Functional capacity, physical activity, and arterial stiffness in patients with systemic sclerosis.

OBJECTIVES: Systemic sclerosis (SSc) is a complex immune-mediated connective tissue disease, involving skin manifestations, vascular features, and organ-based complications that may affect functional capacity and physical activity. Functional capacity and physical activity are associated with arterial stiffness; however, this relationship has not been evaluated in patients with SSc. Therefore, the objective of this study was to investigate the association of functional capacity and physical activity with arterial stiffness in patients with SSc. METHODS: Sixty-five patients with SSc were enrolled in this cross-sectional study. Arterial stiffness was evaluated with carotid-femoral pulse wave velocity (cf-PWV). Functional capacity and physical activity were assessed with a six-min walk test (6MWT) and International Physical Activity Questionnaire-Short Form (IPAQ-SF), respectively. RESULTS: All participants were women, and the mean age was 54.91 ± 11.18 years. 6MWT distance and IPAQ-SF were inversely associated with cf-PWV in crude analysis (p < 0.05). The relationship between 6MWT distance and cf-PWV was maintained in the fully adjusted model (ß = - 0.007, 95% CI, - 0.013 to 0.000). Similarly, the association between IPAQ-SF and cf-PWV remained significant in the fully adjusted model (ß = - 0.001, 95% CI, - 0.002 to - 0.001). CONCLUSION: The present study indicates that functional capacity and self-reported physical activity are independently associated with arterial stiffness in patients with SSc. Exercise interventions targeted to increase functional capacity and physical activity may help to regulate arterial stiffness in patients with SSc. Key Points • Arterial stiffness is an independent predictor of cardiovascular risk. • SSc patients exhibit decreased exercise capacity and functional capacity. • The association of functional capacity and physical activity with arterial stiffness in patients with SSc is unknown. • Functional capacity and self-reported physical activity are independently associated with arterial stiffness in patients with SSc.

Dose-response associations of triglyceride to high-density lipoprotein cholesterol ratio and triglyceride-glucose index with arterial stiffness risk.

BACKGROUND: The triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio and triglyceride-glucose (TyG) index are novel indexes for insulin resistance (IR). We aimed to evaluate associations of TG/HDL-C and TyG with arterial stiffness risk. METHODS: We enrolled 1979 participants from the Rural Chinese Cohort Study, examining arterial stiffness by brachial-ankle pulse wave velocity (baPWV). Logistic and linear regression models were employed to calculate effect estimates. For meta-analysis, we searched relevant articles from PubMed, Embase and Web of Science up to August 26, 2023. The fixed-effects or random-effects models were used to calculate the pooled estimates. We evaluated dose-response associations using restricted cubic splines. RESULTS: For cross-sectional studies, the adjusted ORs (95%CIs) for arterial stiffness were 1.12 (1.01-1.23) and 1.78 (1.38-2.30) for per 1 unit increment in TG/HDL-C and TyG. In the meta-analysis, the pooled ORs (95% CIs) were 1.26 (1.14-1.39) and 1.57 (1.36-1.82) for per 1 unit increment of TG/HDL-C and TyG. Additionally, both TG/HDL-C and TyG were positively related to PWV, with ß of 0.09 (95% CI 0.04-0.14) and 0.57 (95% CI 0.35-0.78) m/s. We also found linear associations of TG/HDL-C and TyG with arterial stiffness risk. CONCLUSIONS: High TG/HDL-C and TyG were related to increased arterial stiffness risk, indicating TG/HDL-C and TyG may be convincing predictors of arterial stiffness.

Early Cardiac Rehabilitation Improves Carotid Arterial Stiffness in Patients with Myocardial Infarction.

Background: Little is known about the effect of cardiac rehabilitation (CR) on carotid arterial stiffness (CAS) in patients with myocardial infarction (MI). Patients and Methods: Rehabilitation group (B) included 90 patients with MI subjected to CR, control group (K) consisted of 30 patients with MI not participating in CR, and healthy group comprised 38 persons without cardiovascular risk factors. CAS was determined using echo-tracking before and after CR. Results: At baseline, patients with MI (B+K) presented with significantly higher mean values of CAS parameters: beta-stiffness index (7.1 vs 6.4, p = 0.004), Peterson's elastic modulus (96 kPa vs 77 kPa, p < 0.001) and PWV-beta (6.1 m/s vs 5.2 m/s, p < 0.001) than healthy persons. Age (beta: r = 0.242, p = 0.008; EP: r = 0.250, p = 0.006; PWV-beta: r = 0.224, p = 0.014) and blood pressure: SBP (EP: r = 0.388, PWV-beta: r = 0.360), DBP (AC: r = 0.225) and PP (PWV-beta: r = 0.221) correlated positively with the initial parameters of CAS. Beta-stiffness index (Rho=-0.26, p = 0.04) and PWV-beta (Rho = 0.29, p = 0.03) correlated inversely with peak exercise capacity expressed in METs. After CR, mean values of beta-stiffness index (6.2 vs 7.1, p = 0.016), EP (78 kPa vs 101 kPa, p = 0.001) and PWV-beta (5.4 m/s vs 6.2 m/s, p = 0.001) in group B were significantly lower than in group K. In group B, CAS parameters decreased significantly after CR. Univariate analysis demonstrated that the likelihood of an improvement in CAS after CR was significantly higher in patients with baseline systolic blood pressure <120 mm Hg (OR = 2.74, p = 0.009) and left ventricular ejection fraction <43% (OR = 5.05, p = 0.005). Conclusion: In patients with MI, CR exerted a beneficial effect on CAS parameters. The improvement in CAS was predicted by lower SBP and LVEF at baseline.

Short-term vascular responses to spring and fall daylight savings time shifts.

Daylight saving time (DST) is a Western biannual time transition, setting the clock back 1 h in the fall and forward 1 h in the spring. There is an epidemiological link between DST and acute myocardial infarction risk in the first week following the spring shift; however, the mechanisms underlying the effect of DST on cardiovascular function remain unclear. The purpose of this study was to explore the short-term cardiovascular changes induced by fall and spring shifts in DST in a convenience sample of healthy adults. We hypothesized that spring, but not fall, DST shifts would acutely increase central pulse wave velocity, the gold standard measurement of central arterial stiffness. Twenty-one individuals (fall: n = 10; spring: n = 11) participated in four visits, occurring 1 wk before and at +1, +3, and +5 days after spring and fall time transitions. Central, brachial, and radial pulse wave velocity as well as carotid augmentation index were assessed with applanation tonometry. Sleep quality and memory function were assessed via questionnaire and the Mnemonic Similarities Task, respectively. Neither fall or spring transition resulted in changes to cardiovascular variables (carotid-femoral pulse wave velocity, carotid-brachial pulse wave velocity, carotid-radial pulse wave velocity, heart rate, mean arterial pressure, or augmentation index), sleep quality, or cognitive function (all P > 0.05). Our findings do not provide evidence that DST shifts influence cardiovascular outcomes in healthy adults. This study emphasizes the need for further research to determine the mechanisms of increased cardiovascular disease risk with DST that help explain epidemiological trends.NEW & NOTEWORTHY The debate of whether to abolish daylight savings time (DST) is, in part, motivated by the population-level increase in all-cause mortality and incidence of cardiovascular events following DST; however, there is an absence of data to support a physiological basis for risk. We found no changes in pulse wave velocity or augmentation index during the subacute window of DST. Large multisite trials are necessary to address the small, but meaningful, effects brought on by a societal event.

CAVI (Cardio-Ankle Vascular Index) as an independent predictor of hypertensive response to exercise.

OBJECTIVES: Hypertensive response to exercise (HRE) is related to the development of future hypertension, cardiovascular morbidity, and mortality, independent of resting blood pressure. We hypothesized that arterial stiffness as measured by cardio-ankle vascular index (CAVI) could be an independent predictor of HRE. MATERIALS AND METHODS: Retrospective chart review of patients participated in the preventive health program at the Bangkok Heart Hospital who underwent both CAVI and treadmill stress testing on the same day between June and December 2018 were performed. Variables for the prediction of HRE were analyzed using univariate analysis, and significant variables were entered into multiple logistic regression. An ROC curve was created to test the sensitivity and specificity of CAVI as a predictor of HRE. RESULTS: A total of 285 participants (55.1% female) were enrolled in this study. There were 58 patients (20.4%) who met the HRE definition (SBP > 210 mmHg in males, SBP > 190 mmHg in females, or DBP > 110 mmHg in both males and females), with a mean age of 46.4 12.8 years. In univariate analysis, age, systolic blood pressure at rest, diastolic blood pressure at rest, pulse pressure at rest, diabetes mellitus, hypertension, dyslipidemia, history of beta-blocker, and CAVI results were statistically significant. Multiple logistic regression revealed that CAVI and systolic blood pressure were statistically significant predictors of HRE with OR of 5.8, 95%CI: 2.9-11.7, P < 0.001 and OR 1.07, 95%CI: 1.03-1.10, P = 0.001 respectively. ROC curve analysis of the CAVI revealed an AUC of 0.827 (95%CI: 0.76-0.89, p < 0.001), and the sensitivity and specificity of cut-point CAVI > 8 were 53% and 92%, respectively. CONCLUSION: This study demonstrated that CAVI is an independent predictor of hypertensive response to exercise. Additionally, the findings suggest that CAVI > 8 can be a valuable tool in identifying individuals at risk for hypertensive responses during exercise.

Screening for Peripheral Vascular Stiffness in Lipedema Patients by Automatic Electrocardiogram-Based Oscillometric Detection.

Body mass index (BMI) is seen as a predictor of cardiovascular disease (CVD) in lipedema patients. A valid predictor of CVD is increased aortic stiffness (IAS), and previous research described IAS in lipedema. However, it is not known if this applies to all patients. In this cross-sectional single-center cohort study, peripheral pulse wave velocity (PWV) as a non-invasive indicator of aortic stiffness was measured in 41 patients with lipedema, irrespective of stage and without pre-existing cardiovascular conditions or a history of smoking and a maximum body mass index (BMI) of 35 kg/m2. Automatically electrocardiogram-triggered oscillometric sensor technology by the Gesenius-Keller method was used. Regardless of the stage of lipedema disease, there was no significant difference in PWV compared to published standard values adjusted to age and blood pressure. BMI alone is not a predictor of cardiovascular risk in lipedema patients. Measuring other anthropometric factors, such as the waist-hip ratio or waist-height ratio, should be included, and the existing cardiovascular risk factors, comorbidities, and adipose tissue distribution for accurate risk stratification should be taken into account. Automated sensor technology recording the PWV represents a valid and reliable method for health monitoring and early detection of cardiovascular risks.

Sex differences in sympathetic activity and pulse wave velocity in adults with chronic kidney disease.

Chronic kidney disease (CKD) is characterized by sympathetic nervous system (SNS) overactivity that contributes to increased vascular stiffness and cardiovascular risk. Although it is well established that SNS activity and vascular stiffness are substantially elevated in CKD, whether sex differences in autonomic and vascular function exist in CKD remains unknown. We tested the hypothesis that compared with females, males with CKD have higher baseline sympathetic activity that is related to increased arterial stiffness. One hundred twenty-nine participants (96 males and 33 females) with CKD stages III and IV were recruited and enrolled. During two separate study visits, vascular stiffness was assessed by measuring carotid-to-femoral pulse wave velocity (cfPWV), and resting muscle sympathetic nerve activity (MSNA) was measured by microneurography. Males with CKD had higher resting MSNA compared with females with CKD (68 ± 16 vs. 55 ± 14 bursts/100 heart beats, P = 0.005), whereas there was no difference in cfPWV between the groups (P = 0.248). Resting MSNA was not associated with cfPWV in both males and females. In conclusion, males with CKD have higher resting sympathetic activity compared with females with CKD. However, there was no difference in vascular stiffness between the sexes. There was no correlation between resting MSNA and cfPWV, suggesting that non-neural mechanisms may play a greater role in the progression of vascular stiffness in CKD, particularly in females.NEW & NOTEWORTHY Males with chronic kidney disease (CKD) have higher resting muscle sympathetic nerve activity (MSNA) compared with females. There was no correlation between MSNA and carotid-to-femoral pulse wave velocity (cfPWV), suggesting that non-neural mechanisms may play a greater role in the progression of vascular stiffness in CKD. Sex differences in SNS activity may play a mechanistic role in observations from epidemiological studies suggesting greater cardiovascular risk in males compared with females with CKD.

Higher arterial stiffness and blunted vagal control of the heart in young women with compared to without a clinical diagnosis of PTSD.

PURPOSE: Young women are typically thought to be protected from cardiovascular disease (CVD) before menopause. However, posttraumatic stress disorder (PTSD) increases CVD risk in women by up to threefold. Data in predominantly male cohorts point to physiological mechanisms such as vascular and autonomic derangements as contributing to increased CVD risk. The purpose of the study reported here was to determine whether young women diagnosed with PTSD, compared to those without, present with arterial stiffness and impaired autonomic control of the heart. METHODS: A total of 73 healthy young women, ranging in age from 18 to 40 years, with a history of trauma exposure were included in this study, 32 with and 41 without a clinical PTSD diagnosis. We measured resting pulse wave velocity (PWV), central hemodynamics, augmentation pressure and augmentation index (AI) via pulse wave analysis using applanation tonometry. Heart rate variability was also assessed via peripheral arterial tone. RESULTS: In comparison to controls, women with PTSD showed higher central arterial pressure (mean ± standard deviation: systolic blood pressure 104 ± 8 vs. 97 ± 8 mmHg, p < 0.001; diastolic blood pressure 72 ± 7 vs. 67 ± 7 mmHg, p = 0.003), PWV (6 ± 0.3 vs. 5 ± 0.6 m/s, p < 0.001) and AI (22 ± 13 vs. 15 ± 12%, p = 0.007) but lower standard deviation of normal-to-normal intervals (SDNN; 44 ± 17 vs. 54 ± 18 ms, p = 0.005) and root mean square of successive differences between normal heartbeats (RMSSD; 37 ± 17 vs. 51 ± 22 ms, p = 0.002). CONCLUSION: PTSD in young women is associated with higher brachial and central pressures, increased arterial stiffness and blunted parasympathetic control of the heart. These findings illustrate potential mechanisms underlying high risk for CVD in young women with PTSD, suggesting possible treatment targets for this at-risk group.

Vascular Responses to Acute Induced Inflammation With Aging: Does Fitness Matter?

Acute inflammation impairs vascular function in an age-dependent manner and affects cardiovascular event risk. Regular aerobic exercise preserves vascular function with aging and potentially modifies how acute inflammation affects the vasculature. We hypothesize high cardiorespiratory fitness may accompany greater arterial responsiveness post-acute inflammation in older adults.

Association between arterial stiffness and autonomic dysfunction in participants underwent treadmill exercise testing: a cross-sectional analysis.

Data on the impact of arterial stiffness on autonomic function are limited. We sought to investigate whether heart rate recovery (HRR), a predictor of autonomic function, is impaired in patients with increased arterial stiffness. A total of 475 participants (mean age 55.8 ± 11.1 years, 34.3% women) who underwent a treadmill exercise test (TET) for the evaluation of chest pain were retrospectively analyzed. All patients underwent brachial-ankle pulse wave velocity (baPWV) measurement on the same day. HRR was defined as the difference in heart rate from maximal exercise to 1 min of recovery. Participants with the lowest HRR tertile were older and had more cardiovascular risk factors than those with the highest HRR tertile. Simple correlation analysis showed that baPWV was negatively correlated with HRR (r = - 0.327, P < 0.001). In multiple linear regression analysis, there was a significant association between baPWV and HRR, even after adjusting for potential confounders (ß = - 0.181, P < 0.001). In participants who underwent TET, baPWV was negatively correlated with HRR. The results of our study indicate a potential relationship between arterial stiffness and the autonomic nervous system.

Arterial Stiffness and Ankle-Brachial Index - Cross-Sectional Study of 259 Primary Care Patients ≥50 Year-Old.

BACKGROUND Lower-extremity arterial disease (LEAD) is the most common form of peripheral artery disease (PAD), and diagnosis relies on the ankle-brachial index (ABI). The objective of our study was to evaluate the correlation between ABI and arterial stiffness parameters, specifically focusing on PWV. Additionally, we aimed to assess the correlation between PWV and established LEAD risk factors. MATERIAL AND METHODS The study included primary care patients aged ≥50 years. Pulse wave velocity was measured with a Mobil-o-Graph Pulse Wave Analyzer (I.E.M. Germany). Two criteria defined abnormal PWV: 1) universal PWV threshold exceeding 10 m/s (uPWVt) and 2) surpassing an individualized threshold calculated by the device, accounting for sex, age, and blood pressure (iPWVt). RESULTS We assessed PWV in 266 individuals and both PWV and ABI in 259. Overall, 6/259 (2.3%) had a diagnosis of LEAD, 44/259(16.9%) had ABI <0.9, and 97/259 (37.5%) had PWV values above iPWVt. Among patients with Doppler ABI <0.9, 25/44 (56.8%) exhibited elevated iPWVt versus 72/215 (33.5%) in those with ABI ≥0.9 (P=0.003, r=0.18 Spearman's correlation). Among patients with ABI <0.9 19/44 (43.2%) had PWV >iPWVt (P=0.003, r=0.18). We observed significant correlation between elevated PWV (both cutoffs) and hypertension (in both P=0.009, r=0.16) and PWV >uPWVt correlated with the presence of diabetes (P=0.004, r=0.18). CONCLUSIONS Elevated PWV correlates with abnormal ABI and some cardiovascular risk factors in primary care patients aged 50 and above. Use of individualized PWV thresholds, factoring in age, appears to be a preferable approach for assessment of arterial stiffness and early diagnosis of LEAD.

Non-invasive parameters of autonomic function using beat-to-beat cardiovascular variations and arterial stiffness in hypertensive individuals: a systematic review.

PURPOSE: Non-invasive, beat-to-beat variations in physiological indices provide an opportunity for more accessible assessment of autonomic dysfunction. The potential association between the changes in these parameters and arterial stiffness in hypertension remains poorly understood. This systematic review aims to investigate the association between non-invasive indicators of autonomic function based on beat-to-beat cardiovascular signals with arterial stiffness in individuals with hypertension. METHODS: Four electronic databases were searched from inception to June 2022. Studies that investigated non-invasive parameters of arterial stiffness and autonomic function using beat-to-beat cardiovascular signals over a period of > 5min were included. Study quality was assessed using the STROBE criteria. Two authors screened the titles, abstracts, and full texts independently. RESULTS: Nineteen studies met the inclusion criteria. A comprehensive overview of experimental design for assessing autonomic function in terms of baroreflex sensitivity and beat-to-beat cardiovascular variabilities, as well as arterial stiffness, was presented. Alterations in non-invasive indicators of autonomic function, which included baroreflex sensitivity, beat-to-beat cardiovascular variabilities and hemodynamic changes in response to autonomic challenges, as well as arterial stiffness, were identified in individuals with hypertension. A mixed result was found in terms of the association between non-invasive quantitative autonomic indices and arterial stiffness in hypertensive individuals. Nine out of 12 studies which quantified baroreflex sensitivity revealed a significant association with arterial stiffness parameters. Three studies estimated beat-to-beat heart rate variability and only one study reported a significant relationship with arterial stiffness indices. Three out of five studies which studied beat-to-beat blood pressure variability showed a significant association with arterial structural changes. One study revealed that hemodynamic changes in response to autonomic challenges were significantly correlated with arterial stiffness parameters. CONCLUSIONS: The current review demonstrated alteration in autonomic function, which encompasses both the sympathetic and parasympathetic modulation of sinus node function and vasomotor tone (derived from beat-to-beat cardiovascular signals) in hypertension, and a significant association between some of these parameters with arterial stiffness. By employing non-invasive measurements to monitor changes in autonomic function and arterial remodeling in individuals with hypertension, we would be able to enhance our ability to identify individuals at high risk of cardiovascular disease. Understanding the intricate relationships among these cardiovascular variability measures and arterial stiffness could contribute toward better individualized treatment for hypertension in the future. SYSTEMATIC REVIEW REGISTRATION: PROSPERO ID: CRD42022336703. Date of registration: 12/06/2022.

Clinical application value of Ultrafast Pulse Wave Velocity in early cardiovascular injury of Immunoglobulin A nephropathy.

AIM: To investigate the application and the related influencing factors of ultrafast pulse wave velocity (ufPWV) in the evaluation of carotid artery elasticity in patients with Immunoglobulin A nephropathy (IgAN). MATERIAL AND METHODS: A total of 156 IgAN patients and 50 healthy individuals were selected as the control group. The ufPWV technique was employed to measure carotid arterial elasticity parameters, including carotid intima-media thickness (cIMT), pulse wave velocity at the beginning of systole (BS-PWV) and pulse wave velocity at the end of systole (ES-PWV). RESULTS: Across the three groups (control group, IgAN patients with normal renal function, and IgAN patients with renal dysfunction) there was an increasing trend observed in cIMT, BS-PWV, and ES-PWV. Additionally, ES-PWV exhibited higher sensitivity than BS-PWV. Correlation analysis revealed that BS-PWV and ES-PWV were positively correlated with age, body mass index (BMI), systolic blood pressure (SBP), high-sensitivity C-reactive protein (hs-CRP), creatinine (Cr), blood urea nitrogen (BUN), and uric acid (UA) and negatively correlated with estimated glomerular filtration rate (eGFR). CONCLUSION: The ufPWV technique allows for the rapid and direct measurement of arterial elasticity parameters in the neck and represents a novel approach for the early diagnosis and quantitative assessment of arterial stiffness risk in IgAN patients.

The Pathogenesis and Impact of Arterial Stiffening in Hypertension: The 2023 John H. Laragh Research Award.

Fifty years ago, Dr. John Laragh brought forward the "vasoconstriction-volume hypothesis" of hypertension. This is Ohm's Law in blood pressure regulation, explicating hypertension as a consequence of increased peripheral vascular resistance, cardiac output, or both. Resistance vessels, those of a diameter less than 200 µm, determines mean arterial pressure by controlling peripheral vascular resistance. In comparison, large capacitance arteries, particularly the aorta, confines the systolic and diastolic blood pressure in physiological range through the "windkessel effect." Loss of this cushioning function results in aortic stiffening and isolated systolic hypertension, both of which are independently associated with increased risk for coronary, cerebral, and renal diseases. Aortic stiffening is both a cause and a consequence of hypertension. On one hand, aortic stiffness precedes the onset of hypertension in populations and experimental models, and hemodynamic derangements related to aortic stiffening contributes to the development of hypertension by promoting renal dysfunction. On the other hand, the vasculature itself is a hypertensive target organ and hypertensive mechanical stretch directly induces the pathogenesis of aortic adventitial remodeling. Various cell types, including bone marrow-derived circulating fibrocytes, vascular stem cell antigen-1 positive progenitors, and endothelial to mesenchymal transition, and to a lesser extent resident fibroblasts, contribute to adventitial matrix deposition and aortic stiffening in hypertension. Vascular smooth muscle stiffness is another important contributor of aortic stiffening. Understanding the roles of immune components and specific signal pathways in the pathogenesis aortic stiffening paves the path to novel antihypertensive and anti-fibrosis therapies.

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

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

Impact of arterial stiffness on cerebrovascular function: a review of evidence from humans and preclincal models.

With advancing age, the cerebral vasculature becomes dysfunctional, and this dysfunction is associated with cognitive decline. However, the initiating cause of these age-related cerebrovascular impairments remains incompletely understood. A characteristic feature of the aging vasculature is the increase in stiffness of the large elastic arteries. This increase in arterial stiffness is associated with elevated pulse pressure and blood flow pulsatility in the cerebral vasculature. Evidence from both humans and rodents supports that increases in large elastic artery stiffness are associated with cerebrovascular impairments. These impacts on cerebrovascular function are wide-ranging and include reductions in global and regional cerebral blood flow, cerebral small vessel disease, endothelial cell dysfunction, and impaired perivascular clearance. Furthermore, recent findings suggest that the relationship between arterial stiffness and cerebrovascular function may be influenced by genetics, specifically APOE and NOTCH genotypes. Given the strength of the evidence that age-related increases in arterial stiffness have deleterious impacts on the brain, interventions that target arterial stiffness are needed. The purpose of this review is to summarize the evidence from human and rodent studies, supporting the role of increased arterial stiffness in age-related cerebrovascular impairments.

Habitual isomaltulose intake reduces arterial stiffness associated with postprandial hyperglycemia in middle-aged and elderly people: a randomized controlled trial.

Endothelin-1 (ET-1), produced by vascular endothelial cells, plays a pivotal role in the regulation of vascular tone. Isomaltulose, a naturally occurring sweetener and structural isomer of sucrose, reduces postprandial hyperglycemia, but its effect on arteriosclerosis due to hyperglycemia is unknown. The effects of 12 weeks of isomaltulose administration on ET-1 levels, a peptide that regulates arterial stiffness, blood pressure, and vascular tone, were tested before and after an oral glucose tolerance test. Fifty-four healthy middle-aged and older adults (30 men and 24 women) were divided into two groups: (1) a 25 g isomaltulose jelly drink intake group (Group I, 27 participants, mean age 55 ± 1 years) and (2) a sucrose jelly drink intake group (Group S, 27 participants, mean age 55 ± 1 years), each consuming isomaltulose or sucrose daily for 12 weeks, and a randomized, controlled study was conducted. Participants visited the laboratory before the intervention and 4, 8, and 12 weeks after the intervention to measure carotid-femoral (cf) and brachial-ankle (ba) pulse wave velocity (PWV), systolic blood pressure (BP), plasma glucose (PG), insulin, and ET-1 levels before and 60 and 120 min after a 75-g OGTT. baPWV, and ET-1 levels before intervention were significantly increased after 75-g OGTT compared to before 75-g OGTT in both groups (p < 0.05). The post-intervention baPWV, and ET-1 levels were significantly increased after 75-g OGTT in Group S compared to before 75-g OGTT (p < 0.05), whereas no significant changes were observed in Group I. These results suggest that consumption of isomaltulose, which has a lower GI than sucrose, is more effective in preventing the increases in systemic arterial stiffness associated with postprandial hyperglycemia in healthy middle-aged and older adults.

Vascular Age Assessed From an Uncalibrated, Noninvasive Pressure Waveform by Using a Deep Learning Approach: The AI-VascularAge Model.

BACKGROUND: Aortic stiffness, assessed as carotid-femoral pulse wave velocity, provides a measure of vascular age and risk for adverse cardiovascular disease outcomes, but it is difficult to measure. The shape of arterial pressure waveforms conveys information regarding aortic stiffness; however, the best methods to extract and interpret waveform features remain controversial. METHODS: We trained a convolutional neural network with fixed-scale (time and amplitude) brachial, radial, and carotid tonometry waveforms as input and negative inverse carotid-femoral pulse wave velocity as label. Models were trained with data from 2 community-based Icelandic samples (N=10 452 participants with 31 126 waveforms) and validated in the community-based Framingham Heart Study (N=7208 participants, 21 624 waveforms). Linear regression rescaled predicted negative inverse carotid-femoral pulse wave velocity to equivalent artificial intelligence vascular age (AI-VA). RESULTS: The AI-VascularAge model predicted negative inverse carotid-femoral pulse wave velocity with R2=0.64 in a randomly reserved Icelandic test group (n=5061, 16%) and R2=0.60 in the Framingham Heart Study. In the Framingham Heart Study (up to 18 years of follow-up; 479 cardiovascular disease, 200 coronary heart disease, and 213 heart failure events), brachial AI-VA was associated with incident cardiovascular disease adjusted for age and sex (model 1; hazard ratio, 1.79 [95% CI, 1.50-2.40] per SD; P<0.0001) or adjusted for age, sex, systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, prevalent diabetes, hypertension treatment, and current smoking (model 2; hazard ratio, 1.50 [95% CI, 1.24-1.82] per SD; P<0.0001). Similar hazard ratios were demonstrated for incident coronary heart disease and heart failure events and for AI-VA values estimated from carotid or radial waveforms. CONCLUSIONS: Our results demonstrate that convolutional neural network-derived AI-VA is a powerful indicator of vascular health and cardiovascular disease risk in a broad community-based sample.

Sexual function scores are associated with arterial stiffness in postmenopausal women.

BACKGROUND: Female sexual dysfunction (FSD) has been suggested to be correlated with the burden of cardiovascular risk factors. AIM: We aimed to evaluate the possible association between functional indices of vascular function and FSD scores in apparently healthy postmenopausal women. METHODS: This cross-sectional study included 116 postmenopausal women who underwent assessment of endothelial function with measurement of flow-mediated dilation (FMD) of the branchial artery and arterial stiffness estimation with measurement of the carotid-femoral pulse wave velocity (PWV). We used the Greene Climacteric Scale to evaluate vasomotor symptomatology, the Female Sexual Function Index (FSFI) to evaluate FSD and the Beck Depression Inventory to evaluate mood disorder. Low sexual function was defined as an FSFI score <26.55. OUTCOMES: These included FSFI and low sexual function scores as well as measures of PWV and FMD. RESULTS: Sexual function scores were associated with measures of blood pressure (normal vs low sexual function; systolic blood pressure: 120.2 ± 15.0 mm Hg vs 113.4 ± 14.6 mm Hg; analysis of covariance P = .026; diastolic blood pressure: 75.9 ± 10.5 mm Hg vs 70.3 ± 9.9 mm Hg; analysis of covariance P = .012; both adjusted for age, body mass index, current smoking, and PWV). Systolic blood pressure, but not diastolic blood pressure, was associated with FSFI (B = 0.249, P = .041) and PWV (B = 0.392, P < .001). PWV measures were associated with FSFI (B = -0.291, P = .047) and pulse pressure (B = 0.355, P = .017). FMD measures were also associated with FSFI (B = 0.427, P = .033). All models were adjusted for age, body mass index, current smoking, insulin resistance, vasomotor symptomatology, and Beck Depression Inventory. CLINICAL IMPLICATIONS: Our findings demonstrate that lower scores of sexual function are associated with deteriorated vascular function mainly manifested as arterial stiffening, further contributing to systolic blood pressure changes. STRENGTHS AND LIMITATIONS: The strength of this study is the carefully selected healthy sample of postmenopausal women, with simultaneous assessment of climacteric symptomatology and mood disorders. The limitations include the small sample size, the cross-sectional design, and the recruitment of consecutive outpatients of a university menopause clinic. CONCLUSION: Longitudinal studies and interventions to improve FSD should further assess the clinical relevance of these findings.