Reduction In Arterial Stiffness Research Articles

Optimizing Exercise Interval for Arterial Stiffness Improve-Ment in Middle-Aged Adults

By decreasing the interval periods and increasing the frequency of exercise bouts, we were able to confirm our hypothesis that middle-aged adults could achieve a greater reduction in arterial stiffness through intermittent exercise. Thirty middle-aged males were randomly divided into a control group (CON), continuous exercise group (CE), interval exercise long-long group (IELL), interval exercise long-short group (IELS), and interval exercise short-short group (IESS). The subjects performed moderate-intensity exercise on the treadmill. Cardio-ankle vascular index (CAVI) was assessed before exercise, right after the session ended, and at 30 and 60 minutes into the recovery period. Changes in values from the baseline (∆CAVI) during each measurement were used for analysis. The control group showed no significant change in ∆CAVI, while all exercise groups showed a significant decrease at 0, 30, and 60 minutes. The exercise groups had significantly lower ∆CAVI than the control group at 0 and 30 minutes. At 60 minutes, the IESS group had a significantly lower ∆CAVI than the control group. Additionally, at 0 and 30 minutes, the IELS and IESS groups had a significantly lower ∆CAVI than the CE group. Hence, interval exercise is more effective than continuous exercise regardless of the total duration, but the effectiveness depends on the interval duration and number of repetitions.

Inflammation and Arterial Stiffness as Drivers of Cardiovascular Risk in Kidney Disease.

Patients with chronic kidney disease (CKD) have an increased cardiovascular (CV) risk. The lower the glomerular filtration rate, the higher the CV risk. Current data suggest that several uremic toxins lead to vascular inflammation and oxidative stress that, in turn, lead to endothelial dysfunction, changes in smooth muscle cells' phenotype, and increased degradation of elastin and collagen fibres. These processes lead to both functional and structural arterial stiffening and explain part of the increased risk of acute myocardial infarction and stroke reported in patients with CKD. Considering that, at least in patients with end-stage kidney disease, the reduction of arterial stiffness is associated with a parallel decrease of the CV risk, vascular function is a potential target for therapy to reduce the CV risk. in this review, we explore mechanisms of vascular dysfunction in CKD, paying particular attention to inflammation, reporting current data in other models of mild and severe inflammation, and discussing the vascular effect of several drugs currently used in nephrology.

Plasma Lipidomic Profiles Improve upon Traditional Risk Factors for the Prediction of Arterial Stiffness Among Patients with Type 2 Diabetes Mellitum: A Randomized, Placebo-Controlled Trial.

Exercise or vitamin D intervention can reduce the risk of arterial stiffness; however, the underlying mechanisms of lipid metabolism remain unexplored. To examine the effects of a 12-week moderate and vigorous exercise program (65-80% maximal heart rate, 60 min/time, 2~3 times/week) with or without vitamin D supplementation (1000 IU/day) on the reduction in arterial stiffness and further explore whether the effects of interventions could be associated with the basal lipidome among patients with Type 2 diabetes mellitum (T2DM). 61 patients with T2DM were randomly assigned to the following groups: control (CON, n = 15), exercise (EX, n = 14), vitamin D (VD, n = 16), and exercise + vitamin D (EX + VD, n = 16). Arterial stiffness risk factors (ankle-brachial index (ABI); brachial-ankle pulse wave velocity (baPWV), systolic blood pressure (SBP), and diastolic blood pressure (DBP)) were evaluated before and after the intervention. The plasma lipidome was determined using ultra-performance liquid chromatography coupled with tandem mass spectrometry. Machine learning was applied to establish prediction models for the responsiveness to arterial stiffness. Vitamin D supplementation could inhibit the decrease in the ankle-brachial index (mean ± SD: EX + VD and VD, -0.001 ± 0.058; EX + CON, -0.047 ± -0.089; p = 0.03). We observed high inter-individual variability in the arterial stiffness risk factors in response to the interventions. We also found that optimally selecting the lipid predictors at baseline, such as SM d44:6, LPE 18:2, and Hex2Cer 29:0, could enhance the predictive power by 100% for arm SBP changes in the exercise group. Basal levels of Cer (33:1) and GM3 (44:4) could enhance the predictive power by 100% for changes in baPWV in the vitamin D group. A 12-week vitamin D supplementation was beneficial in preventing arterial stiffness. Compared with traditional clinical risk factors, specific lipids at baseline could significantly improve the ability to predict intervention-induced changes in the reduction of arterial stiffness.

Exploring the Cardiorenal Benefits of SGLT2i: A Comprehensive Review

The history of sodium-glucose cotransporter 2 inhibitors (SGLT2i) is so long and started in 1835 when Petersen extracted a compound called phlorizin from apple tree bark. About fifty years later, von Mering discovered its glucosuric properties. In the 1980s, it was discovered that the glucosuria resulted from inhibition by phlorizin of glucose reabsorption by the renal tubules, which lowered blood glucose levels in diabetic rats. Nowadays, beyond their glucose-lowering effects, growing evidence suggests significant cardiorenal benefits associated with SGLT2i therapy. Indeed, several clinical trials, including landmark studies such as EMPA-REG OUTCOME, CANVAS Program, and DECLARE-TIMI 58, have demonstrated robust reductions in cardiovascular events, particularly heart failure hospitalizations and cardiovascular mortality, among patients treated with SGLT2i. However, subsequent trials showed that SGLT2i benefits extend beyond the diabetic population, encompassing individuals with and without diabetes. Additionally, SGLT2i exhibit nephroprotective effects, manifesting as a slowing of the progression of chronic kidney disease and a reduction in the risk of end-stage kidney disease. The mechanisms underlying the cardiorenal benefits of SGLT2i are multifactorial and include improvements in glycemic control, reduction in arterial stiffness, modulation of inflammation and oxidative stress, reduction of intraglomerular pression and promotion of natriuresis and diuresis through inhibition of SGLT2 in the luminal brush border of the first segments of the proximal kidney tubule. This narrative review aims to explore the cardiorenal outcomes of SGLT2i, encompassing their mechanisms of action, clinical evidence, safety profile, and implications for clinical practice.

JNK2-MMP-9 axis facilitates the progression of intracranial aneurysms

Intracranial aneurysm (IA) can cause subarachnoid hemorrhage or some other hemorrhagic stroke after rupture. Because of the poor outcome in spite of the intensive medical care after the onset of hemorrhage, the development of a novel therapeutic strategy like medical therapy to prevent the progression of the disease becomes a social need. As the reduction of arterial stiffness due to the degeneration of the extracellular matrix via Matrix Metalloproteinases (MMPs) becomes one of the central machineries leading to the progression of IAs through a series of studies, factors regulating the expression or the activity of MMPs could be a therapeutic target. In the present study, specimens from human IA lesions and the animal model of IAs were used to examine the expression of c-Jun N-terminal kinase (JNK) which might exacerbate expressions of MMPs in the lesions to weaken arterial walls resulting in the progression of the disease. In some human IA lesions examined, the expression of p-JNK, the activated form of JNK, could be detected mostly in the medial smooth muscle cells. In IA lesions induced in rats, the activation of JNK was induced during the progression of the disease and accompanied with the activation of downstream transcriptional factor c-Jun and importantly with the expression of MMP-2 or -9. The genetic deletion of Jnk2, not Jnk1, in mice significantly prevented the incidence of IAs with the suppression of the expression of MMP-2 or MMP-9. These results combined together have suggested the crucial role of JNK in the progression of IAs through regulating the expression of MMPs. The results from the present study provides the novel insights about the pathogenesis of IA progression and also about the therapeutic target.

Acute effects of static stretching exercise-induced decrease in arterial stiffness on maximal aerobic capacity.

We recently have reported that individual day-to-day arterial stiffness variations are associated with maximal aerobic capacity. However, the evidence of this phenomenon was not provided sufficiently. The present study aimed to examine whether a decrease in arterial stiffness through static stretching exercise could enhance maximal aerobic capacity. Twelve healthy young men (age 22±2 years, mean and standard deviation) participated in this study and underwent two separate sessions in a randomized controlled crossover design: a single session of a whole-body static stretching exercise protocol that involved the trunk, upper limb, and lower limb (stretch condition), and sedentary control where they rested in the exercise room. Brachial-ankle pulse wave velocity (baPWV) was measured as an index of systemic arterial stiffness before, immediately after and at 30 min after both conditions. Maximal oxygen uptake (V̇O<inf>2</inf>max) was assessed using a graded power test on an electronically braked cycle ergometer after these measurements. As we expected, there was a significant decrease in the baPWV at 30 min after the stretch trial compared to baseline values (P=0.01). The baPWV in the stretch condition was lower than that of the control condition, while V̇O<inf>2</inf>max in the stretch condition was higher than that of the control condition (P=0.03). Based on these findings, it can be inferred that an acute reduction in arterial stiffness may contribute to change in maximal aerobic capacity.

Limb Position Influences Peripheral Arterial Stiffness Reduction with Reactive Hyperemia

The mechanism behind the acute reduction in peripheral arterial stiffness with reactive hyperemia is presumed to be flow-mediated; however, this has not been clearly demonstrated. We hypothesized that a larger reactive hyperemia magnitude would result in a greater reduction in peripheral arterial stiffness. Fourteen healthy young adults (5 females, 25 ± 5 yrs, mean ± SD) underwent reactive hyperemia with a rapid-release cuff on the upper arm inflated to 220 mmHg for 5 min: once with the arm positioned ~ 50ο above heart level and once with the arm positioned ~ 50ο below heart level. 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. At 5 min after reactive hyperemia, both the absolute (2.31 ± 1.22 vs 1.19 ± 1.19 m/sec, p = 0.007) and relative (24% vs 15%; p = 0.043) changes in brachial to radial PWV were greater with the arm below the heart compared to above the heart. The peak brachial blood flow was higher when the arm was below the heart compared to above the heart (477 ±\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\\pm$$\\end{document} 145 vs 369 ±\\documentclass[12pt]{minimal} \\usepackage{amsmath} \\usepackage{wasysym} \\usepackage{amsfonts} \\usepackage{amssymb} \\usepackage{amsbsy} \\usepackage{mathrsfs} \\usepackage{upgreek} \\setlength{\\oddsidemargin}{-69pt} \\begin{document}$$\\pm$$\\end{document} 137 ml/min; p < 0.001). Reactive hyperemia acutely reduced peripheral arterial stiffness above and below heart level, with a greater decrease observed when the arm was positioned below the heart. These results demonstrate the contribution of conduit artery blood flow to the reduction of peripheral arterial stiffness after reactive hyperemia.

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&lt;0.01) with peripheral PWV higher with the arm below the heart. There was a significant time x condition interaction (p&lt;.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&gt;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&lt;.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.

Acute effects of low-intensity one-legged electrical muscle stimulation on arterial stiffness in experimental and control limbs

The aim of this study was to examine the acute effects of low-intensity one-legged electrical muscle stimulation (EMS) for skeletal muscle on arterial stiffness in EMS and non-EMS legs. Eighteen healthy subjects received two different protocols (Control (CT) and Experimental (ET) trials) in random order on separate days. EMS was applied to the left lower limb at 4 Hz for 20 min at an intensity corresponding to an elevation in pulse rate of approximately 15 beats/min (10.9 ± 5.1% of heart rate reserve). Before and after the experiment, arterial stiffness parameters in the control right leg (CRL) and control left leg (CLL) in CT and non-EMS leg (NEL) and EMS leg (EL) in ET were assessed by pulse wave velocity (baPWV, faPWV) and cardio-ankle vascular index (CAVI). No significant changes in all parameters were observed in either leg in CT. Conversely, in ET, low-intensity, single-leg EMS significantly reduced CAVI, baPWV, and faPWV in the EL, but not in the NEL. Acute, low-intensity single-leg EMS reduces arterial stiffness only in the EL. These data support our idea that physical movement-related regional factors rather than systematic factors are important for inducing acute reductions in arterial stiffness.

Daily Step Count and its Association with Arterial Stiffness Parameters in Older Adults.

Daily step count is a simple parameter for assessing physical activity. However, the potential advantages of setting daily step goals below the traditional 10,000-step threshold remain unclear. The cross-sectional study aimed to determine the relationship between daily step counts and arterial stiffness outcomes in older individuals. Forty-eight older adults recorded their daily step counts over a 7-day period using a pedometer. The participants were classified into two groups based on their daily step count: Group 1 (n = 28) consisted of individuals taking fewer than 5000 steps per day, while Group 2 (n = 20) included those who recorded 5,000 to 9,999 steps per day. To evaluate arterial stiffness parameters, we measured pulse wave velocity (PWV), cardio-ankle vascular index (CAVI), and ankle-brachial index (ABI). Hemodynamic and biochemical parameters were also determined. Participants who accumulated fewer daily steps exhibited higher PWV compared to each group. An inverse association was observed between average steps per day and PWV. However, no significant differences were found between daily step counts and CAVI or ABI. Conclusions: As individuals increase their daily step count, they may experience a reduction in arterial stiffness. Consequently, the assessment of daily steps has benefits for enhancing vascular health and overall well-being among older individuals.

Translating scientific recommendations into reality: a feasibility study using group-based high-intensity functional exercise training in adolescents with cerebral palsy

Purpose To examine the feasibility and effects of a functional high-intensity exercise intervention performed in a group-setting on functionality, cardiovascular health and physical performance in adolescents with cerebral palsy (CP). Methods Ten adolescents with a diagnosis of CP (2 females; 16.6 ± 3.4 years; GMFCS: I-II) participated in a 12-week training intervention, containing progressive resistance training using free weights and high-intensity workouts twice a week. The six-minute walking test, arterial stiffness and physical performance (strength and power tests) were measured before and after the intervention. Results No adverse events were reported. We measured small increases in the six-minute walking test (Δ = 28.8 m, 95% CI [-1.78;52.7]; g = 0.34 [-0.04;0.72]) and a small reduction in arterial stiffness (Δ = −4.65% [-10.90;1.25]; g = −0.46 [-1.36;0.21]). All measures of physical performance increased (0.24 ≤ g ≤ 0.88). Conclusion Functional training with free weights in high-functioning adolescents with CP is safe and effective in increasing parameters of physical performance and cardiovascular health. Positively influenced indicators of everyday independence (i.e. strength parameters) showed a transfer into movements of daily life. Concerns about adverse events through high-intensity training in adolescents with CP appear unjustified when training is performed progressively, following basic training principles.

Clinical efficacy of a fixed-dose combination of amlodipine/indapamide/perindopril in patients with hypertension and multiple risk factors

Aim. To evaluate the antihypertensive and organ protective efficacy of the triple fixed-dose combination of amlodipine/indapamide/perindopril in patients with hypertension (HTN) who did not achieve target blood pressure (BP) on previous antihypertensive therapy (AHT).Material and methods. The study included 47 patients with HTN and multiple risk factors who did not achieve target blood pressure during previous AHT. They were prescribed triple fixed-dose combination of amlodipine/indapamide/perindopril with preliminary prescription of amlodipine, indapamide and perindopril in the free-dose combination. At baseline and after 3 months of AHT, 24-hour ambulatory blood pressure monitoring (ABPM), echocardiography and arterial stiffness were analyzed.Results. Initially, in patients included in the study, the main ABPM parameters were increased, while non dipper and reduced dipper (66% of patients) patterns prevailed. The results of echocardiography indicated left ventricular (LV) hypertrophy (LVH) by left ventricular mass index (LVMI), left ventricular posterior wall thickness (LVPWT), interventricular septum (IVS) and its diastolic dysfunction by E/A, while an increase in CAVI and biological vascular age reflected an increase in arterial stiffness. After 3 months of AHT, significant (p£0,05) ABPM changes and a predominance of the dipper-type 24-hour BP pattern were recorded in more than half of the patients (53%). A decrease in LVMI, LVPWT and IVS by 7%, 12% and 8%, respectively (p£0,05), while an E/A increase by 12% reflected LVH regression and LV diastolic function improvement. A decrease in arterial stiffness was evidenced by a decrease (p£0,05) in CAVI by an average of 10% and biological vascular age by 4 years.Conclusion. Triple fixed-dose therapy of amlodipine/indapamide/perindopril after 3-month treatment made it possible to achieve target blood pressure in 78% of patients, improved ABPM parameters and ensured pronounced cardioand vasoprotective effects, reflected in LVH regression, improvement of LV diastolic function and reduction of arterial stiffness.

Effects of Zofenopril on Arterial Stiffness in Hypertension Patients.

Angiotensin-converting enzyme inhibitors (ACEIs) reduce arterial stiffness beyond their antihypertensive effect. Studies showed that sulfhydryl ACEIs have the antioxidative potential to improve endothelial function, which might have a clinical effect on arterial distensibility. However, there are no studies that directly compare the effects of sulfhydryl (zofenopril) and non-sulfhydryl ACEIs (enalapril) on arterial stiffness. Therefore, this prospective study aims to compare the effects of enalapril and zofenopril on arterial stiffness and oxidative stress in both short- and long-term treatment of arterial hypertension (AH). Baseline and post-treatment peripheral and central arterial pressure indices, augmentation index (Aix), aortic pulse wave velocity (ao-PWV), serum levels of oxidized low-density cholesterol lipoprotein, LDL and uric acid (UA) were measured. The results showed that acute treatment with zofenopril, in contrast to enalapril, significantly decreased peripheral and central Aix (p < 0.001). Chronic treatment with zofenopril showed a superior effect over enalapril on the reduction of the peripheral systolic arterial pressurewith reduction of ao-PWV (p = 0.004), as well as a reduction in peripheral Aix (p = 0.021) and central Aix (p = 0.021). Therefore, this study indicates that zofenopril has beneficial effects on the reduction of arterial stiffness compared to enalapril. It has potent clinical efficacy in AH treatment and further studies should compare its safety and long-term efficacy to other AH drugs that would aid clinicians in treating AH and other various cardiovascular diseases that have arterial stiffness as a common denominator.

Abstract 115: An Action Plan To Improve Biochemically Detected Non-adherence To Antihypertensive Treatment Results In A Short-term Reduction In Arterial Stiffness And A Long-term Reduction In Albuminuria (the ATHAN Clinical Trial)

We previously shown that a specific 3-months(m) intervention improved therapeutic adherence in patients with non-controlled hypertension (HT) decreases blood pressure (BP). We aim to evaluate if there is also a decrease in HT-mediated organ damage (HMOD) at short- and long-term. We conducted a prospective, randomized clinical trial in a HT Unit. Consecutively attended patients with 24h-BP &gt;or=130/80 mmHg despite receiving at least 2 antihypertensive drugs and with therapeutic non-adherence confirmed by determination of antihypertensives in urine (n=47) were randomized (1:1) to receive a specific 3m program to improve adherence (INT=intervention) or routine follow-up (C=control). Antihypertensive treatment was not changed. Prior to randomization, and at 3m and 12m, the presence of antihypertensives in urine and albuminuria were determined. BP and pulse wave velocity (PWV) were evaluated by 24h- ambulatory monitoring in all periods. After 3m, all patients received usual care. At 3m, the adjusted BP differences (mean; 95% CI) from baseline (INT vs. C) were -14.3 mmHg (-5.1 to -23.5), p=0.003, and -10, 0 mmHg (-4.0 to -16.0), p=0.002, for 24h-SBP and 24h-DBP, respectively. The INT group maintained the decrease in BP at 12m. vs baseline: mean change (95% CI) of 24h-SBP = -16.1 mmHg (-22.8 to -9.4), p &lt;0.001 and 24h-DBP change = -7.8 (-12, 8 to -2.7), p=0.002. In the INT group, the percentage of undetected antihypertensive drugs decreased from baseline (median [interquartile range]): 40% [20-100], 0% [0-25], and 18.3% [0-40] at baseline, 3m and 12m, respectively; Z= -3.426 (p&lt;0.001) and Z= -3.055 (p=0.002) for changes at 3m and 12m, respectively. PWV decreased at 3m only in the INT group: mean difference (95% CI) -0.402 m/sec (-0.054 to -0.749), p=0.025, but not at 12m. Albuminuria (median [IQR]) decreased in the INT group at 12m: 27.1 mg/g [11.1-116.2] and 22.4 mg/g [6.4-91.9] at baseline and 12 m, respectively (Z=-2.207, p=0.027). In conclusion, urine biochemical detection of therapeutic non-adherence and a specific 3m-intervention to improve adherence lead to better BP control, which maintains in the long term. In addition, there is a decrease in arterial stiffness in the short term and a regression of albuminuria in the long term, thus reducing the HMOD.

Reduction of arterial stiffness in depressive individuals responding to multimodal treatment

BackgroundDepressive individuals are at higher risk for cardiovascular diseases (CVD). Thus, cardiovascular parameters such as arterial stiffness, often measured by pulse wave velocity (PWV), should be monitored. Recent research indicated that depressive individuals exhibit higher PWV, but there is little data on the changeability of PWV through multimodal treatment. This study investigated PWV in moderately to severe depressive individuals before and after undergoing treatment in dependence on responding or not responding to treatment. Methods47 participants (31 females, 16 males) underwent a PWV measurement and filled out a questionnaire surveying depressive symptom severity before and after a six-week psychiatric rehabilitation treatment including multimodal interventions. Subjects were divided in responders and non-responders, depending on their treatment success. ResultsA mixed ANCOVA analysis indicated no significant main effect of responder status, but a significant main effect of measurement time and a significant interaction between responder status and measurement time. Responders exhibited a significant decrease in PWV across time, while no significant change in PWV across time was found for non-responders. LimitationsResults are limited by the lack of a control group. The influence of medication duration or medication type was not considered in the analyses. Causality of the relationship between PWV and depression cannot be determined. ConclusionThese findings show that PWV can be positively modified in depressive individuals responding to treatment. This effect cannot solely be attributed to pharmacological interventions but rather the combination of multimodal interventions, thus highlighting the clinical relevance of multimodal treatment in depression and comorbid disorders.

Arterial stiffness and peripheral chemoreflex responsiveness in electronic cigarette users

Electronic cigarettes (e-cigarettes) are marketed as less harmful alternatives to tobacco smoking, but the short- and long-term health consequences are unclear. Raised arterial stiffness and increased peripheral chemoreflex sensitivity are pathogenic features of several clinical conditions and associated with adverse outcomes. The aim of this study was to determine if regular e-cigarettes use is associated with increased arterial stiffness and elevated peripheral chemoreflex responsiveness.Eight healthy e-cigarettes users (E-cig; &gt;12 months, 6 women, 27±5yr, 26.0±4.5kg/m2 mean±SD) and 13 healthy non-e-cigarettes user controls (HC; 8 women, 26±4yr, 22.4±3.4kg/m2,) were studied under 3 conditions (each for 5min) in the following order: room-air, isocapnic hyperoxia (1.0 fraction of inspired oxygen [FiO2]; peripheral chemoreflex deactivation) and isocapnic hypoxia (0.1 FiO2; peripheral chemoreflex activation). In each condition, arterial stiffness was evaluated by the aortic augmentation index (AIx) and aortic pulse wave velocity (PWV) (SphygmoCor), while heart rate (HR), mean arterial pressure (MAP), and minute ventilation (V̇E) were monitored.In room air, AIx was higher in E-cig compared to HC (18.4±3.4 vs. 8.1±2.5%, P=0.023), while PWV (5.7±0.3 vs. 5.8±0.8m/sec, P=0.731), HR (68±6 vs. 70±9beats/min, P=0.616), MAP (83±4 vs. 83±7mmHg/min, P=0.920), and V̇E (12.7±2.2 vs. 13.9±3.1L/min, P=0.515) were not different. During isocapnic hyperoxia, AIx was unchanged in both E-cig (21.9±11.2%, P=0.327) and HC (9.2±7.9%, P=1.000) versus room air, with AIx remaining higher in E-cig (P=0.006). There were no changes from isocapnic hyperoxia to room air in both E-cig and HC in aortic PWV (Δ0.1±0.1 and Δ0.1±0.2m/sec, P=0.894), HR (Δ-3±3 and Δ-2±3beats/min, P=0.482), MAP (Δ0.3±2.2 and Δ-0.9±2.1mmHg/min, P=0.528) and V̇E (Δ1.1±2.0 vs. Δ1.2±4.6L/min, P=0.124). During isocapnic hypoxia, AIx was unchanged in E-cig (14.7±9.5%, P=0.288) versus room air, but was decreased in HC (2.8±9.4%, P=0.006), such that AIx remained higher in E-cig than HC (P=0.009). HR increased similarly during isocapnic hypoxia in both E-cig (77±7beats/min, P&lt;0.001) and HC (82±7beats/min, P&lt;0.001) compared to room air. In E-cig and HC no change was observed in aortic PWV (Δ0.4±0.4 and Δ0.2±1.4m/sec, P=0.254), MAP (Δ-0.2±2.0 and Δ0.3±2.3mmHg/min, P=0.609) and V̇E (Δ 1.4±1.0 vs. Δ1.1±1.4L/min, P=0.638) during isocapnic hypoxia relative to room air.These preliminary findings suggest that arterial stiffness is higher in young e-cigarettes users, and that the normal hypoxia-induced reduction in arterial stiffness in young non-e-cigarette users is absent in e-cigarettes users. Future studies are needed to determine if the altered effects of hypoxia on arterial stiffness in young e-cigarettes users is associated with exaggerated peripheral chemoreflex mediated sympatho-excitation and/or local endothelial/vascular smooth muscle mechanisms, and if it is reversible on cessation of e-cigarette use. Health Research Council of New Zealand (Ref# 19/687. JPF, JFRP), and the Sidney Taylor Trust (JFRP). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Reduction in Arterial Stiffness Is Related to Exercise Intensity

Increased arterial stiffness is associated with cardiovascular risk and mortality. Central and peripheral arterial stiffness measured with pulse wave velocity (PWV) are known to be reduced 5 min after a single bout of dynamic exercise using a large muscle mass. The effect of small muscle mass rhythmic handgrip exercise on peripheral stiffness is unknown. In addition, it is not known whether the magnitude of reduction in peripheral arterial stiffness is related to the intensity of exercise. We hypothesized that a higher exercise intensity would result in a larger reduction in post-exercise peripheral arterial stiffness. Eight healthy young volunteers participated in this study (5 females, 28 ± 4 yrs, mean ± SD). Two Millar tonometers were placed simultaneously on the brachial and radial arteries of the exercising arm for measurement of peripheral arterial stiffness. Beat-by-beat arterial pressure was obtained by a photoplethysmographic sensor on the middle finger of the contralateral hand. Brachial-radial PWV and mean arterial pressure (MAP) were recorded before exercise then at 5-, 15-, and 30-min post-exercise. The exercise consisted of two 5-min bouts of rhythmic handgrip exercise (2sec contraction/2sec relaxation) at either 30% or 50% of their maximal voluntary contraction (MVC) performed in randomized order. Baseline brachial-radial PWV before handgrip exercise at 30% MVC was 10.7 ± 2.8 m/sec. Postexercise at 30% MVC, PWV was 9.6±2.6 m/sec at 5min, 9.8 ± 2.7 m/sec at 15min, and 11.5 ± 2.9 m/sec at 30 min (all p&gt;0.05 compared to baseline). Before handgrip exercise at 50% MVC baseline brachial-radial PWV was 13.1 ± 3.2 m/sec. Post-exercise at 50% MVC, PWV was 9.9 ± 3.7 m/sec at 5min (p&lt;0.05), 9.1 ± 2 m/sec at 15min (p&lt;0.05), and 10.2 ± 3 m/sec at 30 min (p&gt;0.05). MAP was not statistically significantly different across all time points (p &gt; 0.05). These results show that peripheral arterial stiffness measured as brachial-radial PWV was reduced after 5-min and 15 min of rhythmic handgrip exercise at 50% MVC, but not at 30% MVC. Thus, the magnitude of reduction in PWV was related to the intensity of exercise. The observed reduction of brachial-radial PWV was not a function of changes in blood pressure which would have confounded the PWV results. This study is the first to show that small muscle mass handgrip exercise reduces peripheral PWV. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Arterial stiffness and blood pressure in treated hypertension: a longitudinal study.

It has been reported that an increase in arterial stiffness precedes an increase in blood pressure (BP) in the general population. Whether BP lowering results from of reducing arterial wall or vice versa in antihypertensive treatment is unclear. This study aimed to investigate the association between arterial stiffness and BP in patients with treated hypertension. This study included 3277 participants who were treated with antihypertensive agents and with repeated measurements of branchial-ankle pulse wave velocity (baPWV) and BP during 2010-2016 from the Kailuan study. Temporal relation between baPWV and BP was assessed by cross-lagged path analyses. After adjustment for potential confounders, the standard regression coefficient from baseline baPWV to follow-up SBP was 0.14 [95% confidence interval (95% CI), 0.10-0.18], which was significantly greater than that from baseline SBP to follow-up baPWV (0.05; 95% CI, 0.02-0.08) ( P < 0.0001 for difference). Similar results were observed for the cross-lagged analysis with changes of baPWV and mean arterial pressure. Further analysis showed that the yearly rate of change in SBP during the follow-up period significantly varied across increasing quartiles of baseline baPWV ( P < 0.0001), whereas the yearly rate of change in baPWV showed a nonsignificantly varied trend across quartiles of baseline SBP ( P = 0.2443). These findings provided strong evidence that reduction in arterial stiffness through antihypertensive treatment could precede BP lowering.

Exploring mechanisms of blood pressure regulation in response to device-guided and non-device-guided slow breathing: A mini review.

Hypertension is a widespread disease that, if persistent, increases the risks of coronary heart disease mortality and morbidity. Slow breathing is a recommended blood pressure-lowering strategy though the mechanisms mediating its effects are unknown. This review aims to evaluate autonomic and vascular function as potential mediators driving BP adaptive responses with slow breathing. We searched EBSCO host, Web of Science, Cochrane Central Register of Controlled Trials, and PubMed using key words for optimized search results. Nineteen studies were included in this review (11 device-guided; 8 non-device-guided breathing). Though some studies showed increased vagally mediated components of heart rate variability during slow breathing, results from acute and long-term studies were incongruent. Increases in baroreflex sensitivity (BRS) following a single device-guided slow breathing bout were noted in normotensive and hypertensive adults. Long-term (4weeks to 3months) effects of slow breathing on BRS were absent. Device-guided breathing resulted in immediate reductions in muscle sympathetic nerve activity (MSNA) in normo- and hyper-tensive adults though results from long-term studies yielded inconsistent findings. Non-device-guided slow breathing posed acute and chronic effects on vascular function with reductions in arterial stiffness in adults with type I diabetes and increases in microvascular endothelial function in adults with irritable bowel syndrome. Non-device guided breathing also reduced pro-inflammatory cytokines in healthy and hypertensive adults in acute and chronic studies. No adverse effects or non-adherence to treatment were noted in these trials. Device-guided slow breathing is a feasible and effective modality in improving BRS, HRV, and arterial stiffness though its long-term effects are obscure. Though less evidence exists supporting the efficacy of non-device-guided slow breathing, acute and chronic studies demonstrate improvements in vascular function and inflammatory cytokines. More studies are needed to further explore the long-term effects of slow breathing in general and non-device-guided breathing in particular.

PS-P15-5: EFFECT OF SODIUM RESTRICTION ON LARGE ARTERY STIFFNESS AND DISTENSIBILITY OF SMALL ARTERIES IN HYPERTENSIVE PATIENTS: A RANDOMIZED TRIAL

Objective: Arterial stiffness is characterized by a decrease in arterial distensibility, resulting from the interaction between the extracellular matrix and cellular elements. Large and small arteries can be differently influenced by extrinsic factors, such as excessive sodium intake. This study aim to evaluate the impact of sodium restriction on large artery stiffness and distensibility of small arteries in young adults diagnosed with arterial hypertension. Methods: Randomized controlled clinical trial, including 20 hypertensive patients, aged between 30 and 59 years, followed up at the hypertension outpatient clinic of a tertiary hospital. Subjects were randomized into two groups: group 1 - low-sodium diet (2 g sodium/day); group 2 - usual diet. To analyze the stiffness and distensibility of the arteries, it was measured aortic pulse wave velocity by Complior®, elasticity of small arteries and vascular resistance by HDI®, and also through the measurement of metalloproteinase-9. For nutritional assessment it were considered blood glucose levels, 24-h urinary sodium, body mass index (BMI) and other anthropometric measurements. For nutritional intake we analized the 24-hour dietary recall. Results and Discussion: In comparison with group 2, it was observed a significant (p &lt; 0.05) reduction in office blood pressure (p = 0,037) and pulse wave velocity (p = 0,010) in group 1 subjects. Also, in group 1 it occurred reduction in blood glucose levels, BMI, waist and neck circumference. Sodium intake was significantly reduced in group 1, taking into account 24 hs urinary sodium and evaluated by dietary recall. It is worth mentioning that excessive sodium intake linked to arterial hypertension causes a remodeling process, increased oxidative stress, inflammation and fibrosis of the arteries, contributing to arterial stiffness. Regarding the distensibility of small arteries, no significant differences were found between the two groups, but the intervention period and the number of individuals in the study should be taken into account, since these factors may have influenced the results. Conclusion: Sodium restriction for a short period of time promoted reduction of arterial stiffness, in parallel to reduction in obesity parameters and blood pressure in adults diagnosed with systemic arterial hypertension.