Peripheral Arterial Stiffness Research Articles

Osteocalcin: A Potential Marker of Peripheral Arterial Stiffness in Hypertensive Patients.

Background and Objectives: Brachial-ankle pulse wave velocity (baPWV) is an established independent risk factor for cardiovascular events, cardiovascular mortality, and all-cause mortality. Osteocalcin (OC) is recognized to be associated with vascular function. The present study assessed the correlation between serum OC levels and peripheral arterial stiffness (PAS) measured through baPWV in hypertensive patients. Materials and Methods: Fasting blood samples were collected from 120 hypertensive participants. The serum total OC levels were measured using a commercial enzyme-linked immunosorbent assay kit, whereas the baPWV device was used to detect PAS. The PAS group had left or right baPWV > 18.0 m/s. Results: Among the hypertensive patients, 24 (20.0%) were classified into the PAS group. The PAS group exhibited a significantly older age (p = 0.011), higher prevalence of diabetes (p = 0.010), systolic blood pressure (p = 0.019), levels of serum fasting glucose (p = 0.003), blood urea nitrogen (p = 0.024), creatinine (p = 0.004), C-reactive protein (p = 0.007), OC (p = 0.002), and lower estimated glomerular filtration rate (p = 0.004) than the non-PAS group. Age (odds ratio [OR]: 1.076, 95% CI: 1.004-1.153, p = 0.037) and serum OC level (OR: 1.797, 95% confidence interval (CI): 1.077-3.000, p = 0.025) were independent factors linked to PAS in hypertensive patients in the multivariate logistic regression analysis. Conclusions: Serum OC levels and older age are positively associated with PAS in hypertensive patients.

Limb Position Influences Peripheral Arterial Stiffness Reduction with Reactive Hyperemia

Reactive hyperemia can acutely reduce peripheral arterial stiffness. The reduction in peripheral arterial stiffness with reactive hyperemia has been suggested to be flow dependent. However, no previous studies have manipulated the magnitude of hyperemia. We manipulated blood flow by altering limb position to test the hypothesis that a larger increase in blood flow would lead to a greater reduction in peripheral arterial stiffness. Fourteen healthy young adults (5 women; age: 25 ± 5 years; mean ± SD) were included in this study. Peripheral arterial stiffness assessed via brachial to radial pulse wave velocity (PWV) was measured by placing pulse tonometers simultaneously over the brachial and radial arteries. Doppler ultrasound was used to measure brachial arterial blood flow. Arterial blood pressure was continuously monitored via photoplethysmography on the middle finger of the contralateral hand. Reactive hyperemia was performed with the right arm positioned below (≍50°) and above (≍50°) heart level using a rapid-release cuff positioned on the upper arm, inflated to 220 mmHg, sustained for 5 min, then released. Measurements were recorded before cuff inflation and at 5, 15, and 30 min after cuff release. Repeated measures ANOVA revealed a significant condition effect (p<0.01) with peripheral PWV higher with the arm below the heart. There was a significant time x condition interaction (p<.05). At 5-min after reactive hyperemia, peripheral PWV was reduced more with the arm below the heart (9.58 ±1.65 to 7.26 ± 1.51 m/sec) than above the heart (7.08 ± 1.79 to 5.88 ± 1.43 m/sec). Mean arterial pressure did not change across time points (p>0.05). Peak brachial artery blood flow was greater with the arm below the heart (477.37 ± 145 vs 368.64 ± 137 ml/min; p<.001). The results show that reactive hyperemia produces an acute reduction in brachial to radial PWV. The reduction in peripheral arterial stiffness was greater when the arm was below the heart. The mechanism for position-related differences in the reduction in peripheral arterial stiffness with reactive hyperemia may be associated with the magnitude of increase in blood flow. REJ was supported by National Heart, Lung, and Blood Institute (5T32HL134634-04). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The effects of prolonged sitting with a mild hypercapnic environment on vascular function in elderly adults: A pilot study

Introduction: Prolonged Sitting (PS), defined a sitting for 2+ hours at a time, has been identified as an independent risk factor for cardiovascular disease (CVD). We previously reported that an acute bout of PS can attenuate macrovascular function in healthy young adults. Additionally, we reported that PS in mild hypercapnic environments (elevated CO2 concentrations) can further exacerbate these impairments in healthy young adults, and these impairments can be partially prevented by intermittent bouts of passive and active leg movements. However, the effects of prolonged sitting with a mild hypercapnic environment in the elderly population have not been studied. Therefore, the purpose of this study was to examine the impact of prolonged sitting with a mild hypercapnic condition on macrovascular function, arterial stiffness, and leg muscle metabolism. Additionally, we have further examined the effects of passive and active movements to negate the negative effects of prolonged sitting in elderly adults. Hypothesis: We hypothesized that 1) prolonged sitting in a hypercapnic environment will attenuate vascular function and leg metabolism, 2) both passive and active leg movements will preserve endothelial function and leg metabolism. Methods: Healthy elderly adults (n=2, 2 males, 69 ± 2.83 yrs) participated in three experimental visits consisting of 2.5h of prolonged sitting in a mild hypercapnic condition (CO2 = 1500ppm): control (CON), passive (PASS, passive leg movement), and active (ACT, active leg movement). Popliteal and brachial artery endothelial function was measured using flow-mediated dilation (FMD). Peripheral and central arterial stiffness was assessed using pulse wave velocity. Leg muscle metabolism was assessed using near infrared spectroscopy and a thermal camera. All measurements were taken pre- and post-siting. Results: Popliteal FMD was reduced in the CON condition compared to both the PASS and ACT (Δ -3.559 ± 0.499 vs Δ -1.799 ± 0.824 vs Δ 0.601 ± 1.958, respectively). Brachial FMD was attenuated in the CON condition compared to both compared to both the PASS and ACT (Δ -2.368 ± 0.215 vs Δ -0.285 ± 1.578 vs Δ 1.116 ± 1.174, respectively). The CON condition showed a greater reduction in leg temperature compared to both the PASS and ACT (Δ -2.4 vs Δ -1.6 ± 0.599 vs Δ 0.1 ± 0.224, respectively). No changes in central or peripheral arterial stiffness were observed. Conclusion: This preliminary data shows that uninterrupted prolonged sitting induces impairments in both local and systemic vascular function, leg muscle metabolism, but not arterial stiffness. Additionally, intermittent bouts of passive and active movements can partially preserve leg vascular function and metabolism during PS. This research was supported by the UNO Graduate Research and Creative Activity Grant, National Institutes of Health (RO1HD106911) and the Great Plains IdeaA-CTR (U54 GM115448). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Home-Based Heat Therapy and Vascular Function of Adults Living with Type 2 Diabetes: Preliminary Analyses of a Randomized Controlled Trial

Background: Several studies indicate that various heat exposure interventions improve peripheral endothelial function and microvascular reactivity, as well as reduce central arterial stiffness and blood pressure in various populations. Nonetheless, few studies have considered the potential therapeutic effects of heat exposure for people living with type 2 diabetes mellitus (T2DM), who are at high cardiovascular risk. In addition, all heat therapy interventions investigated to date have been laboratory-based, which may limit long-term adherence. HYPOTHESES: This study aims is to determine the effects of a 12-week home-based heat therapy intervention on markers of vascular function in adults living with T2DM. The primary hypothesis is that heat therapy improves peripheral endothelial function relative to a sham intervention. Secondary hypotheses include improved microvascular reactivity, central arterial stiffness, and 24h blood pressure. METHODS: Thirteen adults (66 ± 10 years, 28.9 ± 6.0 kg/m2, 9 men/ 4 women) living with TD2M were randomized to 12 weeks of home-based heat therapy (n=7, lower leg immersion in 42°C water) or a thermoneutral sham intervention (n=6, lower leg immersion in 36°C water). Peripheral endothelial function (brachial artery flow-mediated dilation, FMD), microvascular reactivity (post-occlusive reactive hyperemia), arterial stiffness (carotid-femoral pulse wave velocity), and 24h blood pressure (ambulatory blood pressure monitoring), were measured before and after the intervention. RESULTS: Brachial artery FMD changed by 1.72% [95%CI, 0.06; 3.37] in response to heat therapy compared to 0.41% [-1.38; +2.20] in response to the sham intervention. Peak and total reactive hyperemia changed by 0.79 mL/min/mmHg [-0.27; 1.86] and by 1.77 mL/mmHg [0.73; 2.81], respectively, in response to heat therapy compared with 0.76 mL/min/mmHg [-0.38; 1.91] and 1.68 mL/mmHg [0.56; 2.80] in response to the sham intervention. Arterial stiffness changed by 0.55 m/s [-1.62; 2.71] in response to heat therapy compared with -1.60 m/s [-3.75; 0.57] in response to the sham intervention. The 24h-systolic and diastolic blood pressure changed by 6 mmHg [-1; +12] and 2 mmHg [-3; +7], respectively, in response to heat therapy compared with -2 mmHg [-10; +6] and -3 mmHg [-9; +3] in response to the sham intervention. CONCLUSION: These preliminary results suggest that 12 weeks of home-based lower leg hot water immersion improves brachial artery FMD in adults with T2DM. In contrast, the heat therapy intervention does not appear to improve microvascular reactivity, central arterial stiffness, or 24h blood pressure. Cardiometabolic Health Diabetes and Obesity Research Network and Diabète Quebec. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

PERIPHERAL ARTERIAL STIFFNESS PREDICTS INDEPENDENTLY FUNCTIONAL OUTCOME AFTER ISCHEMIC STROKE

Objective: Aortic stiffness is a strong predictor of morbidity in various clinical conditions, including ischemic stroke. However, the prognostic significance of the peripheral arterial stiffness, defined as radial -carotid pulse wave velocity - for functional outcome in ischemic stroke remains unknown. Design and method: We enrolled 189 patients (126 males, age 62.9±11.9 years, mean±SD) with acute ischemic stroke (NIHSS score at admission 6.4±5.1 points). Radial-carotid pulse wave velocity (CR PWV), peripheral blood pressure (BP) and heart rate (HR) were measured (SphygmoCor®) within several (6±2) days after stroke onset. Functional outcome was evaluated 90 days after stroke using the modified Rankin Scale (mRS) with an mRS score of 0 to 1 considered as an excellent outcome. Results: In univariate analysis, age, severity of stroke, heart rate, previous stroke, predicted stroke functional outcome. By contrast, CR PWV had no significant predictive value for stroke outcome (8.91±1.66 vs 8.56±1.50 m/s; p=0.14). In a multivariate analysis, the predictive value of CR PWV was significantly associated with functional outcome (OR, 1.34; 95% CI, 1.77–1.01; p=0.04) after adjustment for covariates, with higher values of CR PWV being associated with better prognosis. Conclusions: We found that the CR PWV in patients in the subacute phase of ischemic stroke is associated with functional outcome independently of traditional neurologic and hemodynamic factors. This PWV index might be useful in clinical practice, including therapeutic decisions, but needs broader studies in patient populations of stroke subtypes.

Serum Malondialdehyde-Modified Low-Density Lipoprotein as a Risk Marker for Peripheral Arterial Stiffness in Maintenance Hemodialysis Patients.

Background and Objectives: Peripheral arterial stiffness (PAS), assessed by brachial-ankle pulse wave velocity (baPWV), is an independent biomarker of cardiovascular diseases (CVD) in patients on maintenance hemodialysis (HD). Malondialdehyde-modified low-density lipoprotein (MDA-LDL), an oxidative stress marker, has been linked to atherosclerosis and CVD. However, the association between serum MDA-LDL and PAS among HD patients has not been fully elucidated. This study aimed to examine the association of serum MDA-LDL with PAS in HD patients and to identify the optimal cutoff value of serum MDA-LDL for predicting PAS. Materials and Methods: A cross-sectional study was conducted in 100 HD patients. Serum MDA-LDL was quantified using an enzyme-linked immunosorbent assay (ELISA), and baPWV was measured using a volume plethysmographic device. Patients were divided into the PAS group (baPWV > 18.0 m/s) and the non-PAS group (baPWV ≤ 18.0 m/s). The associations of baPWV and other clinical and biochemical parameters with serum MDA-LDL were assessed by multivariable logistic regression analyses. A receiver operating characteristic (ROC) curve analysis was performed to determine the optimal cutoff value of serum MDA-LDL for predicting PAS. Results: In multivariable logistic regression analysis, higher serum MDA-LDL, older age, and higher serum C-reactive protein [odds ratios (ORs) and 95% confidence intervals: 1.014 (1.004-1.025), 1.044 (1.004-1.085) and 3.697 (1.149-11.893)] were significantly associated with PAS. In the ROC curve analysis, the optimal cutoff value of MDA-LDL for predicting PAS was 80.91 mg/dL, with a sensitivity of 79.25% and a specificity of 59.57%. Conclusions: Greater serum MDA-LDL levels, particularly ≥80.91 mg/dL, were independently associated with PAS in HD patients. The findings suggest that oxidative stress plays a crucial role in the pathogenesis of PAS, and targeting MDA-LDL may be a potential therapeutic strategy for reducing cardiovascular risk in HD patients.

Home- vs gym-based exercise delivery modes of two multicomponent intensity training regimes on cardiorespiratory fitness and arterial stiffness in adults with intellectual and developmental disability during the COVID-19 pandemic - a randomized controlled trial.

Background: We compared the effects of home- vs gym-based delivery modes of two 8-week supervised multicomponent intensity training regimes on cardiorespiratory fitness and arterial stiffness in 17 adults with intellectual and developmental disability during the COVID-19 pandemic. Methods: Participants were assigned to sprint interval training or continuous aerobic training, both incorporating resistance training. The intervention started with 8-weeks of online training (M1-M2), 1-month of detraining, plus 8-weeks of gym-based training (M3-M4). Results: Peak oxygen uptake decreased from M1-M2 and increased from M2-M4. Central arterial stiffness decreased between M1-M2, and M1-M4, along with peripheral arterial stiffness. Central systolic blood pressure decreased from M1-M2 only with sprint interval training. Conclusion: Home-based training minimized the negative impact of the lockdown on central arterial stiffness and central blood pressure, but it did not match the benefits on cardiorespiratory fitness and peripheral arterial stiffness of a gym-based intervention, irrespective of the multicomponent intensity training regime. Registered in ClinicalTrials.gov NCT05701943.

Evaluation of cardiac and vascular remodeling in patients with arterial hypertension in combination with atherosclerosis of the lower extremity arteries

Objective: to evaluate the features of cardiac and vascular remodeling in patients with arterial hypertension (AH) and atherosclerosis of the arteries of the lower extremities (LAA) of varying severity. Materials and methods: the study involved 120 patients with hypertension. Depending on the presence of AANC, all patients were divided into 3 groups: group 1 — 46 patients with hypertension and clinically manifested AANC, group 2 — 39 patients with hypertension and asymptomatic AANC, group 3 — 35 patients with hypertension without AANC. The characteristics of cardiac and vascular remodeling were assessed based on the results of 24-hour blood pressure monitoring (ABPM) using Vasotens technology, triplex ultrasound scanning (UTS) of the arteries of the lower extremities (LEA), and echocardiographic examination (EchoCG). Statistical data processing was carried out using Microsoft Office Excel 16 (2015, Microsoft, USA), Statistica 10.0 (StatSoft, USA) and IBM SPSS Statistica 26.0 (IBM, USA). Results: in the group of patients with severe circulatory disorders of the lower extremities, compared with patients with asymptomatic AANK, significantly lower values of the indicator — reflected wave propagation time (RWTT, ms) (p = 0.006) and significantly higher values of the indicator — augmentation index (AIX) were revealed) and augmentation index in the aorta (AIXao) (p<0.05). A direct statistically significant correlation of moderate strength was revealed between the degree of stenosis (%) of the ANC and the values of the AIX and AIXao indicators (r = 0.345, p = 0.001). Higher values of the dimensions of the walls of the left ventricle (LV) were determined: the thickness of the interventricular septum (IVS) and the posterior wall of the left ventricle (PLW) in patients of the 1st and 2nd groups in comparison with the indicators in patients of the 3rd group (p<0 .05). Patients of all three groups had thickening of the left ventricle and intraventricular septum (>11 mm) and an increase in LVMI. In patients with hypertension and severe AANC, the maximum values of LVMI were determined, which were significantly higher than the corresponding values in patients of the 2nd (p = 0.004) and 3rd (p = 0.0001) groups. LV systolic function in all patients included in the study was assessed as intact. However, the highest ejection fraction (EF) values were recorded in patients with hypertension without AANC, and were significantly higher than those in patients with hypertension and concomitant asymptomatic AANC (p = 0.02), as well as in patients with hypertension and clinically manifested AANC (p =0.001). Conclusions: the progression of AANK was associated with an increase in the stiffness of both peripheral and main arteries, which was accompanied by an increase in the load on the myocardium, which in 97.8% of cases led to more pronounced myocardial remodeling of the concentric hypertrophy type.

Hyperparathyroidism and Peripheral Arterial Disease.

Primary hyperparathyroidism (PHPT) is presented in various forms, including classic PHPT, characterised by increased parathyroid hormone (PTH) secretion, normohormonal PHPT, and normocalcaemic PHPT. Secondary hyperparathyroidism is characterised by increased PTH secretion triggered by factors such as vitamin D deficiency and kidney failure. This review aims to discuss the involvement of hyperparathyroidism (HPT) in atherosclerosis, including peripheral arterial disease (PAD). The increased level of PTH is involved in developing subclinical and overt vascular diseases, encompassing endothelial dysfunction, vascular stiffness, hypertension, and coronary and peripheral arterial diseases. It has been consistently associated with an augmented risk of cardiovascular morbidity and mortality, independent of classical risk factors for atherosclerosis. Chronic hypercalcemia associated with increased levels of PTH contributes to the development of calcification of vessel walls and atherosclerotic plaques. Vascular calcification can occur in the intima or media of the arterial wall and is associated with stiffness of peripheral arteries, which the formation of atherosclerotic plaques and narrowing of the vessel lumen can follow. For treating hyperparathyroidism, particularly SHPT, calcimimetics, novel phosphorus binders and novel vitamin D receptor activators are used. However, they are ineffective in severe PHPT. Therefore, parathyroidectomy remains the primary therapeutic option of PHPT.

Effects of pre-exercise intake of plant- and animal-based foods on arterial function and aerobic exercise capacity in healthy young men: a randomized cross-over trial.

The purpose of this study was to examine the effects of plant- versus animal-based food intake before exercise on arterial function and subsequent aerobic exercise capacity. Eleven healthy adult males (mean age, 22.6±1.8 years) participated in this study. A plant- or animal-based randomized meal type crossover comparison was conducted on separate days with a uniform protein, fat, and carbohydrate balance. Both carotid-femoral pulse wave velocity (cfPWV), femoral-ankle pulse wave velocity (faPWV), and brachial artery flow-mediated dilatation (FMD) were measured as indexes of aortic and peripheral arterial stiffness and vascular endothelial function, respectively, before and at 120min after the meal. After these measurements, maximal oxygen uptake was assessed using a graded power test on an electronically braked cycle ergometer. The results revealed that cfPWV was significantly lower, whereas FMD was significantly higher, at 120min after compared with before the plant-based meal (p=0.01 and 0.02, respectively). By contrast, cfPWV and FMD did not change at 120min after compared with before the animal-based meal. In addition, faPWV did not change at 120min after compared with before the meal for either meal type. Maximal oxygen uptake was higher in the plant- than in the animal-based meal type (p=0.02). These results suggest that pre-exercise plant-based food intake may improve central arterial stiffness and vascular endothelial function, which may have favorable implications for aerobic exercise capacity.

Neuroimaging-based evidence for sympathetic correlation between brain activity and peripheral vasomotion during pain anticipation

Anticipation of pain engenders anxiety and fear, potentially shaping pain perception and governing bodily responses such as peripheral vasomotion through the sympathetic nervous system (SNS). Sympathetic innervation of vascular tone during pain perception has been quantified using a peripheral arterial stiffness index; however, its innervation role during pain anticipation remains unclear. This paper reports on a neuroimaging-based study designed to investigate the responsivity and attribution of the index at different levels of anticipatory anxiety and pain perception. The index was measured in a functional magnetic resonance imaging experiment that randomly combined three visual anticipation cues and painful stimuli of two intensities. The peripheral and cerebral responses to pain anticipation and perception were quantified to corroborate bodily responsivity, and their temporal correlation was also assessed to identify the response attribution of the index. Contrasting with the high responsivity across levels of pain sensation, a low responsivity of the index across levels of anticipatory anxiety revealed its specificity across pain experiences. Discrepancies between the effects of perception and anticipation were validated across regions and levels of brain activity, providing a brain basis for peripheral response specificity. The index was also characterized by a 1-s lag in both anticipation and perception of pain, implying top-down innervation of the periphery. Our findings suggest that the SNS responds to pain in an emotion-specific and sensation-unbiased manner, thus enabling an early assessment of individual pain perception using this index. This study integrates peripheral and cerebral hemodynamic responses toward a comprehensive understanding of bodily responses to pain.

Circulating leptin is associated with adverse vascular changes in young adult survivors of childhood cancer.

Proteomics may help discover novel biomarkers and underlying mechanisms for cardiovascular disease. This could be useful for childhood cancer survivors as they show an increased risk of cardiovascular disease. The aim of this study was to investigate circulating cardiovascular proteins in young adult survivors of childhood cancer and their relationship to previously reported subclinical cardiovascular disease. Ninety-two cardiovascular proteins were measured in 57 childhood cancer survivors and in 52 controls. For proteins that were significantly different between childhood cancer survivors and controls, we performed correlations between protein levels and measures of peripheral arterial stiffness (carotid distensibility and stiffness index, and augmentation index) and endothelial dysfunction (reactive hyperemia index). Leptin was significantly higher in childhood cancer survivors compared to controls (normalized protein expression units: childhood cancer survivors 6.4 (1.5) versus 5.1 (1.7), p < 0.0000001) after taking multiple tests into account. Kidney injury molecule-1, MER proto-oncogene tyrosine kinase, selectin P ligand, decorin, alpha-1-microglobulin/bikunin precursor protein, and pentraxin 3 showed a trend towards group differences (p < 0.05). Among childhood cancer survivors, leptin was associated with anthracycline treatment after adjustment for age, sex, and body mass index (p < 0.0001). Higher leptin correlated with lower carotid distensibility after adjustment for age, sex, body mass index, and treatments with radiotherapy and anthracyclines (p = 0.005). This proteomics approach identified that leptin is higher in young asymptomatic adult survivors of childhood cancer than in healthy controls and is associated with adverse vascular changes. This could indicate a role for leptin in driving the cardiovascular disease burden in this population.

Uninterrupted prolonged sitting and arterial stiffness: moderating effect of prior aerobic exercise in physically active adults.

Prolonged sitting acutely increases arterial stiffness, with interruption strategies only providing limited success in offsetting these rises. Acute aerobic exercise is a potent stimulus to decrease arterial stiffness. However, limited information exists on the effectiveness of acute exercise to maintain arterial stiffness when performed prior to prolonged sitting, particularly within physically active individuals. Using a randomized crossover design, 22 young, active individuals (50% female) performed two conditions 30min of walking at 55-65% of heart rate reserve (EX) and 30min of standing (STAND) followed by 2.5-h of sitting. Brachial-femoral (bfPWV) and femoral-ankle pulse wave velocity (faPWV) were assessed at Baseline, post-exercise and pre-sitting (Pre), and post-sitting (Post) as estimates of central and peripheral arterial stiffness, respectively. For bfPWV, no interaction, condition, or time effects were observed. For faPWV, an interaction was present (p < 0.001); compared to Baseline, there was a 6.1% decrease for EX (- 0.4m/s, p < 0.001) and a 4.6% increase for STAND (0.3m/s, p = 0.016) for STAND such that there was an 11.3% difference between conditions at Pre (0.7m/s, p < 0.001). From Pre to Post, EX then increased by 11.7% (0.9m/s p < 0.001) while STAND remained unchanged, resulting in no difference between conditions (0.1m/s, p = 0.569). While aerobic exercise resulted in a significant decrease in faPWV prior to sitting, the prior exercise bout did not confer a protective effect against the deleterious effects of uninterrupted sitting. Future work should investigate the combined effect of prior exercise and sitting interruption strategies on markers of arterial stiffness.

Assessment of aortic and peripheral arterial stiffness in patients with knee osteoarthritis by ultrasound Doppler derived pulse wave velocity

Information regarding regional arterial stiffness assessment in osteoarthritis (OA) was scarce and sometimes contradictory. We aimed to investigate the aortic, lower limb peripheral arterial stiffness and their associations with knee OA. Patients with primary knee OA and matched non-OA controls were prospectively enrolled from two medical centers in China. The carotid-femoral pulse wave velocity (cfPWV) and femoral-ankle pulse wave velocity (faPWV) were measured using a novel ultrasound technique. A total of 238 participants (including 128 patients with knee OA and 110 controls) were included. In OA patients, cfPWV was significantly higher than that of non-OA controls (9.40 ± 1.92 vs 8.25 ± 1.26 m/s, P < 0.0001). However, faPWV measurements in OA patients (12.10 ± 2.09 m/s) showed no significant difference compared with that of the controls (11.67 ± 2.52 m/s, P = 0.130). Multiple regression analysis revealed that cfPWV was independently associated with knee OA (P < 0.0001) after adjusting for the confounding factors including age, gender, smoking, mean blood pressure, body mass index, heart rate, high-sensitivity C-reactive protein and lipids profiles. In contrast, faPWV did not show independent association with knee OA (P = 0.372) when after adjusting for confounding factors. In addition, Spearman’s correlation analysis showed cfPWV had a significant correlation with Kellgren-Lawrence score (rs = 0.2333, P = 0.008), but no correlation was founded between faPWV with Kellgren-Lawrence score (rs = 0.1624, P = 0.067) in OA patients. This study demonstrated that stiffening of aorta, but not lower limb arteries, was independently associated with knee OA. Our findings may call for further implementation of routine aortic stiffness assessments so as to evaluate cardiovascular risk in patients with OA.

Noninvasive characterization of peripheral sympathetic activation across sensory stimuli using a peripheral arterial stiffness index.

Introduction: The peripheral arterial stiffness index has been proposed and validated as a noninvasive measure quantifying stimulus intensity based on amplitude changes induced by sympathetic innervation of vascular tone. However, its temporal response characteristics remain unclear, thus hindering continuous and accurate monitoring of the dynamic process of sympathetic activation. This paper presents a study aimed at modeling the transient response of the index across sensory stimuli to characterize the corresponding peripheral sympathetic activation. Methods: The index was measured using a continuous arterial pressure monitor and a pulse oximeter during experiments with local pain and local cooling stimuli designed to elicit different patterns of sympathetic activation. The corresponding response of the index was modeled to clarify its transient response characteristics across stimuli. Results: The constructed transfer function accurately depicted the transient response of the index to local pain and local cooling stimuli (Fit percentage: 78.4% ± 11.00% and 79.92% ± 8.79%). Differences in dead time (1.17 ± 0.67 and 0.99 ± 0.56 s, p = 0.082), peak time (2.89 ± 0.81 and 2.64 ± 0.68 s, p = 0.006), and rise time (1.81 ± 0.50 and 1.65 ± 0.48 s, p = 0.020) revealed different response patterns of the index across stimuli. The index also accurately characterized similar vasomotor velocities at different normalized peak amplitudes (0.19 ± 0.16 and 0.16 ± 0.19 a.u., p = 0.007). Discussion: Our findings flesh out the characterization of peripheral arterial stiffness index responses to different sensory stimuli and demonstrate its validity in characterizing peripheral sympathetic activation. This study valorizes a noninvasive method to characterize peripheral sympathetic activation, with the potential to use this index to continuously and accurately track sympathetic activators.

Acute inflammation elicits decreased blood pressure but similar arterial stiffness in young African American adults.

African Americans (AA) have a higher risk for cardiovascular disease (CVD) as compared to their White (W) counterparts. CVD is characterized by increased blood pressure (BP), arterial stiffness and systemic inflammation. An acute inflammatory stimulus may explain physiological manifestations responsible for amplified CVD in AA that are not apparent at rest. The purpose of this study was to evaluate central and peripheral BP, central and local arterial stiffness, and indices of pulse wave morphology in young healthy AA and W participants in response to acute inflammation. Concentrations of the inflammatory cytokine interleukin-6 (IL-6) and measures of central and peripheral BP, central arterial stiffness (carotid-femoral pulse wave velocity (cfPWV)), local carotid arterial stiffness (β-stiffness, elastic modulus (Ep)), and indices of pulse wave morphology were assessed in 28 participants (21±2years, AA: n = 11) at baseline (BL), 24h and 48h post-inflammation. Changes in IL-6 concentrations (ΔIL-6) were significantly greater at 24h as compared to 48h post-inflammation (0.652±0.644 vs. -0.146±0.532pg/μl, P≤0.0001). Among AA participants, central and peripheral diastolic BP were significantly decreased at 24h post-inflammation as compared to BL (aortic diastolic BP: -4±4mmHg, P=0.016; brachial diastolic BP: -4±4mmHg, P=0.014). AA participants also experienced a significant decrease in central and peripheral mean arterial BP at 48h post-inflammation as compared to BL (aortic mean arterial pressure: -4±4mmHg, P=0.009; brachial mean arterial pressure: -4±4mmHg, P=0.012). Despite haemodynamic changes, there were no differences in central or local carotid arterial stiffness or indices of pulse wave morphology.

Reduction in peripheral arterial stiffness after reactive hyperemia is dependent on increases in blood flow.

The acute reduction in peripheral arterial stiffness during reactive hyperemia is assumed to be flow-mediated; however, the mechanism remains unproven. We hypothesized that restricting the blood flow increase during reactive hyperemia would abolish the reduction in peripheral arterial stiffness. Fourteen healthy young adults (5 females, 25 ± 5 years, mean ± SD) underwent reactive hyperemia with a rapid-release cuff on the upper arm inflated to 220 mmHg for 5 min: once with unrestricted blood flow and once with restricted blood flow by manually applying pressure to the brachial artery. Brachial-radial pulse wave velocity (PWV) was measured with tonometers over brachial and radial arteries before cuff inflation and at 5, 15, and 30 min after release. Brachial blood flow was monitored with Doppler ultrasound. Baseline brachial-radial PWV was similar between conditions (10.3 ± 1.8 vs. 10.7 ± 1.7 m/s). With unrestricted flow, PWV decreased 5 min post-reactive hyperemia (8.6 ± 1.1 m/s; p < 0.05) and returned near baseline at 15 and 30 min post (p < 0.05). With restricted flow, PWV did not change (p > 0.05) post-reactive hyperemia. Reactive hyperemia acutely reduced peripheral arterial stiffness, but not when brachial artery blood flow increase was restricted. This suggests that the reduction in peripheral arterial stiffness during reactive hyperemia depends on increased blood flow.

The Influence of Aging – Related Decrease in Endothelial Function on the Stiffness of Peripheral Conducting Arteries for CME Credit December 2023

The Influence of Aging – Related Decrease in Endothelial Function on the Stiffness of Peripheral Conducting Arteries for CME Credit December 2023

Assessment of aortic to peripheral vascular stiffness and gradient by segmented upper limb PWV in healthy and hypertensive individuals

Theoretically pulse wave velocity (PWV) is obtained by calculating the distance between two waveform probes divided by the time difference, and PWV ratio is used to assess the arterial stiffness gradient (SG) from proximal to distal. The aim was to investigate segmental upper-limb PWV (ulPWV) differences and the effects of hypertension and or aging on each ulPWV and SG. The study collected multi-waveform signals and conduction distances from 167 healthy individuals and 92 hypertensive patients. The results showed significant differences between ulPWVs (P < 0.001), with increased and then decreased vascular stiffness along the proximal transmission to the distal peripheral artery and then to the finger. Adjusted for age and sex, ulPWVs in hypertension exceeded that of healthy individuals, with significant differences between groups aged ≥ 50 years (P < 0.05). The hrPWV/rfPWV (heart-radial/radial-finger) was reduced in hypertension and differed significantly between the aged ≥ 50 years (P = 0.015); the ratio of baPWV (brachial-ankle) to ulPWV differed significantly between groups (P < 0.05). Hypertension affected the consistency of rfPWV with hfPWV (heart-finger). The findings suggest that segmented ulPWV is instrumental in providing stiffness corresponding to the physiological structure of the vessel. The superimposition of hypertension and or aging exacerbates peripheral arterial stiffness, as well as alteration in stiffness gradient.

The Influence of Aging-Related Decrease in Endothelial Function on the Stiffness of Peripheral Conducting Arteries

Introduction: The aim of this study is to determine the degree of aging-related decrease in endothelial capacity for endothelium-dependent vasodilatation and its mutual inter-relation with increase in the stiffness of peripheral arteries. Methods: The reactive hyperemia test is useful for noninvasively evaluating the degree of endothelium-dependent vasodilatation. Stiffness index is a parameter used to evaluate vascular tonus and structural changes in the peripheral vasculature. The examination was done on 30 healthy respondents of both sexes and different ages, with no manifested risk factors and/or symptoms of cardiovascular diseases, to evaluate the influence of endothelium-dependent vasodilatation on the brachial artery and the influence of stiffness index on the common carotid artery. Results: With aging, the functional capacity of the endothelium for endothelium-dependent vasodilatation declines, in men as early as in their 20s, and in women more considerably after the age of 50 years. Over the course of aging, a significant stiffness increase was recorded in respondents of both sexes, the correlations being summarized in the following formulas: stiffness index = 0.028 × years of age + 5.0992 in male respondents, and stiffness index = 0.028 × years of age + 5.1991 in female respondents. Conclusion: Decrease in the capacity of peripheral arteries for endothelium-dependent vasodilatation correlates with increase in the stiffness of peripheral arteries.