness was lower in Has2 knockout compared to wild-type mice (P<0.05). Has2 reduction induced arterial dysfunction, demonstrated by impaired endothelium-dependent dilation (EDD) and elevated aortic stiffness (P<0.05). To augment glycocalyx properties, old mice received 10 weeks of a glycocalyx-targeted therapy via Endocalyx™ (old+ECX), which contains HMW-HA and other glycocalyx components. Compared to old control mice, glycocalyx properties and EDD were augmented, and aortic stiffness decreased in old+ECX mice (P<0.05). Old+ECX mice had a more youthful aortic phenotype, demonstrated by lower collagen content and higher elastin content than old control mice (P<0.05). Functional outcomes were repeated in old mice that underwent a diet supplemented solely with HMW-HA (old+HA). Compared to old controls, glycocalyx properties and EDD were augmented, and aortic stiffness was lower in old+HA mice (P<0.05). We did not observe any differences between old+HA and old+ECX mice (P>0.05). Has2 reduction phenocopies age-related arterial dysfunction, while 10 weeks of glycocalyx-targeted therapy that restores the glycocalyx also ameliorates age-related arterial dysfunction. These findings suggest that the glycocalyx may be a viable therapeutic target to ameliorate age-related arterial dysfunction. [ABSTRACT FROM AUTHOR]

Age-associated cardiovascular (CV) dysfunction, namely arterial dysfunction, is a key antecedent to the development of CV disease (CVD). Arterial dysfunction with aging is characterized by impaired vascular endothelial function and stiffening of the large elastic arteries, each of which is an independent predictor of CVD. These processes are largely mediated by an excess production of reactive oxygen species (ROS) and an increase in chronic, low-grade inflammation that ultimately leads to a reduction in bioavailability of the vasodilatory molecule nitric oxide. Additionally, there are other fundamental aging mechanisms that may contribute to excessive ROS and inflammation termed the “hallmarks of aging”; these additional mechanisms of arterial dysfunction may represent therapeutic targets for improving CV health with aging. Aerobic exercise is the most well-known and effective intervention to prevent and treat the effects of aging on CV dysfunction. However, the majority of mid-life and older (ML/O) adults do not meet recommended exercise guidelines due to traditional barriers to aerobic exercise, such as reduced leisure time, motivation, or access to fitness facilities. Therefore, it is a biomedical research priority to develop and implement time- and resource-efficient alternative strategies to aerobic exercise to reduce the burden of CVD in ML/O adults. Alternative strategies that mimic or are inspired by aerobic exercise, that target pathways specific to the fundamental mechanisms of aging, represent a promising approach to accomplish this goal.

Western diet (WD), characterized by excess saturated fat and sugar intake, is a major contributor to obesity and metabolic and arterial dysfunction in humans. However, these phenotypes are not consistently observed in traditional inbred, genetically identical mice. Therefore, we sought to determine the effects of WD on visceral adiposity and metabolic/arterial function in UM-HET3 mice, an outbred, genetically diverse strain of mice. Male and female UM-HET3 mice underwent normal chow (NC) or WD for 12 weeks. Body mass and visceral adiposity were higher in WD compared to NC (P < 0.05). Female WD mice had greater visceral adiposity than male WD mice (P < 0.05). The results of glucose and insulin tolerance tests demonstrated that metabolic function was lower in WD compared to NC mice (P < 0.05). Metabolic dysfunction in WD as was driven by male mice, as metabolic function in female WD mice was unchanged (P > 0.05). Systolic blood pressure (BP) and aortic stiffness were increased in WD after 2 weeks compared to baseline and continued to increase through week 12 (P < 0.05). Systolic BP and aortic stiffness were higher from weeks 2-12 in WD compared to NC (P < 0.05). Aortic collagen content was higher in WD compared to NC (P < 0.05). Carotid artery endothelium-dependent dilation was lower in WD compared to NC (P < 0.05). These data suggest sex-related differences in visceral adiposity and metabolic dysfunction in response to WD. Despite this, arterial dysfunction was similar in male and female WD mice, indicating this model may provide unique translational insight into similar sex-related observations in humans that consume WD.

Background: Our aim was to assess the relationships of cardiovascular health metrics, cardiorespiratory fitness, lean mass, and fat percentage with arterial structure and function from childhood to adolescence., Methods and Results: Five hundred four children aged 6 to 9 years were examined in the PANIC (Physical Activity and Nutrition in Children) study at baseline, 2 and 8 years later. The associations of adjusted American Heart Association cardiovascular health metrics (smoking status, body mass index-SD score, moderate-to-vigorous physical activity, diet quality, plasma total cholesterol, systolic blood pressure, plasma glucose categorized into poor, intermediate, and ideal), the American Heart Association cardiovascular health score, cardiorespiratory fitness measured by maximal oxygen uptake in a bicycle exercise test, lean mass and fat percentage with carotid intima-media thickness (cIMT) and pulse wave velocity (PWV) were analyzed cross-sectionally and longitudinally in 277 participants at age 15 to 17 years. Higher American Heart Association cardiovascular health score at baseline was associated with lower PWV at 8-year follow-up (ß, -0.19 [95% CI, -0.32 to -0.05]). Higher body mass index-SD score and systolic blood pressure were associated with higher cIMT (ß, 0.18 [95% CI, 0.05-0.31]); and (ß, 0.13 [95% CI, 0.00-0.25]; respectively) and PWV (ß, 0.20 [95% CI, 0.07-0.34]) and (ß, 0.13 [95% CI, 0.00-0.26]; respectively) at 8-year follow-up. Higher moderate-to-vigorous physical activity was associated with higher cIMT (ß, 0.25 [95% CI, 0.07-0.43]); yet lower PWV (ß, -0.25 [95% CI, -0.44 to -0.06]) at 8-year follow-up. Better cardiorespiratory fitness (ß, 0.29 [95% CI, 0.08-0.51]) and higher lean mass (ß, 0.51 [95% CI, 0.03-0.98]) were associated with higher cIMT after accounting for American Heart Association cardiovascular health score at 8-year follow-up., Conclusions: While our results suggest that higher cardiometabolic risk factors in childhood may exert unfavorable effects on arterial health during adolescence, we demonstrated the complexity of relationships between cardiovascular health metrics and arterial health indicators in childhood and adolescence. We found different associations of cardiovascular health metrics with cIMT and PWV in childhood and adolescence, calling for caution when interpreting the results of various cardiovascular risk factors with measures of arterial health, particularly in youth., Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT01803776.

High blood pressure (HBP) has been identified as a major risk factor for cardiovascular events such as stroke and myocardial infarction. To understand the pathophysiology of high blood pressure and other diseases which affect the cardiovascular system, it is necessary to understand how they occur. Here, we discuss pathophysiological elements which lead to HBP including a discussion on arterial stiffness, as well as the biophysical and hemodynamic components which lead to the sustenance and increase in systemic blood pressure levels in adults. We also discuss humoral components which regulate blood pressure and which, when dysregulated, play a pivotal role in the pathophysiology of HBP. [ABSTRACT FROM AUTHOR]

Sedentary behavior (SB) and physical activity (PA) are important risk factors of cardiovascular disease morbidity and mortality. In addition to increasing the amount of moderate-to-vigorous PA (MVPA), the current PA guidelines recommend that adults should reduce SB, or any waking activity performed while sitting, reclining, or lying, with low energy expenditure. While mounting evidence has emphasized the benefits of increasing MVPA, little has focused on the effect of SB on health. Therefore, this review discusses the pathophysiological effects of SB and the potential physiological benefits of reducing/breaking up SB at the levels below the current guidelines for PA. Such knowledge is important, given that the majority of the United States population performs insufficient or no MVPA and is at high risk of being negatively impacted by SB. Interventions targeting sedentary time, such as breaking up SB by standing and moving, may be safe, feasible, and applicable to execute daily for a wide range of the population. This review also discusses the importance of monitoring SB in the era of the coronavirus disease 2019 (COVID-19) pandemic and the clinical implications of sitting less and moving more. [ABSTRACT FROM AUTHOR]

Abstract The study was to compare age‐related alterations in cardiac and arterial structure and function by sex and to explore the impacts of achieved systolic blood pressure (SBP;

IntroductionPreeclampsia, an endothelial disorder of pregnancy, predisposes to remote cardiovascular diseases (CVD). Whether there is an accelerated effect of aging on endothelial decline in former preeclamptic women is unknown. We investigated if the arterial aging regarding endothelial-dependent and -independent vascular function is more pronounced in women with a history of preeclampsia as compared to women with a history of solely normotensive gestation(s).MethodsData was used from the Queen of Hearts study (ClinicalTrials.gov Identifier NCT02347540); a large cross-sectional study on early detection of cardiovascular disease among young women (≥18 years) with a history of preeclampsia and a control group of low-risk healthy women with a history of uncomplicated pregnancies. Brachial artery flow-mediated dilation (FMD; absolute, relative and allometric) and sublingually administered nitroglycerine-mediated dilation (NGMD; absolute and relative) were measured using ultrasound. Cross-sectional associations of age with FMD and NGMD were investigated by linear regression. Models were adjusted for body mass index, smoking, antihypertensive drug use, mean arterial pressure, fasting glucose, menopausal state, family history of CVD and stress stimulus during measurement. Effect modification by preeclampsia was investigated by including an interaction term between preeclampsia and age in regression models.ResultsOf the 1,217 included women (age range 22–62 years), 66.0% had a history of preeclampsia and 34.0% of normotensive pregnancy. Advancing age was associated with a decrease in relative FMD and NGMD (unadjusted regression coefficient: FMD: −0.48%/10 years (95% CI:−0.65 to −0.30%/10 years), NGMD: −1.13%/10 years (−1.49 to −0.77%/10 years)) and increase in brachial artery diameter [regression coefficient = 0.16 mm/10 years (95% CI 0.13 to 0.19 mm/10 years)]. Similar results were found when evaluating FMD and NGMD as absolute increase or allometrically, and after confounder adjustments. These age-related change were comparable in former preeclamptic women and controls (p-values interaction ≥0.372). Preeclampsia itself was independently associated with consistently smaller brachial artery diameter, but not with FMD and NGMD.ConclusionIn young- to middle-aged women, vascular aging in terms of FMD and NGMD was not accelerated in women after preeclampsia compared to normotensive pregnancies, even though former preeclamptic women consistently have smaller brachial arteries.

Purpose: Carcinoid heart disease (CHD) is a life-threatening complication of carcinoid syndrome (CS) characterised by tricuspid regurgitation (TR). However, there is an unmet need for earlier diagnosis of CHD. We cross-sectionally assessed the prevalence and potential predictive or diagnostic markers for CS and CHD in a contemporary cohort of patients with small intestinal neuroendocrine tumours (SI-NETs). Methods: Biochemical characteristics, hepatic tumour load, measures of arterial and endothelial function, atherosclerosis, and transthoracic echocardiography were analysed in a prospective cross-sectional setting. Results: Among the 65 patients studied, 29 (45%) had CS (CS+), and 3 (5%) CHD. CS+ was characterised by significantly higher hepatic tumour load, S-5-HIAA and fP-CgA, higher frequency of diarrhoea and flushing, and more frequent PRRT compared to CS− (for all, P < 0.05). Central systolic, central mean, and central end-systolic blood pressures were significantly higher in CS+ than in CS− (for all, P < 0.05). Subjects with grades 2–4 TR had higher hepatic tumour burden, fP-CgA, and S-5-HIAA compared to those with grades 0–1 TR, but measures of vascular function did not differ. fP-CgA (P = 0.017) and S-5-HIAA (P = 0.019) but not proBNP increased significantly according to the severity of TR. Conclusion: Although CS is common, the prevalence of CHD was found to be lower in a contemporary cohort of SI-NET patients than previously anticipated. Measures of arterial or endothelial function or carotid atherosclerosis do not identify subjects with mild TR. Echocardiography remains the most sensitive means to diagnose CHD in CS patients with high tumour burden and elevated CgA and 5-HIAA. [ABSTRACT FROM AUTHOR]

The opinion on the mechanisms underlying the pathogenesis of preeclampsia still divides scientists and clinicians. This common complication of pregnancy has long been viewed as a disorder linked primarily to placental dysfunction, which is caused by abnormal trophoblast invasion, however, evidence from the previous two decades has triggered and supported a major shift in viewing preeclampsia as a condition that is caused by inherent maternal cardiovascular dysfunction, perhaps entirely independent of the placenta. In fact, abnormalities in the arterial and cardiac functions are evident from the early subclinical stages of preeclampsia and even before conception. Moving away from simply observing the peripheral blood pressure changes, studies on the central hemodynamics reveal two different mechanisms of cardiovascular dysfunction thought to be reflective of the early-onset and late-onset phenotypes of preeclampsia. More recent evidence identified that the underlying cardiovascular dysfunction in these phenotypes can be categorized according to the presence of coexisting fetal growth restriction instead of according to the gestational period at onset, the former being far more common at early gestational ages. The purpose of this review is to summarize the hemodynamic research observations for the two phenotypes of preeclampsia. We delineate the physiological hemodynamic changes that occur in normal pregnancy and those that are observed with the pathologic processes associated with preeclampsia. From this, we propose how the two phenotypes of preeclampsia could be managed to mitigate or redress the hemodynamic dysfunction, and we consider the implications for future research based on the current evidence. Maternal hemodynamic modifications throughout pregnancy can be recorded with simple-to-use, noninvasive devices in obstetrical settings, which require only basic training. This review includes a brief overview of the methodologies and techniques used to study hemodynamics and arterial function, specifically the noninvasive techniques that have been utilized in preeclampsia research. [ABSTRACT FROM AUTHOR]

Systemic sclerosis (SSc) is a rare, auto-immune disease with variably progressive fibrosis of the skin and internal organs, as well as vascular dysfunction. Recently, we demonstrated a decrement in exercising skeletal muscle blood flow and endothelium-dependent vasodilation in SSc, but the mechanisms responsible for these impairments have not been investigated. Thus, we sought to determine if acute administration of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase (eNOS), would improve hyperemia and brachial artery vasodilation during progressive handgrip exercise in SSc. Thirteen patients with SSc (63 ± 11 years) participated in this placebo-controlled, randomized, double-blind, crossover study. Tetrahydrobiopterin (10 mg/kg) administration resulted in a ~4-fold increase in circulating BH4 concentrations (P < 0.05). Cardiovascular variables at rest were unaffected by BH4 (P > 0.05). During handgrip exercise, BH4 administration increased brachial artery blood flow (placebo: 200 ± 87; BH4: 261 ± 115 ml/min; P < 0.05) and vascular conductance (placebo: 2.0 ± 0.8; BH4: 2.5 ± 1.0 ml/min/mmHg; P < 0.05), indicating augmented resistance artery vasodilation. Tetrahydrobiopterin administration also increased brachial artery vasodilation in response to exercise (placebo: 12 ± 6; BH4: 17 ± 7%; P < 0.05), resulting in a significant upward shift in the slope relationship between Δ brachial artery vasodilation and Δ shear rate (placebo: 0.030 ± 0.007; BH4: 0.047 ± 0.007; P < 0.05) that indicates augmented sensitivity of the brachial artery to vasodilate to the sustained elevations in shear rate during handgrip exercise. These results demonstrate the efficacy of acute BH4 administration to improve both resistance and conduit vessel endothelial function in SSc, suggesting that eNOS recoupling may be an effective strategy for improving vasodilatory capacity in this patient group.

Sex and gender are important modifiers of cardiovascular system physiology, pathophysiology, and disease development. The atherosclerosis process, together with the progressive loss of arterial elasticity with age, is a major factor influencing the development of overt cardiovascular, renal, and cerebrovascular disease. While differences between women and men in epidemiology and pathophysiology of vascular ageing are increasingly reported, sex-disaggregated data are still scarcely available for prospective studies. A better knowledge of sex differences in physiological ageing as well as in disease-related changes in vascular ageing trajectories is crucial to avoid misdiagnosis and mistreatment. This review presents key concepts and knowledge gaps identified in vascular ageing due to gonadal function, vascular physiology, pathophysiology, psychosocial factors, pregnancy, and prognostic relevance. Gender roles determine the effectiveness of any cardiovascular preventive strategy and acceptance for non-invasive or invasive diagnostics and therapeutics. Gender differences in health behaviour, also due to sociocultural norms conditioned by society, contribute to behaviours that may lead to premature arterial vascular ageing. These include differences in risk behaviours like smoking, diet, exercise, and in stress, but also conditions such as housing, noise pollution, poverty, disability, and any kind of stigmatisation. The VascAgeNet Gender Expert Group aims to advance the use of non-invasive vascular ageing measures in routine clinical settings by providing facts to fill in the gaps concerning sex and gender differences at each step of this process, and to search for solutions. [ABSTRACT FROM AUTHOR]

The integrity of endothelial function in major arteries (EFMA) is a powerful independent predictor of heart attack and stroke. Existing ultrasound-based non-invasive assessment methods are technically challenging and suitable only for laboratory settings. EFMA, like blood pressure (BP), is both acutely and chronically affected by factors such as lifestyle and medication. Consequently, laboratory-based measurements cannot fully gauge the effects of medical interventions on EFMA. EFMA and BP have, arguably, comparable (but complementary) value in the assessment of cardiovascular health. Widespread deployment of EFMA assessment is thus a desirable clinical goal. To this end, we propose a device based on modifying the measurement protocol of a standard electronic sphygmomanometer. The protocol involves inflating the cuff to sub-diastolic levels to enable recording of the pulse waveform before and after vasodilatory stimulus. The mechanical unloading of the arterial wall provided by the cuff amplifies the distension that occurs with each pulse, which is measured as a pressure variation in the cuff. We show that the height of the rising edge of each pulse is proportional to the change in lumen area between diastole and systole. This allows the effect of vasodilatory stimuli on the artery to be measured with high sensitivity. We compare the proposed cuff flow-mediated dilation (cFMD) method to ultrasound flow-mediated dilation (uFMD). We find significant correlation (r = 0.55, p = 0.003, N = 27) between cFMD- and uFMD-based metrics obtained when the release of a 5 min cuff occlusion is employed to induce endothelial stimulus via reactive hyperemia. cFMD is approximately proportional to the square of uFMD, representing a typical increase in sensitivity to vasodilation of 300-600%. This study illustrates the potential for an individual to conveniently measure his/her EFMA by using a low-cost reprogrammed home sphygmomanometer.

The study was to compare age‐related alterations in cardiac and arterial structure and function by sex and to explore the impacts of achieved systolic blood pressure (SBP; <130 mm Hg vs. <140 mm Hg) level on age‐related alterations in cardiac and arterial structure and function in hypertensive women and men. Community hypertensive individuals without cardiovascular disease who had echocardiographic examination were included. Age‐related alterations in cardiac and arterial structure and function were compared by sex, and interplay between age and sex was analyzed according to achieved SBP level. The mean age of the cohort was 66.5 years, and women accounted for 62% (n = 602) of the cohort (n = 971). Compared to men, women had worse left ventricular (LV) diastolic function and greater LV and arterial stiffness. After adjusting for covariates, the magnitude of the associations between age with septal E/e′ ratio, septal S′ velocity, effective arterial elastance (Ea) and LV end‐diastolic elastance (Eed) were greater in women. Sex differences in the magnitude of association between age with these four indices varied according to achieved SBP level. When achieved SBP <130 mm Hg, the magnitude of the associations between age with septal E/e′ ratio, septal S′ velocity, Ea and Eed did not differ by sex. Since age and sex are non‐modifiable, achieving SBP target, especially at a lower level, might be beneficial to attenuate sex differences in age‐related alterations in cardiac and arterial structure and function. [ABSTRACT FROM AUTHOR]

Adipose tissue and arterial dysfunction are common in the obese state. Perivascular adipose tissue (PVAT) plays an important role in mediating arterial health, and with obesity, the PVAT dysfunction negatively affects arterial health. Exercise training exerts direct and beneficial effects on PVAT, providing an additional and novel pathway by which exercise can improve arterial health in diseased populations. [ABSTRACT FROM AUTHOR]

Background: Peripartum cardiomyopathy (PPCM) is idiopathic pregnancy‐associated heart failure (HF) with reduced left ventricular ejection fraction (LVEF). We aimed to assess arterial stiffness and left ventricular (LV) function in women recovered from PPCM compared with controls. Methods: Twenty‐two PPCM patients were compared with 15 age‐matched controls with previous uncomplicated pregnancies. Eleven of the patients were at inclusion in the study recovered and off medication since at least 6 months and still free from cardiovascular symptoms with normal LVEF and normal NT‐proBNP. All underwent echocardiography, including LV strain, left atrial (LA) reservoir strain and tissue Doppler early diastolic velocity (e´) and non‐invasive assessment for arterial stiffness and central aortic systolic blood pressure (AoBP) at rest and immediately postexercise. Results: The patients off medication showed alterations compared with controls. AoBP was higher (120 ± 9 mm Hg vs. 104 ± 13 mm Hg; p =.001), a difference which persisted postexercise. The arterial elastance was higher (1.9 ± 0.4 mm Hg/ml vs. 1.3 ± 0.2 mm Hg/ml; p <.001), while there were lower e´ septal (8.9 ± 1.7 cm/s vs. 11.0 ± 1.1 cm/s; p = 0. 002), LV global strain (18.7 ± 3.9% vs. 23.1 ± 1.6%; p =.004) and LA reservoir strain (24.8 ± 9.1% vs. 37.7 ± 6.3%; p =.002). Conclusions: Compared with healthy controls, PPCM patients considered recovered and off medication had increased arterial stiffness, decreased LV longitudinal function and reduced LA function. [ABSTRACT FROM AUTHOR]

About 20% of patients with a history of atherosclerotic cardiovascular disease will experience further cardiovascular events despite maximal pharmacological treatment with cardioprotective drugs. This highlights the presence of residual cardiovascular risk in a significant proportion of patients and the need for novel, more effective therapies. These therapies should ideally target different pathophysiological pathways involved in the onset and the progression of atherosclerosis, particularly the inflammatory and immune pathways. Methotrexate is a firstline disease-modifying antirheumatic drug that is widely used for the management of autoimmune and chronic inflammatory disorders. There is some in vitro and in vivo evidence that methotrexate might exert a unique combination of antiinflammatory, blood pressure lowering, and vasculoprotective effects. Pending the results of large prospective studies investigating surrogate end-points as well as morbidity and mortality, repurposing methotrexate for cardiovascular risk management might represent a cost-effective strategy with immediate public health benefits. This review discusses the current challenges in the management of cardiovascular disease; the available evidence on the effects of methotrexate on inflammation, blood pressure, and surrogate markers of arterial function; suggestions for future research directions; and practical considerations with the use of methotrexate in this context.

BACKGROUND Aortic stiffness as measured by carotid–femoral pulse wave velocity (cfPWV) is known to depend on blood pressure (BP), and this dependency may change with age. Therefore, the hydrostatic BP gradient resulting from a change in body posture may elicit a cfPWV change that is age-dependent. We aimed to analyze the relationship between BP gradient—induced by head-up body tilting—and related changes in cfPWV in individuals of varying age. METHODS cfPWV and other hemodynamic parameters were measured in 30 healthy individuals at a head-up tilt of 0° (supine), 30°, and 60°. At each angle, the PWV gradient and resulting cfPWV were also estimated (predicted) by assuming a global nonlinear, exponential, pressure–diameter relationship characterized by a constant β 0, and taking into account that (diastolic) foot-to-foot cfPWV acutely depends on diastolic BP. RESULTS cfPWV significantly increased upon body tilting (8.0 ± 2.0 m/s supine, 9.1 ± 2.6 m/s at 30°, 9.5 ± 3.2 m/s at 60°, P for trend <0.01); a positive trend was also observed for heart rate (HR; P < 0.01). When the observed, tilt-induced cfPWV change measured by applanation tonometry was compared with that predicted from the estimated BP hydrostatic gradient, the difference in observed-vs.-predicted PWV change increased nonlinearly as a function of age (R 2 for quadratic trend = 0.38, P < 0.01, P vs. linear = 0.04). This result was unaffected by HR tilt-related variations (R 2 for quadratic trend = 0.37, P < 0.01, P vs. linear = 0.04). CONCLUSIONS Under a hydrostatic pressure gradient, the pulse wave traveling along the aorta undergoes an age-related, nonlinear PWV increase exceeding the increase predicted from BP dependency. [ABSTRACT FROM AUTHOR]

The goal of this work is to assess the impact of vascular anatomy definition degree in the predictions of blood flow models of the arterial network. To this end, results obtained with an anatomically detailed network containing over 2000 vessels are systematically compared with those obtained with an anatomically simplified network containing the main 86 vessels, the latter being a truncated version of the former one. The comparison is performed quantitatively and qualitatively in terms of pressure and flow rate waveforms, wave intensity analysis and impedance analysis. Comparisons are performed under physiological conditions and for the case of common carotid artery occlusion. Mechanisms of blood flow delivery to the brain, as well as different blood flow steal phenomena, are unveiled in light of model predictions. Results show that detailed and simplified models are in reasonable agreement regarding the hemodynamics in larger vessels and in healthy scenarios. The anatomically detailed arterial network features improved predictive capabilities at peripheral vessels. Moreover, discrepancies between models are substantially accentuated in the case of anatomical variations or abnormal hemodynamic conditions. We conclude that physiologically meaningful agreement between models is obtained for normal hemodynamic conditions. This agreement rapidly deteriorates for abnormal blood flow conditions such as those caused by total arterial occlusion. Differences are even larger when modifications of the vascular anatomy are considered. This rational comparison allows us to gain insight into the need for anatomically detailed arterial networks when addressing complex hemodynamic interactions. [ABSTRACT FROM AUTHOR]

Purpose: Optimal assessment of cardiovascular performance requires simultaneous measurement of load independent left ventricular (LV) contractility, arterial function and LV/arterial coupling. We aimed to demonstrate feasibility of non-invasive ventricular pressure–volume and aortic pressure-flow-impedance measurements using simultaneous arterial tonometry (AT) and cardiovascular magnetic resonance imaging (CMRI). Methods: 21 consecutive patients referred for CMRI were enrolled to undergo a simultaneous AT and CMRI protocol. A CMRI compatible AT apparatus provided aortic end-systolic pressure, taken to be equivalent to LV end-systolic pressure in the absence of aortic stenosis. CMRI provided LV volume and aortic flow at the time of pressure acquisition. Pressure–volume relationships were determined and correlated to traditional parameters of LV function including ejection fraction and circumferential strain. Aortic pressure-flow relationships were used to determine aortic characteristic impedance and systemic vascular resistance. Results: Simultaneous AT and CMRI permitted measurement of LV end-systolic elastance, preload recruitable stroke work, arterial elastance, aortic characteristic impedance and systemic vascular resistance. Absolute values were within the expected range for our cohort, were highly reproducible and showed appropriately directed correlation to traditional parameters. Conclusion: Non-invasive assessment of LV pressure–volume and aortic pressure-flow relationships are both feasible and reproducible using simultaneous AT and CMRI. Methods permit assessment of load independent LV contractility, arterial function and LV/arterial coupling from a single non-invasive diagnostic encounter. [ABSTRACT FROM AUTHOR]

New Findings: What is the topic of this review?Patients with advanced heart failure who are implanted with left ventricular assist devices (LVADs) present an opportunity to understand the human circulation under extreme conditions.What advances does it highlight?LVAD patients have a unique circulation that is characterized by a reduced or even absent arterial pulse. The remarkable survival of these patients is accompanied by circulatory complications, including stroke, gastrointestinal bleeding and right‐heart failure. Understanding the mechanisms related to the complications in LVAD patients will help the patients and also advance our fundamental understanding of the human circulation in general. Some humans with chronic, advanced heart failure are surgically implanted with a left ventricular assist device (LVAD). Because the LVAD produces a continuous flow, a palpable pulse is often absent in these patients. This allows for a unique investigation of the human circulation and has created a controversy around the 'need' for a pulse. The medical debate has also generated a more generic, fundamental discussion into what is 'normal' arterial physiology and health. The comprehensive study and understanding of the arterial responses to drastically altered haemodynamics due to continuous‐flow LVADs, at rest and during activity, presents an opportunity to significantly increase our current understanding of the fundamental components of arterial regulation (flow, blood pressure, sympathetic activity, endothelial function, pulsatility) in a way that could never have been studied previously. In a series of four articles, we summarize the talks presented at the symposium entitled 'Bionic women and men – Physiology lessons from implantable cardiac devices' presented at the 2019 Annual Meeting of The Physiological Society in Aberdeen, UK. The articles highlight the novel questions generated by physiological phenomena observed in LVAD patients and propose future areas of interest within the field of cardiovascular physiology. [ABSTRACT FROM AUTHOR]

Diagnosis and treatment for coronary artery disease (CAD) often involves angiography and/or percutaneous coronary intervention. However, the radial artery catheterization required during both procedures may result in acute artery dysfunction/damage. While exercise-based rehabilitation is recommended for CAD patients following catheterization, it is not known if there is a period when exercise may be detrimental due to catheter-induced damage. Animal studies have demonstrated exercise-induced paradoxical vasoconstriction postcatheterization. This study aimed to examine arterial responses to acute exercise following catheterization. Thirty-three CAD patients (65.8 ± 7.3 yr, 31.5 ± 6.3 kg/m2, 82% men) undergoing transradial catheterization were assessed before and 1 wk postcatheterization. Radial artery (RA) diameter and shear rate were assessed during handgrip exercise (HE), in both the catheterized (CATH) and control (CON) arms. Endothelial function was also assessed via simultaneous bilateral radial flow-mediated dilation (FMD) at both time points. We found that the increase in RA diameter and shear stress in response to HE (P < 0.0001) was maintained postcatheterization in both the CATH and CON arms, whereas FMD following catheterization was impaired in the CATH [6.5 ± 3.3 to 4.7 ± 3.5% (P = 0.005)] but not in the CON [6.2 ± 2.6 to 6.4 ± 3.5% (P = 0.797)] limb. While endothelial dysfunction, assessed by FMD, was apparent 1 wk postcatheterization, the ability of the RA to dilate in response to exercise was not impaired. The impact of catheterization and consequent endothelial denudation on vascular dys/function in humans may therefore be stimulus specific, and a highly level of redundancy appears to exist that preserves exercise-mediated vasodilator responses. [ABSTRACT FROM AUTHOR]

“Structure and Function of Arteries”—is a topic of great importance to those who deal with arterial hypertension, since it links the source of flow, the left ventricle of the heart (whose output is pulsatile) to the peripheral tissues (whose flow is near continuous). The arterial tree acts passively as a conduit and cushion, and the interaction of heart, arterial tree, and organs is conventionally gauged on the basis of blood pressure measured by cuff in a conveniently located place (the brachial artery). For any precision and perspective to be gained, measurements of brachial systolic and diastolic pressure need be supplemented by other information. When such information is gained, one can understand how beautifully the arterial tree is tuned to the beat of the heart in animals of different size and shape and in humans at age 30 through the first third of a 3 billion beat lifetime. After age 30, the beats themselves progressively destroy the human arteries and their tuning to the heart, with emergence of clinical syndromes. In this review, the subject is tackled quantitatively on the basis of published numerical, physical, physiological, and pathophysiological basis, with principal focus on the beat of the heart, the pulse of the arteries, and their interaction. [ABSTRACT FROM AUTHOR]

To determine whether arterial responsiveness is impaired among patients with gout, and whether arterial responsiveness inversely correlates with serum urate and inflammatory measures. This is a cross-sectional study of untreated gout subjects (n = 34) and non-gout healthy controls (n = 64). High-resolution dynamic ultrasound-measured flow-mediated dilation (FMD) and nitroglycerin-mediated dilation (NMD) assessed endothelium-dependent and endothelium-independent arterial responsiveness respectively. Serum urate (sUA) and high-sensitivity C-reactive protein (hsCRP) were measured in the gout group, and correlated with FMD and NMD responses. Both FMD (2.20 ± 0.53 vs 3.56 ± 0.31, p = 0.021) and NMD (16.69 ± 1.54 vs 24.51 ± 0.90, p = 0.00002) were impaired in the gout versus control group. Stratification for individual comorbidities suggested that no single risk factor accounted for impaired FMD/NMD in the gout subjects. However, the degree of association between gout and FMD, but not NMD impairment, was dampened after multivariable adjustment (FMD unadjusted beta = − 1.36 (SE 0.58), p = 0.02; adjusted beta = − 1.16 (SE 0.78), p = 0.14 and NMD unadjusted beta = − 7.68 (SE 1.78), p < 0.0001; adjusted beta = − 5.33 (SE 2.46), p = 0.03). Within the gout group, there was an inverse correlation between FMD and sUA (R = − 0.5, p = 0.003), and between FMD and hsCRP (R = − 0.42, p = 0.017), but not between NMD and sUA or hsCRP. Compared with healthy controls, subjects with gout have reduced arterial function. Individual comorbidities are insufficient to account for differences between gout and control groups, but multiple comorbidities may collectively contribute to impairment in endothelium-dependent arterial responsiveness. Endothelial impairment is also related to sUA and hsCRP, markers of gout severity and inflammation respectively. Studies to determine whether gout therapy may improve arterial responsiveness are warranted. [ABSTRACT FROM AUTHOR]

Objectives: The objective of this study was the analysis of B-Cell Activating Factor (BAFF) levels in pregnancies affected by PE, and in pregnancies affected by fetal growth restriction without Hypertensive disorders and its possible correlation with pulse wave velocity and cardiac output.Study Design: Prospective study of 69 women at 24-40 weeks gestation. Haemodynamic function was assessed in those with Pre-eclampsia (PE, n = 19), fetal growth restriction (FGR, n = 10) and healthy pregnancies (n = 40). Maternal venous BAFF levels at recruitment were measured using ELISA. We analysed the relationship between BAFF and cardiac output (CO), and BAFF and PWV (pulse wave velocity); the gold standard for assessing arterial stiffness. PWV was measured with an oscillometric device and CO using inert gas rebreathing technique. PWV and CO were converted to gestation adjusted indices (z scores).Main Outcome Measures: The association between BAFF levels in PE and FGR, and the relationship of BAFF with PWV and CO.Results: BAFF was higher in PE (p = 0.03) but not in FGR (p = 0.83) when compared to healthy pregnancies. There was a positive correlation between BAFF levels and z score PWV (r = 0.25, p = 0.04), but not CO (r = -0.01, p = 0.91). BAFF levels did not change with gestational age. (r = 0.012, p = 0.925).Conclusions: These findings provide evidence of a possible contribution of BAFF to both maternal inflammation and arterial dysfunction associated with PE. Though no relationship was found with another disorder of placentation: normotensive FGR, this condition is not thought to be associated with maternal inflammation. [ABSTRACT FROM AUTHOR]

Apelin can improve arterial function by enhancing the expression of endothelial nitric oxide synthase but this effect depends markedly on endothelial integrity. We hypothesized that inflammation influences the potential impact of apelin on arterial function in rheumatoid arthritis (RA). We assessed the associations of apelin concentrations with arterial stiffness (pulse wave velocity), wave reflection (augmentation index, reflected wave pressure, and reflection magnitude), and pressure pulsatility (central systolic pressure (CSP), central pulse pressure (CPP), peripheral pulse pressure (PPP), pulse pressure amplification (PPamp), and forward wave pressure (Pf)) among 170 RA patients without cardiovascular disease. In multivariable regression models, apelin concentrations were not independently associated with arterial function measures (p ≥ 0.15) in all patients. Inflammation markers were not consistently associated with apelin levels but joint deformity counts, Disease Activity Score in 28 joints (DAS28), and erythrocyte sedimentation rate (ESR) impacted apelin-pressure pulsatility relations (interaction p ≤ 0.05). In stratified analysis, apelin was associated with CSP (partial r = − 0.33, p = 0.01), CPP (partial r = − 0.26, p = 0.04), PPamp (partial r = 0.27, p = 0.03), and Pf (partial r = − 0.33, p = 0.01) in patients without but not with joint deformities; apelin was related to CSP (partial r = − 0.24, p = 0.05) in those with a DAS28 joint < 2.8 (median value) (partial r = − 0.24, p = 0.05) but not ≥ 2.8, and to CSP (partial r = − 0.36, p = 0.003) in those with an erythrocyte sedimentation rate < 13 mm/h (median value) but not ≥ 13 mm/h. Apelin is associated with reduced pressure pulsatility in RA patients without but not with a high inflammatory burden. A loss of apelin protective effects on arterial function may contribute to the link between RA severity and cardiovascular risk. [ABSTRACT FROM AUTHOR]

Background: Multiple sclerosis (MS) is associated with increased risk of cardiovascular disease (CVD) and approximately 25–54% of patients report poor sleep quality. There is evidence from the general population of an association between poor sleep and increased CVD risk, but this is poorly understood in MS. Purpose: This study examined the association between self-reported sleep quality and arterial health in persons with MS. Methods: MS subjects (n = 31) and control subjects (n = 23) were recruited. Control subjects were age and body size matched. All subjects were administered the Pittsburgh Sleep Quality Index (PSQI) to assess self-reported sleep quality. Subjects with a global score >5 were classified as “poor sleepers”. Blood pressure, arterial stiffness, and the forearm blood flow responses following 5-min ischemic occlusion (endothelial function) were measured. Results: Nineteen MS subjects and 5 control subjects were classified as “poor sleepers”. AIx was significantly higher in MS subjects who had poor sleep quality (32.5 ± 8.8 vs 22.0 ± 13.2; P < 0.05). Conclusions: Markers of arterial dysfunction were significantly higher in MS subjects with poor sleep quality compared to those with good sleep quality. This study suggests novel evidence for the association of CVD risk and sleep quality in MS.