Changes In Arterial Stiffness Research Articles

A study protocol for evaluating aortic stiffness modifications in patients treated with endovascular aortic repair.

Arterial stiffness, particularly aortic stiffness (AoS), is associated with an increased risk of cardiovascular disease. Endovascular repair for abdominal (EVAR) and thoracic (TEVAR) aortic disease may increase AoS. This study protocol aims to assess changes in AoS before and after interventions for aortic disease. Patients scheduled for EVAR or TEVAR during a three-year period will be enrolled. An indirect AoS indicator, carotid-to-femoral pulse wave velocity (cf-PWV) will be measured non-invasively using applanation tonometry and reported with others perioperative data before and after the endovascular treatment. Moreover, cardiological data will be collected through echocardiography. Fifty EVAR and 50 TEVAR will be enrolled. We will primarily analyze changes in cf-PWV. To ensure the reliability of our findings, we will also include supplementary data such as clinical information, morphological data, and functional echocardiographic data. By examining AoS modifications before and after endovascular aortic repair, this study aims to enhance our understanding of how arterial stiffness changes following endoprosthesis deployment. The findings from the applied protocol are expected to be informative for innovative graft designs with minimized mechanical mismatch with the aortic wall and with improved vascular hemodynamic, aligning with the current trend in improving patient outcomes. Moreover, understanding these modifications is important for predicting and improving long-term cardiovascular outcomes in patients undergoing such interventions.

Longitudinal Changes in Arterial Stiffness Associated with Physical Activity Intensity: The Toon Health Study.

Several studies have revealed an association between moderate-to-vigorous physical activity (MVPA) and arterial stiffness, which is a known risk factor for cardiovascular disease. However, a few studies have considered the difference in the longitudinal effect of its intensity in a large general population. Therefore, we examined the effect of MVPA intensity on longitudinal changes in arterial stiffness. We conducted a prospective cohort study involving 1,982 Japanese men and women. Arterial stiffness was measured using the cardio-ankle vascular index (CAVI) at baseline and 5-year follow-up. Physical activity was quantified using the Japan Arteriosclerosis Longitudinal Study Physical Activity Questionnaire and categorized into quartiles as MVPA levels. Linear mixed models were used to examine the differences at baseline and the rate of changes in CAVI associated with MVPA levels for over 5 years. The multivariable-adjusted mean differences in CAVI at baseline were significantly lower in the third (β=-0.019 [95% confidence interval {CI}=-0.033 to -0.005]) and fourth (β=-0.018 [95% CI=-0.035 to -0.001]) quartiles of the MVPA group compared with those in the lowest quartile of MVPA, and the significant effect persisted 5 years later. In summary, this study provides evidence to support the existence of a threshold for beneficial levels of MVPA in the prevention of arterial stiffness. Furthermore, this study suggests that exceeding this threshold may exert similar effects on arterial stiffness. These findings suggest that an optimal level of MVPA exists for preventing arterial stiffness, and exceeding this threshold may not engender additional benefits.

Genetic and biomarker modulation of arterial stiffness change in the SardiNIA population cohort.

Arterial stiffness (AS), quantified by pulse wave velocity (PWV), arises due to impaired arterial elastic tissue and smooth muscle dysfunction. We aimed to examine the longitudinal association of genetic, lipid and inflammation biomarkers with PWV and how these associations may change with aging. We utilized genotype and four time-point biomarker data from the SardiNIA cohort [n = 6,301; mean baseline age 43.3 (SD 17.3); 58% females]. To investigate the association of PWV with genetic variants, lipid, and inflammation biomarkers, we employed linear mixed modeling, using age as the time scale. Biomarkers exhibiting significant longitudinal associations were categorized into tertiles and individuals within the second tertile or those with heterozygous alleles were excluded, leaving a cohort of 2,000 individuals. This cohort was further divided into four risk groups: low genetic and low biomarker (L-L), low genetic and high biomarker (L-H), high genetic and low biomarker (H-L), and high genetic and high biomarker risk (H-H). Subsequent analyses focused on these risk groups to assess their association to PWV with time. Using the complete dataset, we found a significant longitudinal association of total cholesterol (TC), triglycerides (TG), fibrinogen (FGN), and total white blood cell count (TWBC) with PWV, all with p < 3.33 × 10-3. After grouping, individuals with homogeneous risk alleles of SNP rs3742207 and high baseline TG levels (H-H group) exhibited a 1.39-fold higher PWV (m/s) (95% CI, 1.17-1.64, p = 1.21 × 10-4) compared to the L-L group. Similarly, individuals in the H-H group of rs3742207-TWBC combination showed 1.75 times higher PWV (95% CI, 1.48-0.2.07, p = 1.01 × 10-10) compared to the L-L group. Similar patterns were observed for groups based on SNP rs7152623-TWBC risk. Furthermore, these associations became more pronounced with increasing age (p < 3.33 × 10-3). The longitudinal association of TG and TWBC biomarkers with PWV varied by SNPs rs3742207 and rs7152623 genotype. Further studies are warranted to investigate the function of genetics, lipids, and inflammation biomarkers on PWV change.

The Responses of Arterial Stiffness Parameter Beta-Derived Index of the Aorta and Illiac-Femoral Artery to Acute Hypovolemia in Rabbits

Introduction: Acute hemorrhage decreases blood pressure (BP) and sometimes causes hypovolemic shock. At this time, peripheral arteries are supposed to contract and increase peripheral vascular resistance to raise BP. However, there has not been an adequate index of a degree of arterial stiffness. We assessed changes in arterial stiffness during rapid bleeding using new BP-independent vascular indices, aBeta and ifBeta, determined by applying the cardio-ankle vascular index theory to the elastic (aorta) and muscular (common iliac-femoral) arteries, respectively, in rabbits. Methods: Eleven Japanese white male rabbits were fixed at the supine position under pentobarbital anesthesia. Fifteen percent of the total blood volume was depleted at a rate of 2 mL/kg/min for 6 min; 15 min later, the withdrawn blood was re-transfused at the same rate. Pressure waves at the origin of the aorta (oA), distal end of the abdominal aorta (dA), distal end of the left common iliac artery (fA), and flow waves at oA were measured simultaneously. Beta was calculated using the following formula: beta = 2ρ/PP × ln(SBP/DBP) × PWV2, where ρ, SBP, DBP, and PP are blood density, systolic, diastolic, and pulse pressures, respectively. aBeta, ifBeta, and aortic-iliac-femoral beta (aifBeta) were calculated using aPWV, ifPWV, and aifPWV, respectively. Results: BP declined significantly at oA, dA, and fA during the acute bleeding. aBeta and aifBeta increased significantly from 3.7 and 5.0 before the bleeding (control) to 5.0 (about 34%) and 6.3 (about 26%) on average, while ifBeta decreased significantly from 20.5 before the bleeding to 17.1 (about 17%) after the completion of the bleeding. Reverse reactions of those indices were observed by transfusing the removed blood. Conclusion: Total arterial stiffness (aifBeta) increased; however, the elastic and muscular arteries stiffened and softened during the bleeding, respectively. These results would give useful diagnostic information during fall in BP.

Effects of low-pressure Valsalva maneuver on changes in cerebral arterial stiffness and pulse wave velocity.

The Valsalva maneuver (VM), commonly used to assess cardiovascular and autonomic nervous system functions, can induce changes in hemodynamic function that may affect cerebral vascular functionality, such as arterial elasticity. This study aimed to investigate the effects of low-pressure VM on cerebral arterial stiffness and cerebral vascular dynamics. Thirty-one healthy young participants (average age 21.58±1.72 years) were recruited for this study. These participants were instructed to maintain an expiratory pressure of 30-35 mmHg for 15 seconds. We measured the vasoconstriction and vasodilation diameters (VCD and VDD) of the common carotid artery (CCA), as well as systolic and diastolic blood pressures (SBP and DBP), before and after VM (PRE_VM and POST_VM). Additionally, we assessed mean arterial pressure (MAP), pulse pressure (PP), pulse wave velocity (PWV), and arterial stiffness. Our findings revealed significant increases in both the VCD and VDD of the CCA (2.15%, p = 0.039 and 4.55%, p<0.001, respectively), MAP (1.67%, p = 0.049), and DBP (1.10%, p = 0.029) following low-pressure VM. SBP showed an increasing trend, but this was not statistically significant (p = 0.108). Interestingly, we observed significant decreases in arterial stiffness and PWV in POST_VM when comparing with PRE_VM (p<0.001 and p<0.001, respectively). In conclusion, our study demonstrated the effectiveness of low-pressure VM in reducing the PWV and stiffness of the CCA. This suggests that low-pressure VM can be a simple and cost-effective method to reduce cerebrovascular stiffness in a brief interval, without the need for specific environmental conditions.

Short-Term Changes in Arterial Stiffness Measured by 2D Speckle Tracking in Patients Undergoing Transcatheter Aortic Valve Implantation.

Arterial stiffness has received increasing interest as a cardiovascular marker in patients with aortic valve stenosis (AS). So far, studies on the impact of aortic valve replacement (AVR) on arterial stiffness have been equivocal. Two-dimensional speckle tracking (2DST) is a novel, non-invasive method to measure the motion of the vessel wall. In this prospective observational study, we aimed to assess the change in arterial stiffness of the common carotid artery (CCA) measured by 2DST in patients undergoing transcatheter aortic valve implantation (TAVI). A total of 47 patients were included in the study (age 80.04 ± 6.065 years). Peak circumferential strain (CS) was significantly improved after TAVI (4.50 ± 2.292 vs. 5.12 ± 2.958, p = 0.012), as was the peak strain rate (CSR) (0.85 ± 0.567 vs. 1.35 ± 0.710, p = 0.002). Body mass index (BMI), mean arterial pressure (MAP) and hemodynamic parameters were associated with this change. 2DST results did not correlate with aortic pulse wave velocity (aPWV) or augmentation index normalized to heart rate (AIx@75), suggesting a distinct difference between arterial stiffness of the CCA and other stiffness parameters. 2DST seems to be a promising new tool to assess arterial stiffness in TAVI patients.

Changes of vascular stiffness and central blood pressure after endovascular aneurysm repair in patients with hypertension. Results of one-year follow-up

Aim. To assess the changes of arterial stiffness, central blood pressure (CBP), and determine the factors potentially influencing them in patients with descending thoracic and abdominal aortic aneurysm, in combination with hypertension, one year after endovascular aneurysm repair ((T)EVAR).Material and methods. Patients ≥18 years of age without clinically significant cardiac arrhythmias were included. Before surgery and a year later, we determined peripheral blood pressure, heart rate (HR), CBP, augmentation index (AIx), pressure at the point of maximum rise of the direct pulse wave (PT1h), time to return of the reflected pressure wave (Tr) and carotid femoral pulse wave velocity (cfPWV).Results. Fifty patients were included (mean age, 68±9 years; 41 men; 16 with descending thoracic aortic aneurysm, 34 with abdominal aortic aneurysm), 23 patients were reexamined. After (T)EVAR, an increase in cfPWV (+2,6 m/s, p&lt;0,001), PT1h (+5 mm Hg, p=0,026), peripheral pulse pressure (+7 mm Hg, p=0,039), heart rate (+5 beats/min, p=0,025). The CBP and AIx values have not changed. The dependence of Tr decrease on the stent-graft length (β=0,42) and the decrease in heart rate (β=-0,52) was found. During the year, 6 cardiovascular events were registered.Conclusion. Graft implantation is accompanied by an increase in cfPWV, regardless of aneurysm location. An increase in PT1h one year after (T)EVAR may reflect a decrease in aortic distensibility and worsening damping function. No changes of CBP and AIx is probably explained by reflected wave characteristics after surgery. Predictors of Tr are — increase in heart rate and implantation of longer stent grafts.

Features of the arterial hypertension course and arterial stiffness in patients with ankylosing spondylitis who get infected COVID-19

Objective: to evaluate the features of development and course of arterial hypertension (AH) and changes in vascular stiffness in patients with ankylosing spondylitis (AS) who underwent COVID-19. Materials and methods: 60 patients with a reliable diagnosis of AS were included in the study. Patients were divided into 2 groups depending on the presence of COVID - 19 in anamnesis. The main group consisted of 30 patients with AS who had suffered COVID-19 of varying severity during the previous 12 months. The comparison group consisted of 30 patients with AS who had no laboratory and clinically confirmed COVID-19 infection within the last year. Patients were interviewed regarding the severity of their previous coronavirus infection and persisting symptoms in the post-COVID-19 period. AS activity was evaluated by ASDAS (CRB, BASDAI-index). BP measurement and study of arterial stiffness parameters by oscillographic method, evaluation of the results of ambulatory BP measurement were performed. Results: 6 (20%) patients had BP destabilization at the outpatient stage during home BP measurement early after COVID-19. After 12 months, BP elevation persisted in only 2 (7%) patients, the rest had BP stabilization with withdrawal of antihypertensive drugs. No correlation between BP level, arterial stiffness and AS activity was found. There was a weak inverse correlation between the severity of coronavirus infection and the level of systolic blood pressure, between age and pulse wave velocity. No significant differences in systolic, diastolic blood pressure, pulse wave velocity, aortic augmentation index were found in patients with AS with and without coronavirus infection. In the main group, 1 fatal outcome due to the development of acute ST-elevation myocardial infarction 6 months after COVID-19 was recorded, and no adverse cardiovascular events were registered among patients in the comparison group. Conclusion: it was hypothesized that patients with AS who underwent COVID-19 would be more likely to show BP elevation than those who did not undergo COVID-19. It was found that early after COVID-19 (first three months) a reversible increase in BP without significant changes in arterial stiffness is possible. However, no significant differences in the frequency of BP elevation, BP level, and arterial stiffness were found in patients with AS and COVID-19 or without COVID-19 in anamnesis.

Changes in Arterial Stiffness in Response to Blood Flow Restriction Resistance Training: A Narrative Review.

Arterial stiffness naturally increases with age and is a known predictor of cardiovascular morbimortality. Blood flow restriction (BFR) training involves decreasing muscle blood flow by applying a strap or a pneumatic cuff during exercise. BFR induces muscle hypertrophy even at low intensities, making it an appealing option for older, untrained individuals. However, BFR use in patients with cardiovascular comorbidities is limited by the increased pressor and chronotropic response observed in hypertensive elderly patients. Furthermore, the impact of BFR on vascular function remains unclear. We conducted a comprehensive literature review according to PRISMA guidelines, summarizing available data on the acute and long-term consequences of BFR training on vascular function. Although evidence is still scarce, it seems that BFR has a mild or neutral long-term impact on arterial stiffness. However, current research shows that BFR can cause an abrupt, albeit transient, increase in PWV and central blood pressure. BFR and, preferably, lower-body BFR, should be prescribed with caution in older populations, especially in hypertensive patients who have an exacerbated muscle metaboreflex pressor response. Longer follow-up studies are required to assess the chronic effect of BFR training on arterial stiffness, especially in elderly patients who are usually unable to tolerate high-intensity resistance exercises.

Type 2 diabetes exacerbates changes in blood pressure-independent arterial stiffness: cross-sectional and longitudinal evidence from the SUMMIT study.

Greater central artery stiffness is observed in people with type 2 diabetes (T2DM). Elevated blood pressure (BP) and altered arterial wall structure/composition in T2DM are generally considered as main drivers for this alteration. However, because conventional arterial stiffness measures are BP-dependent and as such an influence of BP remains in a measure, it is unclear if greater central artery stiffness is a function of greater BP, or due to changes in the structure and composition of the arterial wall. We aimed to measure BP-independent arterial stiffness (β0) cross-sectionally and longitudinally in T2DM. We studied 753 adults with T2DM (DM+) and 436 adults without (DM-) at baseline (Phase 1), and 310 DM+ and 210 DM- adults at 3-yr follow-up (Phase 2). We measured carotid-femoral pulse wave velocity and used it to calculate β0. In Phase 1, β0 was significantly greater in DM+ than DM- after adjusting for age and sex [27.5 (26.6-28.3) vs. 23.6 (22.4-24.8) au, P < 0.001]. Partial correlation analyses after controlling for age and sex showed that β0 was significantly associated with hemoglobin A1c (r = 0.15 P < 0.001) and heart rate [(HR): r = 0.23 P < 0.001)] in DM+. In Phase 2, percentage-change in β0 was significantly greater in DM+ than DM- [19.5 (14.9-24.0) vs. 5.0 (-0.6 to 10.6) %, P < 0.001] after adjusting for age, sex, and baseline β0. β0 was greater in DM+ than DM- and increased much more in DM+ than in DM- over 3 yr. This suggests that T2DM exacerbates BP-independent arterial stiffness and may have a complemental utility to existing arterial stiffness indices.NEW & NOTEWORTHY We demonstrate in this study a greater BP-independent arterial stiffness β0 in people with type 2 diabetes (T2DM) compared to those without, and also a greater change in β0 over 3 yr in people with T2DM than those without. These findings suggest that the intrinsic properties of the arterial wall may change in a different and more detrimental way in people with T2DM and likely represents accumulation of cardiovascular risk.

Intensive blood pressure control on arterial stiffness among older patients with hypertension.

Arterial stiffening increases with age and blood pressure and is associated with cardiovascular disease (CVD), but the relationship between blood pressure lowering and arterial stiffening is still uncertain, especially in older people. This study aimed to evaluate the effect of intensive blood pressure treatment on the progression of arterial stiffness and risk of CVD in older patients with hypertension. The Strategy of Blood Pressure Intervention in the Elderly Hypertensive Patients (STEP) trial was a multicenter, randomized, controlled trial performed at 42 clinical centers throughout China, and 8511 patients aged 60-80 years with essential hypertension were enrolled and randomly assigned to systolic blood pressure (SBP) target of 110 mmHg to <130 mmHg (intensive treatment) or 130 mmHg to <150 mmHg (standard treatment). Patients underwent repeated examinations of the brachial-ankle pulse wave velocity (baPWV) and ankle-brachial index (ABI) at baseline, and the arterial stiffness was evaluated at the 3-year follow-up. A total of 5339 patients who had twice repeated measurements were included in this study. Changes in arterial stiffness between the intensive and standard treatment groups were analyzed using a multivariate linear regression model. The Cox proportional hazard regression model was used to evaluate the effect of intensive treatment on primary CVD outcomes. The changes in baPWV were 61.5 cm/s (95% confidence interval [CI]: 49.8-73.2 cm/s) in the intensive treatment group and 98.4 cm/s (95% CI: 86.7-110.1 cm/s) in the standard treatment group ( P <0.001). Intensive treatment significantly delayed the progression of arterial stiffness, with an annual change of 23.1 cm·s -1 ·year -1vs. 36.7 cm·s -1 ·year -1 of baPWV in the intensive and standard treatment groups, respectively. During a median follow-up period of 3.36 years, primary CVD outcomes occurred in 77 (2.9%) patients in the intensive treatment group compared with 93 (3.5%) in the standard treatment group. Intensive treatment resulted in a significantly lower CVD risk in patients aged 70-80 years or with SBP <140 mmHg. Intensive blood pressure control with an SBP target of 110 mmHg to <130 mmHg could delay the progression of arterial stiffness and reduce the risk of CVD in older patients with hypertension. http://www.clinicaltrials.gov ; No. NCT03015311.

Non-hyperaemic coronary flow velocity acceleration indices correlate with hyperaemic microvascular resistance in patients with INOCA

Abstract Background Coronary microvascular dysfunction (CMD) is associated with an overall worse prognosis. While the diagnosis and endo-typing of CMD currently rely on hyperaemic physiological indices, the search for accurate non-hyperaemic techniques continues. Flow velocity acceleration pattern is mechanistically associated with changes in shear stress, endothelial function, arterial stiffness and pressure in pulsatile flow systems (1-3). Purpose We aim to interrogate whether resting flow velocity acceleration indices correlate with hyperaemic microvascular resistance (HMR) in patients with Ischemia and no obstructive coronary artery disease (INOCA). Methods In 21 Patients with INOCA (all of whom had presented with typical angina pectoris, had no significant epicardial stenoses but positive myocardial perfusion scan test for ischemia) invasive physiological assessment was performed by means of intracoronary Doppler. Hyperaemia was induced with intracoronary adenosine administration. Coronary flow reserve (CFR) and HMR were calculated per their definitions. Flow velocity acceleration indices were derived from the first derivative of the averaged resting flow velocity waveforms with respect to time. We have defined 6 wave peaks of interest in all patients (peak diastolic acceleration (initial prominent peak with ventricular relaxation, referred as A), early diastolic deceleration (B), early re-acceleration wave (C), peak presystolic deceleration (seen just before initial systolic acceleration peak, J), initial systolic acceleration peak (X) and pre-diastolic deceleration nadir (Z)) and calculated the ratios between them as well as adjusted them with respect to resting mean flow velocity (Figure 1). Results The mean age was 59 ± 8 years and the majority of the study group was female (%81). Cardiovascular risk factors were common amongst the study group.All patients had CFR &amp;lt; 2.5. Mean CFR and HMR were 2.05 ± 0.32 and 2.20 ± 0.60 mmHg.cm.sec-1 respectively. Raw C peak magnitude was significantly correlated with APVh (rho:-0.457 p:0.037) and HMR (rho:0.612 p:0.004). Adjusting the C magnitudes with APVb at patient level yielded better correlations (APVh rho:-0.496 p:0.022 ; HMR:0.642 p:0.002). The ratio between diastolic reacceleration peak (C) and presystolic peak deceleration (J), C/J , adjusted with the APVb ((C/J)/APVb) showed the most pronounced correlation with HMR (rho: 0.758 p &amp;lt; 0.001) (unadjusted C/J – HMR rho: 0.718 p&amp;lt;0.001)(Figure 2). Conclusion(s) Acceleration characteristics of resting coronary flow velocity correlate with hyperaemic microvascular resistance indicating structurally impaired coronary microcirculation, hence their utilisation may aid developing non-hyperaemic physiological markers for coronary microvascular dysfunction in patients with INOCA.Derived Acceleration WaveformsCorrelations between HMR and C/J Ratio

Cumulative accelerometer-based sedentary time from childhood through young adulthood with increased arterial stiffness and carotid intima-media thickness in youth: a 13-year longitudinal study

Abstract Background Arterial stiffness and carotid intima-media thickness (cIMT) progression have been associated with cardiovascular morbidity and mortality in adulthood. Arterial stiffness is a strong risk factor for elevated blood pressure and hypertension, and insulin resistance in adolescents and young adults. It remains unclear whether cumulative sedentary time independently worsens arterial health in the paediatric population. Purpose To investigate the longitudinal association of cumulative sedentary time from childhood through young adulthood with arterial stiffness and cIMT changes during post-pubertal growth. Methods From the Avon Longitudinal Study of Parents and Children (ALSPAC), UK birth cohort, 1399 children aged 11 years who had at least two follow-up time-points accelerometer-measured sedentary time over 13 years follow-up, and complete cardiac structural measures at age 17 years clinic visit were included. Sedentary time was assessed with ActiGraph accelerometer worn for 4-7 days at the 11-, 15-, and 24-year clinic visits and sex-categorized in tertiles as low (reference), moderate, and high. Carotid femoral pulse wave velocity (cfPWV), a measure of arterial stiffness, and cIMT were assessed with Vicorder and ultrasound, respectively at ages 17 and 24 years. Multivariable adjusted associations were examined using generalized linear mixed-effect models and adjusted for sex, and time-varying covariates measured at both baseline and follow-up such as age, insulin, high-sensitivity C-reactive protein, heart rate, systolic blood pressure, glucose, fat mass, lean mass, smoking status, family history of hypertension/diabetes/high cholesterol/vascular disease, socioeconomic status, triglyceride, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, light physical activity, and moderate to vigorous physical activity, Results Among 1339 participants (mean [SD] age, 11.75 [0.24] years; [54.6% females]) males spent on average 358, 461, and 536 minutes/day sedentary at ages 11, 15, and 24 years, respectively. Females spent 369, 484, and 525 minutes/day sedentary at ages 11, 15, and 24 years respectively. cfPWV was significantly higher among males than females at ages 17 and 24 years. cIMT was higher in males than females at 17 years but not at age 24 years. In a fully adjusted model, the highest tertile of sedentary time from ages 11 – 24 years was cumulatively associated with progressively increased changes in cfPWV (effect estimate 0.009m/s [CI 0.006 – 0.012] p&amp;lt;0.001) from ages 17 – 24 years in the total cohort and females (0.047m/s [CI 0.005 – 0.090] p=0.030), but not in males. There was no statistically significant association between cumulative sedentary time and changes in cIMT in the total cohort, males, and females. Conclusion Cumulative increase in sedentary time during growth from childhood through young adulthood was independently associated with progressively worsening arterial stiffness in youth.

Changes in Arterial Stiffness Monitored Using the Cardio-Ankle Vascular Index in Patients with Rheumatic Disease Receiving Initial Glucocorticoid Therapy: A Clinical Pilot Study.

Systemic inflammatory rheumatic diseases predispose to premature birth, accelerated atherosclerosis, and increased cardiovascular disease (CVD). While glucocorticoids (GCs) are used in various rheumatic diseases, and the associations between GC excess and increased prevalence of CVD complications are well established, the mechanisms underlying GCs' role in atheroma development are unclear. We conducted an observational study to address GC therapy's effect on arterial stiffness using the cardio-ankle vascular index (CAVI) in patients with rheumatic diseases. Twenty-eight patients with rheumatic disease received initial GC therapy with prednisolone at doses ranging from 20 to 60 mg/d. CAVI was examined at baseline and 3 and 6 months after GC therapy. Changes in CAVI and inflammatory parameters were evaluated. GC therapy increased the mean CAVI after 3 months but decreased it to pretreatment levels after 6 months. The mean CAVI substantially decreased with GC treatment in patients <65 years but increased in patients ≥65 years. Alterations in CAVI during the 6-month GC treatment negatively correlated with the lymphocyte-to-monocyte ratio (LMR) at baseline. Conversely, no correlation was observed between alterations in CAVI values and conventional inflammatory markers (C-reactive protein and erythrocyte sedimentation rate). Multivariate analysis of factors related to changes in CAVI highlighted young age, high prednisolone dosage, and LMR at baseline. GC temporarily exacerbates but eventually improves arterial stiffness in rheumatic diseases. Particularly in young patients, GC may improve arterial stiffness by reducing inflammation. Therefore, the LMR before GC therapy in rheumatic diseases may be a potential predictor of arterial stiffness.

Impact of sleep-disordered breathing on overnight changes in arterial stiffness in patients with acute heart failure.

Overnight increases in arterial stiffness associated with sleep-disordered breathing may adversely affect patients with acute heart failure. Thus, we investigated overnight changes in arterial stiffness and their association with sleep-disordered breathing in patients hospitalized for acute heart failure. Consecutive patients with acute heart failure were enrolled. All participants underwent overnight full polysomnography following the initial improvement of acute signs and symptoms of acute heart failure. The arterial stiffness parameter, cardio-ankle vascular index (CAVI), was assessed before and after polysomnography. Overall, 60 patients (86.7% men) were analyzed. CAVI significantly increased overnight (from 8.4 ± 1.6 at night to 9.1 ± 1.7 in the morning, P < 0.001) in addition to systolic and diastolic blood pressure (from 114.1 mmHg to 121.6 mmHg, P < 0.001; and from 70.1 mmHg to 78.2 mmHg, P < 0.001, respectively). Overnight increase in CAVI (ΔCAVI ≥ 0) was observed in 42 patients (70%). The ΔCAVI ≥ 0 group was likely to have moderate-to-severe sleep-disordered breathing (i.e., apnea-hypopnea index ≥15, 55.6% vs 80.9%, P = 0.047) and greater obstructive respiratory events (29.4% vs 58.5%, P = 0.041). In multivariable analysis, moderate-to-severe sleep-disordered breathing and greater obstructive respiratory events were independently correlated with an overnight increase in CAVI (P = 0.033 and P = 0.042, respectively). In patients hospitalized for acute heart failure, arterial stiffness, as assessed by CAVI, significantly increased overnight. Moderate-to-severe sleep-disordered breathing and obstructive respiratory events may play an important role in the overnight increase in cardio-ankle vascular index.

Nocturnal Blood Pressure Estimation from Sleep Plethysmography Using Machine Learning.

Elevated nocturnal blood pressure (BP) is a risk factor for cardiovascular disease (CVD) and mortality. Cuffless BP assessment aided by machine learning could be a desirable alternative to traditional cuff-based methods for monitoring BP during sleep. We describe a machine-learning-based algorithm for predicting nocturnal BP using single-channel fingertip plethysmography (PPG) in healthy adults. Sixty-eight healthy adults with no apparent sleep or CVD (53% male), with a median (IQR) age of 29 (23-46 years), underwent overnight polysomnography (PSG) with fingertip PPG and ambulatory blood pressure monitoring (ABPM). Features based on pulse morphology were extracted from the PPG waveforms. Random forest models were used to predict night-time systolic blood pressure (SBP) and diastolic blood pressure (DBP). Our model achieved the highest out-of-sample performance with a window length of 7 s across window lengths explored (60 s, 30 s, 15 s, 7 s, and 3 s). The mean absolute error (MAE ± STD) was 5.72 ± 4.51 mmHg for SBP and 4.52 ± 3.60 mmHg for DBP. Similarly, the root mean square error (RMSE ± STD) was 6.47 ± 1.88 mmHg for SBP and 4.62 ± 1.17 mmHg for DBP. The mean correlation coefficient between measured and predicted values was 0.87 for SBP and 0.86 for DBP. Based on Shapley additive explanation (SHAP) values, the most important PPG waveform feature was the stiffness index, a marker that reflects the change in arterial stiffness. Our results highlight the potential of machine learning-based nocturnal BP prediction using single-channel fingertip PPG in healthy adults. The accuracy of the predictions demonstrated that our cuffless method was able to capture the dynamic and complex relationship between PPG waveform characteristics and BP during sleep, which may provide a scalable, convenient, economical, and non-invasive means to continuously monitor blood pressure.

Age-associated increases in middle cerebral artery pulsatility differ between men and women.

Mechanisms underlying sex differences in brain aging remain unclear but may relate to changes in cerebral pulsatile blood flow. Sex differences in the stiffening of the large arteries and expansion of pulse pressure with age may accelerate changes in pulsatile (i.e., discontinuous) blood flow in the brain that contribute to brain health. The purpose of this cross-sectional, secondary analysis was to examine sex differences in age-associated changes in large artery (aorta and carotid) stiffness, carotid pulse pressure, and cerebral pulsatility in 206 men and 217 women between 18 and 72 yr of age. Outcomes included aortic stiffness [carotid-femoral pulse wave velocity (cfPWV)] and carotid pulse pressure via tonometry, carotid β-stiffness via ultrasound, and middle cerebral artery (MCA) pulsatility index via transcranial Doppler. Regression analyses revealed a significant age-by-sex interaction, with women exhibiting a slower rate of change compared with men for cfPWV (β = -0.21, P = 0.04), and greater rate of change for carotid stiffness (β = 0.27, P = 0.02), carotid pulse pressure (β = 0.98, P < 0.001), and MCA pulsatility index (β = 0.49, P = 0.002) after adjustment for covariates. The significant age-by-sex interaction for MCA pulsatility was abolished after further adjustment for carotid pulse pressure. Women exhibit accelerated increases in cerebral pulsatility during midlife, likely driven by exaggerated increases in carotid stiffness and pulse pressure compared with men. These data suggest that there are disproportionate increases in cerebral pulsatility in women during midlife that could contribute to accelerated brain aging compared with men.NEW & NOTEWORTHY We identify sex-specific associations between increasing age and cerebral pulsatility and its vascular mechanisms. When compared with men, women in our cross-sectional analysis exhibited greater age-associated increases in carotid stiffness, carotid pulse pressure, and cerebral pulsatility particularly during midlife. These data suggest that the rapid expansion of pulse pressure during midlife contributes to an exaggerated increase in cerebral pulsatility among women and suggest a potential mechanism contributing to sex differences in brain aging.

Vascular and autonomic function as early predictive biomarkers of the progression to gestational hypertension

BackgroundThe changes in endothelial function, arterial stiffness, and heart rate variability (HRV) produced in the first trimester of pregnancy in women who develop gestational hypertension (GH) are still being investigated. Objective: to evaluate the HVR, endothelial function, and arterial stiffness changes during the first trimester of pregnancy and their relationship with the development of GH MethodsA group of women normotensive during the first trimester (n = 43), who later did (GH; n = 11) or did not (no-GH; n = 32) develop GH in that pregnancy, were enrolled. In the first trimester, endothelial function and arterial stiffness were evaluated through photoplethysmography. HRV, parasympathetic (PNS), and sympathetic (SNS) indexes were measured in a 5-minute continuous electrocardiogram record at rest sitting. The Griess reaction measured urinary nitrite excretion (NOx). ResultsSystolic blood pressure (SBP) values were higher in GH (no-GH: 105.8 ± 2.0 vs. GH: 112.7 ± 3.0 mmHg; p < 0.05). Endothelial function was decreased, and arterial stiffness was increased in GH. Only in GH the arterial stiffness was correlated with SBP (Pearson’s r: 0.5594; 95%CI: 0.06106–0.8681; p < 0.05). In HRV, GH decreased low-frequency power and the ratio SD2/SD1. The inhibition of PNS was lower in GH. The NOx was reduced in GH (no-GH: 3.4 ± 0.4 vs. GH: 0.3 ± 0.1 μM/L; p < 0.001). NOx was correlated negatively with the SNS index only in GH. ConclusionsDeveloped GH is preceded early in pregnancy by endothelial dysfunction and increased arterial stiffness. In this context, there are SNS-PNS interrelation modifications with less inhibition of PNS.

Post-Doc Competition (Knowledge Generation) ID 1985177

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

Abstract P303: Contribution Of Adrenal Leptin Receptor To The Control Of Aldosterone Synthase Expression And Endothelial Function In Female Mice

While premenopausal women are severally affected by the current obesity epidemic, the mechanisms whereby obesity promotes vascular dysfunction in this population remain ill-defined. We previously demonstrated that the adipokine leptin acts on the adrenal gland to promote aldosterone production and that leptin-mediated aldosterone production impairs endothelial function in female mice only. Herein, we investigated whether these mechanisms are dependent on the presence of leptin receptors (lepR) in adrenal glands. We generated lean female mice exhibiting a selective deficiency in LepR in adrenals (AdKO), and obese mice expressing LepR in adrenal glands (db/ad + ) only. Under baseline conditions, AdKO exhibited no alteration in adrenal CYP11B2, renal renin level, aortic endothelial function (measured by acetylcholine-mediated relaxation), arterial stiffness (pulse wave velocity test, PWV), or metabolic parameters including heart and visceral adipose tissue (VAT) weights, fluid amount, glycemia, and HbA1c. Chronic leptin infusion for a week induced trends towards increases in adrenal CYP11B2 (ΔΔCt 1.10±0.12 vs 2.01±0.51, P=0.077), aldosterone (557±95 vs 918±526 pg/ml, P=0.859), and renin levels in WT. AdKO conferred no protection against any of these changes. Leptin infusion impaired endothelial function in WT (Emax 73.3±3.9 vs 52.8±3.1%, P=0.019), which was exacerbated in AdKO (52.8±3.1 vs 34.3±4.1%, P=0.052). However, leptin infusion did not change PWV in WT (3.93±0.22 vs 4.17±0.32 m/s, P=0.999), but induced a trend towards a decrease in AdKO (4.17±0.32 vs 3.11±0.44 m/s, P=0.228). Restoration of adrenal LepR in db/db mice did not alter CYP11B2 nor aldosterone levels but increased renin (ΔΔCt 1.04±0.11 vs 1.48±0.12, P=0.029), heart weight, VAT weight (5.14±0.29 vs 6.52±0.62 g/g, P=0.052), and HbA1c (5.7±0.2 vs 6.9±0.4 %, P=0.035). Although PWV was worsened in db/ad + (5.40±0.27 vs 6.39±0.49 m/s, P=0.035), db/ad + presented improved relaxation compared to db/db (58.5±5.6 vs 73.0±2.2%, P=0.067), inconsistent with our hypothesis. Collectively these data indicate that adrenal LepR might not directly control adrenal CYP11B2 levels expression but latently contributes to changes in endothelial function and arterial stiffness.