Changes In Arterial Stiffness Research Articles

Long term worsening of arterial stiffness from monitoring of QKD interval predicts the occurrence of cardiovascular events.

Arterial stiffness is an independent predictor of cardiovascular events in different populations. Destiffening appears to be possible through the control of the main cardiovascular risk factors, with however important individual variations. There are so far too few data available on the prognostic importance of changes in arterial stiffness. We tested the consequences of changes in arterial stiffness assessed with the QKD method on the incidence of cardiovascular events in a cohort of hypertensive patients. The change of QKD100-60 was calculated as the difference between baseline and last follow-up value. Patients were classified as group 0 with stable or increased QKD100-60 and group 1 with decreased QKD100-60 (increased arterial stiffness). The prognostic of these two groups was analysed with a Cox model including age, baseline QKD100-60, 24 h SBP (baseline and change), delay between first and last recording, sex, diabetes, smoking, and hypercholesterolemia. We included 555 essential hypertensive patients with 24 h ambulatory measurement of BP and QKD at baseline and follow-up. The follow-up period was 12.28 ± 7.38 years with an average time between baseline and last recording of 8.86 ± 6.48 years. 94 cardiovascular events occurred. The group with increased arterial stiffness shows the double risk of occurrence of cardiovascular event than the group with stable or reduced arterial stiffness independently of other factors including changes in 24 h SBP.

Do Photopletysmographic Parameters of Arterial Stiffness Differ Depending on the Presence of Arterial Hypertension and/or Atherosclerosis?

Background: Hypertension and atherosclerotic cardiovascular diseases (ASCVD) increase cardiovascular risk and worsen patients’ prognoses. One early predictor of increased risk is a change in arterial stiffness. This study aimed to evaluate arterial stiffness parameters using the non-invasive photoplethysmography (PPG) method in Polish patients with arterial hypertension (AH) and/or atherosclerosis (AS). Methods: The study group consisted of 333 patients (Caucasians, both sexes, aged 30–85 years old). Patients were analyzed in four groups depending on AH and AS (Group I: patients without AH or AS, Group II: AH patients, Group III: AS patients, and Group IV: AH/AS patients) and, in addition, according to sex and history of SARS-CoV-2 infection. Arterial stiffness parameters, i.e., reflection index (RI), peak-to-peak time (PPT), and stiffness index (SI) were automatically calculated with PPG based on the analysis of the pulse wave contour. Results: Mean values of RI and SI were higher in men than women (p < 0.001 each). Diastolic blood pressure (DBP) also differed between sexes (p = 0.010). Mean SI values differed between the study groups (p = 0.038) with the highest SI found in AS/AH patients and the lowest—in patients without AH or AS. The mean SI values were significantly lower in women compared to men in both Group I and Group II (p = 0.006 and p < 0.001, respectively). The mean values of RI were also greater in men than in women in Group I and Group II (p < 0.001 for each group). Regarding COVID-19 history, only HR values differed between patients with and without COVID-19 in AH patients (p = 0.012). In AH patients, men had higher values of RI and SI compared to women (p < 0.001 and p < 0.001). On the other hand, AS women with COVID-19 had significantly greater mean values of SI (9.66 m/s ± 1.61) than men with COVID-19 (7.98 m/s ± 1.09) (p = 0.045). Conclusions: The present study confirmed that sex had a significant impact on arterial stiffness parameters. Both AH and AS affected arterial stiffness. Heart rate was greater in hypertensive patients after COVID-19 compared to hypertensive patients without COVID-19.

Characterizing phenotypic data of Peromyscus leucopus compared to C57BL/6J Mus musculus and diversity outbred (DO) Mus musculus.

Translational research is commonly performed in the C57B6/J mouse strain, chosen for its genetic homogeneity and phenotypic uniformity. Here, we evaluate the suitability of the white-footed deer mouse (Peromyscus leucopus) as a model organism for aging research, offering a comparative analysis against C57B6/J and diversity outbred (DO) Mus musculus strains. Our study includes comparisons of body composition, skeletal muscle function, and cardiovascular parameters, shedding light on potential applications and limitations of P. leucopus in aging studies. Notably, P. leucopus exhibits distinct body composition characteristics, emphasizing reduced muscle force exertion and a unique metabolism, particularly in fat mass. Cardiovascular assessments showed changes in arterial stiffness, challenging conventional assumptions and highlighting the need for a nuanced interpretation of aging-related phenotypes. Our study also highlights inherent challenges associated with maintaining and phenotyping P. leucopus cohorts. Behavioral considerations, including anxiety-induced responses during handling and phenotyping assessment, pose obstacles in acquiring meaningful data. Moreover, the unique anatomy of P. leucopus necessitates careful adaptation of protocols designed for Mus musculus. While showcasing potential benefits, further extensive analyses across broader age ranges and larger cohorts are necessary to establish the reliability of P. leucopus as a robust and translatable model for aging studies.

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.

The Effect of Surgical Aortic Valve Replacement on Arterial Stiffness: Does the Valve Type Matter?

Background: Despite the increasing use of transcatheter aortic valve procedures, many patients still require surgical aortic valve replacement (SAVR). Assessing arterial properties in patients undergoing SAVR for aortic valve stenosis can be challenging, and the existing evidence is inconclusive. Our study aimed to investigate the impact of SAVR on vascular stiffness and the quality of life, as well as the different effects of valve type on arterial properties. Methods: We included 60 patients (mean age 70.25 ± 8.76 years, 65% men) with severe symptomatic aortic stenosis who underwent SAVR. Arterial stiffness (cfPWV, baPWV) and vascular parameters (AIx@75, central pressures, SEVR) were measured at baseline, pre-discharge, and 1-year post-operation. The QOL was assessed using the generic questionnaire-short-form health survey 36 (SF-36) pre-operatively and at 1 year. Results: Post-SAVR, cfPWV increased immediately (7.67 ± 1.70 m/s vs. 8.27 ± 1.92 m/s, p = 0.009) and persisted at 1 year (8.27 ± 1.92 m/s vs. 9.29 ± 2.59 m/s, p ≤ 0.001). Similarly, baPWV (n = 55) increased acutely (1633 ± 429 cm/s vs. 2014 ± 606 cm/s, p < 0.001) and remained elevated at 1 year (1633 ± 429 cm/s vs. 1867 ± 408 cm/s, p < 0.001). Acute decrease in Alx@75 (31.16 ± 10% vs. 22.48 ± 13%, p < 0.001) reversed at 1 year (31.16 ± 10% vs. 30.98 ± 9%, p = 0.71). SEVR improved (136.1 ± 30.4% vs. 149.2 ± 32.7%, p = 0.01) and persisted at 1 year (136.1 ± 30.4% vs. 147.5 ± 30.4%, p = 0.01). SV had a greater cfPWV increase at 1 year (p = 0.049). The QOL improved irrespective of arterial stiffness changes. Conclusions: After SAVR, arterial stiffness demonstrates a persistent increase at 1-year, with valve type having a slight influence on the outcomes. These findings remain consistent despite the perceived QOL.

Factors associated with change in arterial stiffness in patients with rheumatoid arthritis: the JointHeart study

Background Rheumatoid arthritis (RA) predominantly affects women and is associated with hypertension and arterial stiffness. We explored factors associated with change in arterial stiffness in patients with RA treated with disease-modifying antirheumatic drug (DMARD) therapy. Methods Seventy-seven outpatients with RA (age 55 ± 11, 69% women), with indication for treatment with biological or targeted synthetic DMARDs, were included. Pulse wave velocity (PWV), augmentation pressure (AP), augmentation index (AIx) and Disease Activity Score in 28 joints (DAS28) were measured at baseline and after a mean of 22 months of follow-up. Results At follow-up, 83% used DMARDs and 73% had achieved remission or low disease activity. DAS28 decreased from 3.8 ± 1.3 to 2.8 ± 1.2 (p < 0.001). Mean PWV increased from 7.8 ± 1.6 m/s at baseline to 8.5 ± 1.8 m/s at follow-up (p < 0.001), while AP and AIx were stable. Increase in PWV during follow-up was associated with increase in systolic blood pressure (BP), diabetes, higher DAS28 and body mass index (BMI) at baseline, independent of achieved remission/low disease activity and use of DMARDs at follow-up. In multivariable analyses at follow-up, female sex was associated with higher AP and AIx, but with lower PWV, after adjusting for possible confounders. Conclusion In patients with RA, higher disease activity, BMI and diabetes at baseline, together with increase in office systolic BP were associated with an increase in arterial stiffness during follow-up, despite DMARD therapy. This highlights the need for management of cardiovascular risk factors in addition to reducing the inflammatory load in patients with RA to preserve arterial function.

High altitude sojourn elicits divergent effects in aortic and carotid stiffness in healthy-young adults

High altitude exposure challenges the cardiovascular system to compensate for barometric pressure-mediated reductions in arterial oxygen content. Reductions in oxygen content elicit simultaneous increases in sympathetic nervous system activity and vasodilation that may have competing effects on changes in large artery stiffness. The objective of this study was to examine changes in aortic and carotid stiffness during high altitude sojourn in healthy, young adults. We hypothesized that short-term high-altitude sojourn would increase both aortic and carotid stiffness. 17 Generally healthy adults (23±4 yrs, 25.0±3.0 BMI, n=9 females) underwent vascular assessments in the supine position at 1400 m and after an 8-day incremental ascent to 4300 m. Aortic stiffness and carotid β-stiffness were derived from carotid-femoral pulse wave velocity (cfPWV) via applanation tonometry and right common carotid artery ultrasonography, with blood pressure assessed via oscillometry. Ascent from 1400 m to 4300 m resulted in decreased arterial oxygen saturation (-11±4 %, p&lt;0.001) and carotid β-stiffness (-4.48±2.73 au, p&lt;0.001), and increased cfPWV, (+54.98±78.10 cm/s, p=0.01) and mean arterial pressure (+4±7 mmHg, p=0.02). Changes in cfPWV, arterial oxygen saturation, and blood pressure were moderately to strongly correlated (r=-0.425-0.503, p=0.09-0.04). Our data suggest that short term exposure to high altitude has differential effects on carotid versus aortic stiffness despite increases in mean blood pressure. Increases in aortic stiffness appear related to hypoxia-induced reductions in arterial oxygen saturation and concomitant increases in blood pressure, while reductions in carotid stiffness may stem, in-part, from compensatory carotid artery dilation necessary to increase cerebral blood flow at high altitude. Additional research is necessary to further understand mechanisms underlying differential changes in large artery stiffness during high altitude sojourn. 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.

BREAKFAST SKIPPING IS ASSOCIATED WITH INCREASED RISK OF TYPE 2 DIABETES AMONG ADULTS : A SYSTEMATIC REVIEW

Background: While certain lifestyle habits may be associated with arterial stiffness, there is limited literature investigating the relationship between lifestyle habits and longitudinal changes in arterial stiffness in patients with type 2 diabetes mellitus (T2DM). Aims : This systematic review is to review the association of breakfast skipping and the risk of type 2 diabetes in adults. Methods: This study demonstrated compliance with all requirements by means of a comparison with the standards established by the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) 2020. Thus, the specialists were able to guarantee that the research was as current as feasible. Publications released between 2014 and 2024 were considered for this search strategy. This was accomplished by utilizing a number of distinct online reference sites, including Pubmed, ScienceDirect, and SagePub. It was determined that reviews, previously published works, and partially completed works would not be included. Result: In the PubMed database, the results of our search brought up 569 articles, whereas the results of our search on SAGEPUB brought up 2731 articles, our search on SCIENCE DIRECT brought up 1382 articles. The results of the search conducted for the last year of 2014 yielded a total 335 articles for PubMed, 1173 articles for SAGEPUB and 864 articles for SCIENCE DIRECT. In the end, we compiled a total of 7 papers, 4 of which came from PubMed, 1 of which came from SAGEPUB and 2 of which came from SCIENCE DIRECT. We included seven research that met the criteria. Conclusion: In summary, breakfast skipping is associated in increasing of type 2 diabetes in adults but also need more studies because the studies of this topic is limited and less reported.

Arterial Stiffness Changes in Adult Cancer Patients Receiving Anticancer Chemotherapy: A Real-World Bicentric Experience.

Background Chemotherapy correlates to acute and long-term cardiotoxicity, is reflected clinically by myocardial and vascular endothelial dysfunction, and can cause cardiovascular complications. Thus, early diagnosis of cardiovascular disease in cancer patients undergoing anti-cancer treatment is necessary to enhance long-term survival. Our principal objective in this study was to discern the impact of specific anti-cancer chemotherapeutics and biologics on arterial stiffness alterations before and after the administration. Methods Conducted at Mustafa Bacha University Hospital, Algeria, the study focused on arterial stiffness in anti-cancer chemotherapy patients. Assessments included blood pressure, diabetes, and dyslipidemia, with precise measurements using validated systems, particularly pulse wave velocity (PWV). Various chemotherapy protocols were applied, and statistical analysis with R software (R Foundation for Statistical Computing, Vienna, Austria) maintained a significance level of p=0.05. Key outcomes centered on carotid-femoral PWV and secondary endpoints such as central and peripheral pressures and pulse pressure (PP). Univariate and bivariate analyses were conducted using appropriate statistical tests. Results A comparative prospective observational study was completed on 58 patients (34 women and 24 men; mean age: 52.64 +/- 12.12 years) treated with anti-cancer chemotherapy agents. Our evaluation included a complete clinical exam, electrocardiogram, Doppler echocardiography, and applanation tonometry with arterial stiffness measurement using PWV. Patients presented significantly higher levels of carotid-femoral PWV, regardless of the chosen chemotherapy protocol, with no return to the initial level after one year of stopping treatment (p-value < 0.01). Moreover, this increase was more significant in patients with diabetes and hypertension and patients treated with monoclonal antibodies or intercalants. Conclusion This prospective study shows that chemotherapy patients have elevated arterial stiffness, emphasizing the need to assess PWV and monitor cardiovascular risk factors. PP measurement with PWV could improve risk management.

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.

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