Carotid Pulse Pressure Research Articles

Inverse association between arterial stiffness and perceived fatigue independent of disability status and BMI in multiple sclerosis.

Multiple sclerosis (MS) is an immune-mediated, neurodegenerative disease of the central nervous system. Fatigue represents one of the most prevalent and limiting symptoms of MS, and is associated with vascular dysfunction, notably increased arterial stiffness. This study examined the relationship between arterial stiffness and perceived fatigue in persons with MS. The sample of 52 persons with MS (71.2% Female; Age: 46.7 ± 12.3 yrs.) completed arterial stiffness and fatigue assessments as baseline for an exercise training intervention. Applanation tonometry measured arterial stiffness, pulsatility and waveform characteristics, and yielded the following outcomes: carotid-femoral pulse wave velocity (cfPWV), carotid pulse-pressure (cPP), and aortic augmentation pressure (AP). Perceived fatigue was measured using the Fatigue Severity Scale (FSS). The mean (SD) scores for cfPWV, cPP, and AP were 7.0 ± 1.8m/s, 35.7 ± 8.8mmHg, 8.2 ± 6.2mmHg, respectively. The mean (SD) FSS score was 4.6 ± 1.4 and indicated elevated fatigue. There were statistically significant (p < .05) inverse correlations between cfPWV (r = -.32), cPP (r = -.37) and AP (r = -.32) with FSS scores, and the correlations remained significant even after controlling for disability, body mass index, age, and sex. Our results indicate a consistent pattern of inverse relationships between arterial stiffness, pulsatility, and waveforms with fatigue independent of disability, body mass index, age, and sex in MS. This could be explained by lower sympathetic activation linking higher arterial stiffness, pulsatility and augmentation pressure with lower fatigue in persons with MS.

Effects of Perceived Social Stress on Cerebrovascular Hemodynamics in Young and Middle-Aged Adults

Depression is associated with altered cerebrovascular hemodynamics, including lower cerebral blood flow, higher cerebral pulsatility, and greater arterial stiffness. There is evidence that perceived stress may contribute to depressive symptomology, but it is unknown if stress may directly impact cerebrovascular hemodynamics. The purpose of this investigation was to examine associations among middle cerebral artery (MCA) hemodynamics, arterial stiffness, and perceived stress in young and middle-aged adults. It was hypothesized that individuals with higher reported social stress would have lower MCA mean velocity and higher MCA pulsatility and arterial stiffness. Methods: 168 adults (range 18-64 years; 40 ± 16 years; BMI 26.6 ± 4.6 kg/m2; n=88 females) underwent resting cerebrovascular measures and completed the self-reported perceived stress scale (PSS-10). Brachial blood pressure and carotid pulse pressure were assessed via oscillometric cuff and tonometry, respectively. Arterial stiffness was assessed as carotid-femoral pulse wave velocity (cfPWV) via tonometry and MCA mean velocity and pulsatility index were assessed via Transcranial Doppler. Results: The sample contained 4 adults with high (PSS score ≥27; mean, 28 ± 1), 38 adults with moderate (PSS score 14-26; mean, 17 ± 2), and 126 adults with low stress (PSS score &lt;13; mean, 8 ± 3). Self-reported perceived stress was not significantly linearly associated with MCA mean velocity (r=-0.10), MCA Pulsatility Index (r=-0.08), or arterial stiffness (r=0.05). A secondary analysis comparing adults with moderate/high stress (n=42) to adults with low stress (n=126) revealed a significantly lower MCA mean velocity among moderate/high stress adults (p&lt;0.05), however this difference was attenuated and no longer statistically significant after covarying for age. Conclusions: This data suggests that perceived stress 1) is not associated with altered cerebrovascular hemodynamics or arterial stiffness in our sample of generally healthy young and middle-aged adults, and 2) may not play a major role in altering cerebrovascular hemodynamics in the context of stress-related disorders (e.g., depression), however future research is required to directly test this hypothesis. Iowa State University College of Human Sciences Faculty Seed Grant. 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.

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 determinants of hippocampal viscoelastic properties in healthy adults across the lifespan

Arterial stiffness and cerebrovascular pulsatility are non-traditional risk factors of Alzheimer’s disease. However, there is a gap in understanding the earliest mechanisms that link these vascular determinants to brain aging. Changes to mechanical tissue properties of the hippocampus (HC), a brain structure essential for memory encoding, may reflect the impact of vascular dysfunction on brain aging. We tested the hypothesis that arterial stiffness and cerebrovascular pulsatility are related to HC tissue properties in healthy adults across the lifespan. Twenty-five adults underwent measurements of brachial blood pressure (BP), large elastic artery stiffness, middle cerebral artery pulsatility index (MCAv PI), and magnetic resonance elastography (MRE), a sensitive measure of HC viscoelasticity. Individuals with higher carotid pulse pressure (PP) exhibited lower HC stiffness (β = −0.39, r = −0.41, p = 0.05), independent of age and sex. Collectively, carotid PP and MCAv PI significantly explained a large portion of the total variance in HC stiffness (adjusted R2 = 0.41, p = 0.005) in the absence of associations with HC volumes. These cross-sectional findings suggest that the earliest reductions in HC tissue properties are associated with alterations in vascular function.

Social isolation and subclinical vascular pathways to cerebrovascular disease

ABSTRACT Social isolation and lack of social support are risk factors for cardiovascular and cerebrovascular disease (CVD). This study explored the relationship between measures of social support and subclinical measures of CVD risk. 58 healthy adults ages 18 to 85 years participated in this study. The Berkman-Syme Social Network Inventory (SNI) was used to assess social isolation, with higher scores signifying less isolation. Social support was defined using the 12-Item Interpersonal Support Evaluation List (ISEL-12) with a higher score signifying higher social support. Subclinical CVD measures included carotid-femoral pulse wave velocity (cfPWV), carotid beta-stiffness index, and middle cerebral artery (MCA) pulsatility index. Path analysis models for both the SNI and ISEL appraisal domain predicting cfPWV and cerebrovascular pulsatility fit the data well. Path analyses showed significant direct paths from the SNI (β = −.363, t = −2.91) and ISEL appraisal domain (β = −.264, t = −2.05) to cfPWV. From cfPWV, both models revealed significant direct paths to carotid stiffness (β = .488, t = 4.18) to carotid pulse pressure (β = .311, t = 2.45) to MCA pulsatility (β = .527, t = 4.64). Social isolation and appraisal of social support are related to unfavorably higher aortic stiffness, with subsequent detrimental effects on cerebrovascular hemodynamic pulsatility.

Aerobic exercise training reduces cerebrovascular impedance in older adults: a 1-year randomized controlled trial.

Older adults have higher cerebrovascular impedance than young individuals which may contribute to chronic brain hypoperfusion. Besides, middle-aged athletes exhibit lower cerebrovascular impedance than their sedentary peers. We examined whether aerobic exercise training (AET) reduces cerebrovascular impedance in sedentary older adults. We conducted a proof-of-concept trial that randomized 73 older adults to 1 yr of AET (n = 36) or stretching and toning (SAT, n = 37) interventions. Cerebrovascular impedance was estimated from simultaneous recordings of carotid artery pressure (CAP) via applanation tonometry and cerebral blood flow velocity (CBFV) in the middle cerebral artery via transcranial Doppler using transfer function analysis. Fifty-six participants completed 1-yr interventions, and 41 of those completed cerebrovascular impedance measurements. AET group showed a significant increase in V̇o2peak after the intervention [estimated marginal mean (95% confidence interval); from 22.8 (21.6 to 24.1) to 24.9 (23.6 to 26.2) mL·kg-1·cm-1, P < 0.001], but not SAT [from 21.7 (20.5 to 22.9) to 22.3 (21.1 to 23.7) mL·kg-1·cm-1, P = 0.114]. Coherence between changes in CBFV and CAP was >0.90 in the frequency range of 0.78-3.12 Hz. The averaged cerebrovascular impedance modulus (Z) in this frequency range decreased after 1-yr AET [from 1.05 (0.96 to 1.14) to 0.95 (0.92 to 1.06) mmHg·s·cm-1, P = 0.023], but not SAT [from 0.96 (0.87 to 1.04) to 1.01 (0.92 to 1.10) mmHg·s·cm-1, P = 0.138]. Reductions in Z were correlated positively with reductions in carotid pulse pressure (r = 0.628, P = 0.004) and inversely with mean CBFV (r = -0.563, P = 0.012) in the AET group. One-year AET reduces cerebrovascular impedance in older adults, which may benefit brain perfusion.NEW & NOTEWORTHY Estimation of cerebrovascular impedance is essential for understanding dynamic cerebral blood flow regulation. This randomized controlled trial demonstrated that aerobic exercise training reduced cerebrovascular impedance in older adults, which may benefit brain perfusion.

Influence of sex and presence of cardiovascular risk factors on relations between cardiorespiratory fitness and cerebrovascular hemodynamics.

Cerebral hemodynamics and pulsatility are important mechanisms of cerebrovascular and brain health. Cardiorespiratory fitness may improve cerebrovascular pulsatility in healthy females, but not in males. Whether cardiovascular disease (CVD) risk factors modify sex-specific associations of fitness with cerebral hemodynamics and vascular contributors to cerebral hemodynamics is unknown. We assessed V̇o2peak and cerebrovascular hemodynamics in 157 adults without (42 ± 13 yr, BMI 24.5 ± 2.7 kg/m2), and 66 adults with modifiable CVD risk factors (54 ± 8 yr, BMI 29.9 ± 4.0 kg/m2). Intracranial [middle cerebral artery (MCA) pulsatility index (PI), mean velocity, conductance, and pulsatile damping] and extracranial hemodynamics [carotid artery wave transmission/reflection, PI, pulse wave velocity (PWV)-β, and carotid-femoral PWV] were assessed via transcranial Doppler/ultrasound and tonometry. Cardiorespiratory fitness was assessed via V̇o2peak during an incremental exercise test. Multiple regression was used to assess contributions of V̇o2peak to cerebrovascular outcomes after adjustment for relevant covariates. V̇o2peak was inversely associated with MCA PI among females (β = -0.39, P = 0.01) but not males (β = -0.16, P = 0.25) without CVD risk factors. V̇o2peak was positively associated with MCA PI among females (β = 0.44, P = 0.01) and not associated in males with CVD risk factors (β = -0.06, P = 0.079). V̇o2peak was beneficially associated with vascular contributors to cerebral hemodynamics but had sex-specific associations with carotid stiffness and pulse pressure in females without CVD risk factors only. These results suggest that sex-specific associations between fitness and cerebral pulsatility among females without CVD risk factors may relate to the differential effects of fitness on carotid stiffness and pulse pressure. In addition, the presence of modifiable CVD risk factors may influence the protective relations of fitness on cerebrovascular hemodynamics.NEW & NOTEWORTHY We identify beneficial associations between cardiorespiratory fitness and lower carotid stiffness and pulse pressure as potential mechanisms underlying sex-specific associations of fitness and cerebral pulsatility in females without modifiable risk factors. Greater fitness is beneficially associated with conductance, pulsatile damping, and forward wave energy among adults without risk factors; however, associations are attenuated among adults with modifiable risk factors. These data suggest sex and risk factors may alter cerebrovascular sensitivity to cardiorespiratory fitness.

Aortic Stiffness is Negatively Associated with Microvascular Glycocalyx Thickness and Microvascular Perfusion among Older Adults: Role of Carotid Pressure Pulsatility

IntroductionThe glycocalyx layer is essential to the maintenance of a healthy microvascular endothelium and diminishes with advancing age. Similarly, the aorta stiffens with aging and increases the risk of cardiovascular disease and target organ damage, possibly through pressure pulsatility‐associated microvascular damage. However, whether aortic stiffness and/or pressure pulsatility are associated with microvascular endothelial glycocalyx structure/function among older adults is unknown. Therefore, the objective of this analysis was to investigate the potential relation between aortic stiffness and pressure pulsatility with glycocalyx thickness and microvascular perfusion in older adults. We hypothesized that increased aortic stiffness and pressure pulsatility would be associated with less glycocalyx thickness and microvascular perfusion in older adults.MethodsSublingual microvessels were assessed using intravital microscopy in older adults (n=24; age 61 ± 6y, 46% women). Perfused boundary region (PBR) and red blood cell (RBC) filling %, indirect indices of glycocalyx thickness (larger PBR=smaller thickness) and microvascular perfusion respectively, were determined in vessels between 5‐25 µm RBC column width. Aortic stiffness was quantified by carotid‐femoral pulse wave velocity (cfPWV) and carotid pressure pulsatility as carotid pulse pressure (PP)/mean arterial pressure (MAP).ResultsAdjusting for age, sex and MAP, cfPWV was associated with larger PBR 5‐25 (β: 0.08; p=0.001) and lower RBC filling % (β: ‐0.02, p=0.002). Higher carotid pressure pulsatility was associated with lower RBC filling % (β: ‐0.12; p=0.03), but this relation was attenuated after adjusting for sex (p=0.11). Upon stratification by sex, higher carotid pressure pulsatility was associated with larger PBR 5‐25 (r=0.66, P=0.03) and lower RBC filling % (r=‐0.73, P=0.01) in women, but not men (P=0.94 and P=0.77 respectively).ConclusionHigher aortic stiffness was negatively associated with microvascular glycocalyx thickness and microvascular perfusion among older adults. Additionally, carotid pressure pulsatility was negatively associated with glycocalyx thickness and microvascular perfusion in women only. The mechanisms that contribute to sex differences in the relation between pressure pulsatility and glycocalyx structure/function in older adults require further study.

Influence of lipid profile and statin administration on arterial stiffness in renal transplant recipients.

BackgroundHyperlipidemia is one of the major risk factors for developing a cardiovascular disease (CVD) and it is a frequent post-transplant complication, occurring in up to 60% of the renal transplant recipients (RTRs). Lipid lowering therapy with HMG-CoA reductase inhibitors (statins) is generally recommended and may reduce the overall cardiovascular risk. The aim of this study was to evaluate the lipid profile, statin administration and their relationship with arterial stiffness parameters in RTRs.MethodsThree hundred and forty-four stable RTRs (62.5% male) transplanted between 1994 and 2018 were randomly enrolled to the study. The following parameters of arterial stiffness was measured in each patient: ankle brachial index, carotid femoral pulse wave velocity (baPWV left and right, cfPWV) and pulse pressure (PP right and left). The study group was divided based on the use statins: 143 (41.6%) and 201 (58.4%). RTRs were qualified to the statin (+) and the statin (−) group, respectively.ResultsIn the statin (+) as compared to statin (−) group there were more patients with a CVD (32.9% vs. 14.9%) and diabetes (25.2% vs. 14.4%). In the whole study group, CVD was associated with a significant increase of both baPWV and cfPWV as well as PP (8.5 mmHg). There were significant differences in arterial stiffness parameters (baPWV, cfPWV, PP) between the statin (+) and the statin (−) group.ConclusionsArterial stiffness was increased in RTRs with CVD and hyperlipidemia. The control of hyperlipidemia was poor in RTRs.

Body height determines carotid stiffness following resistance exercise in young Japanese men.

Height is inversely associated with an increase in arterial stiffness after habitual resistance exercise (RE). Considering that RE is performed during exercise prescriptions, the association between height and the acute effects of RE on arterial stiffness should be clarified. We investigated the effects of height on arterial stiffness following transient RE. Thirty-nine young Japanese men were studied under parallel experimental conditions [sham control (seated rest) and RE (5 sets of 10 repetitions at 75% of one-repetition maximum)], which were randomly ordered on two separate days. The subjects were divided into tertiles of height (each group, n = 13). The β-stiffness index (index of arterial stiffness), assessed by carotid pulse pressure and distension, was measured in all subjects. A significant interaction between time, height, and RE was found for the β-stiffness index (P = 0.01). RE significantly increased the β-stiffness index in the lower-height group (P < 0.001), but not in the middle- and higher-height groups. Height was negatively associated with an increase in β-stiffness index following RE, even after controlling the confounders, including exercise volume and changes in heart rate and carotid pulse pressure (P = 0.003). The mediation analysis demonstrated a mediating effect of carotid distension on the relationship between height and changes in the β-stiffness index. These results suggest that short height individuals have increased arterial stiffness following RE due to decreased mechanical distension, rather than through the widening of pulsatile pressure.

High-frame-rate A-mode ultrasound for calibration-free cuffless carotid pressure: feasibility study using lower body negative pressure intervention

Purpose Existing technologies to measure central blood pressure (CBP) intrinsically depend on peripheral pressure or calibration models derived from it. Pharmacological or physiological interventions yielding different central and peripheral responses compromise the accuracy of such methods. We present a high-frame-rate ultrasound technology for cuffless and calibration-free evaluation of BP from the carotid artery. The system uses a pair of single-element ultrasound transducers to capture the arterial diameter and local pulse wave velocity (PWV) for the evaluation of beat-by-beat BP employing a novel biomechanical model. Materials and methods System’s functionality assessment was conducted on eight male subjects (26 ± 4 years, normotensive and no history of cardiovascular risks) by perturbing pressure via short-term moderate lower body negative pressure (LBNP) intervention (−40 mmHg for 1 min). The ability of the system to capture dynamic responses of carotid pressure to LBNP was investigated and compared against the responses of peripheral pressure measured using a continuous BP monitor. Results While the carotid pressure manifested trends similar to finger measurements during LBNP, the system also captured the differential carotid-to-peripheral pressure response, which corroborates the literature. The carotid diastolic and mean pressures agreed with the finger pressures (limits-of-agreement within ±7 mmHg) and exhibited acceptable uncertainty (mean absolute errors were 2.4 ± 3.5 and 2.6 ± 4.0 mmHg, respectively). Concurrent to the literature, the carotid systolic and pulse pressures (PPs) were significantly lower than those of the finger pressures by 11.1 ± 9.4 and 11.3 ± 8.2 mmHg, respectively (p < .0001). Conclusions The study demonstrated the method’s potential for providing cuffless and calibration-free pressure measurements while reliably capturing the physiological aspects, such as PP amplification and dynamic pressure responses to intervention.

FLOW MEDIATED DILATATION, CAROTID INTIMA MEDIA THICKNESS, ANKLE BRACHIAL PRESSURE INDEX AND PULSE PRESSURE IN YOUNG MALE POST MYOCARDIAL INFARCTION PATIENTS

Introduction:Due to increase in Coronary Artery Disease (CAD) at a younger age, we should try to diagnose atherosclerotic process and population at risk, at the earliest. Flow Mediated Dilatation (FMD), Carotid Intima-Media Thickness (CIMT) and Ankle-Brachial Pressure Index (ABI) are probable markers for early atherosclerosis and may be useful in coronary risk stratification Objectives: To compare and correlate the FMD, CIMT, ABI and Pulse Pressure (PP) in young male patients of Myocardial Infarction (MI) with age and sex matched healthy controls Method50 patients of MI aged ≤45 years, who presented to iccu of Department of Medicine Indira Gandhi medical college Nagpur India, were recruited consecutively for this case control study and same number of age and sex matched healthy controls were also analyzed. 3 days after Myocardial infarction FMD of the brachial artery, intima media thickness of carotid artery, ABPI and PP were measured in the cases and compared with healthy control Results: The FMD was lower among young patients of MI than controls . CIMT was higher among cases than controls . ABI was lower among cases than controls . Compared to controls, PP was higher among cases . In all subjects, a negative correlation between FMD and CIMT and a positive correlation between FMD and ABPI was found. A statistically significant negative correlation was found between endothelial dependent FMD and PP among cases and control groups Conclusion: Biophysical parameters were deranged in young post MI patients. Majority of our young male patients fell in low risk Framingham risk score but still they manifested with CAD. Despite 3 days of treatment among young male patients of MI, various biophysical parameters were stillderanged.

Ability of Carotid Corrected Flow Time to Predict Fluid Responsiveness in Patients Mechanically Ventilated Using Low Tidal Volume after Surgery.

Predicting fluid responsiveness in patients under mechanical ventilation with low tidal volume (VT) is challenging. This study evaluated the ability of carotid corrected flow time (FTc) assessed by ultrasound for predicting the fluid responsiveness during low VT ventilation. Patients under postoperative mechanical ventilation and clinically diagnosed with hypovolemia were enrolled. Carotid FTc and pulse pressure variation (PPV) were measured at VT of 6 and 10 mL/kg predicted body weight (PBW). FTc was calculated using both Bazett’s (FTcB) and Wodey’s (FTcW) formulas. Fluid responsiveness was defined as a ≥15% increase in the stroke volume index assessed by FloTrac/Vigileo monitor after administration of 8 mL/kg of balanced crystalloid. Among 36 patients, 16 (44.4%) were fluid responders. The areas under the receiver operating characteristic curves (AUROCs) for the FTcB at VT of 6 and 10 mL/kg PBW were 0.897 (95% confidence interval [95% CI]: 0.750–0.973) and 0.895 (95% CI: 0.748–0.972), respectively. The AUROCs for the FTcW at VT of 6 and 10 mL/kg PBW were 0.875 (95% CI: 0.722–0.961) and 0.891 (95% CI: 0.744–0.970), respectively. However, PPV at VT of 6 mL/kg PBW (AUROC: 0.714, 95% CI: 0.539–0.852) showed significantly lower accuracy than that of PPV at VT of 10 mL/kg PBW (AUROC: 0.867, 95% CI: 0.712–0.957; p = 0.034). Carotid FTc can predict fluid responsiveness better than PPV during low VT ventilation. However, further studies using automated continuous monitoring system are needed before its clinical use.

Baroreflex Sensitivity Assessment: How Many Sit‐Stand Maneuvers to Evaluate Cardiovascular Disease Risk?

OBJECTIVE Although recent evidence suggests that 15 cycles of repeated sit-stand maneuvers may be a useful method for baroreflex sensitivity (BRS) assessment, it remains unclear how many times the maneuver should be performed to estimate BRS for cardiovascular disease (CVD) risk assessment with minimal effort. The purpose of this study was to explore the minimal cycles of sit-stand maneuvers for BRS assessment. We hypothesized that less than 15 cycles of repeated sit-stand maneuvers can evaluate the BRS for CVD risk assessment. METHODS 183individuals (62 ± 12 years, 72% Women) were analyzed cross-sectionally in this study. In the assessment of BRS, the beat-to-beat changes of R-R interval and SBP were measured during 1) 5 minutes of resting seat condition and 2) 5 minutes of the repeated sit-stand maneuvers at 0.05 Hz (i.e. 15 cycles of 10-second sit and 10-second stand). BRS gain, power spectral density (PSD) of R-R interval and SBP were calculated from the 6 conditions: seated rest, 3, 6, 9, 12, 15 cycles of the repeated sit-stand maneuvers using spectral and transfer function analyses. In addition to traditional CVD risk measurements, including hemodynamics and blood biomarker measures, carotid distensibility was calculated from carotid pulse pressure and intra-beat changes of carotid diameter. The associations of age and carotid distensibility with BRS gains calculated from the 6 conditions were tested through partial correlation analysis adjusted for sex. The partial correlation coefficients were compared by Fisher r-to-z transformation analysis. RESULTS The PSDs of R-R interval and SBP were progressively increased as the cycles of repeated sit-stand maneuvers increased. The BRS gains calculated from all the 6 conditions were negatively associated with age and carotid distensibility (all tests were P < 0.001). The BRS gain calculated from the 6 cycles and over of repeated sit-stand maneuvers were strongly associated with age and carotid distensibility compared to the equivalents calculated from the seated rest and 3 cycles of repeated sit-stand maneuvers (P < 0.05). The strength of the correlation did not increase with the greater number of 6 cycles of sit-stand maneuvers. Furthermore, forward stepwise regression analysis showed that age, sex, carotid distensibility, brachial systolic pressure, heart rate, and HDL-cholesterol were selected as the covariates of BRS gains calculated from 6 cycles of the sit-stand maneuvers, and these covariates explained over 60% variance of the BRS gain. CONCLUSION Our results suggest that BRS gain calculated from at least 6 cycles of repeated sit-stand maneuvers is strongly associated with CVD risk factors. We also observed that variabilities of R-R interval and SBP progressively increased as the number of sit-stand cycles increased.

Physical activity is associated with lower pulsatile stress but not carotid stiffness in children.

The cardiovascular disease (CVD) process may begin early in life when accompanied by atherosclerotic risk factors. CVD risk factors in children are associated with stiffening of the large elastic arteries, a reflection of subclinical atherosclerosis. Physical activity is a preventative lifestyle strategy that may benefit arterial stiffness by attenuating the hemodynamic stress on the artery wall. This study examined the relations between physical activity, carotid pulsatile stress, and carotid stiffness in children. One hundred and forty children (9-11 yrs; 50.0% male, 57.9% African American, 42.10% Caucasian, body mass index (BMI) 20.1±4.7 kg/m2) participated in this study. Physical activity counts were measured using a wrist-worn accelerometer and averaged over 7 days. Carotid artery β-stiffness and pulse pressure (calibrated to brachial mean and diastolic pressure) were assessed as via ultrasound and tonometry, respectively. Pulsatile stress was calculated as the product of carotid pulse pressure and heart rate. Physical activity counts were correlated with pulsatile stress (r= -0.27), and BMI (r= -0.23), but were unrelated to carotid stiffness. In multivariate models, associations between physical activity counts and pulsatile stress remained (B= -1.3 [95%CI, -2.4, -0.2], β= -0.20, p<0.05) after covariate adjustment for age, race, sex, pubertal stage and BMI. Carotid pulsatile stress was related to regional carotid stiffness (r=0.45, p<0.05). These data suggest that higher levels of physical activity at young age are associated with lower hemodynamic stress in the carotid artery. Findings are discussed in the context of an inverse relationship between hemodynamic pulsatile stress and carotid stiffness in children.

Carotid pulse pressure and intima media thickness are independently associated with cerebral hemodynamic pulsatility in community-living older adults.

Vascular aging is associated with markers of cerebrovascular impairment. Whether discrete characteristics of arterial structure and function have independent and/or additive effects on cerebral hemodynamics, however, is not completely understood. We examined the association of cerebral hemodynamics with common carotid artery intima-media thickness (IMT) and pulse pressure (PP) in 61 older adults with prevalent cardiometabolic risk but no history of cerebrovascular disease. We calculated pulsatility index (PI) and hypercapnic reactivity of the middle cerebral artery, as well as global blood flow through the extracranial arteries. The dominant effects were related to hemodynamic pulsatility. In adults with metabolic syndrome, PI was related to IMT (r = 0.48, P = 0.003) after adjustment for age and sex. Without metabolic syndrome, PI was directly related to PP (r = 0.63, P = 0.003). Across the whole cohort, PP [β (95%CI) = 0.42 (0.18, 0.67), P = 0.001] and IMT [0.42 (0.18, 0.67), P < 0.001] remained significant predictors of PI, after accounting for individual cardiometabolic risk factors. The independent and combined effects of IMT and PP were tested by binarizing PP and IMT at the sample median. Participants with both IMT and PP above their respective medians had elevated PI compared with those with both vascular markers below the median [median (interquartile range) = 1.06 (0.22) vs. 0.84 (0.14), P = 0.003)]. PI was not different from the low risk group if only one of IMT or PP were above the median. Although overall vascular burden was low, moderate associations with PI persisted, suggesting pulsatile characteristics represent one of the earliest markers linking vascular aging to changes in brain health.

Perturbations of pulsatile hemodynamics and clinical outcomes in patients with acute heart failure and reduced, mid-range or preserved ejection fraction.

BackgroundHeart failure with mid-range ejection fraction (HFmrEF) has been proposed as a new phenotype of heart failure. We therefore investigated the pulsatile hemodynamic characteristics and outcomes in patients with HFmrEF, in comparison with those with reduced (HFrEF) or preserved (HFpEF) ejection fraction.MethodsThe study was composed of two cohorts of patients hospitalized due to acute heart failure. Pulsatile hemodynamic measures, including carotid-femoral pulse wave velocity (cf-PWV), carotid pulse pressure (cPP), amplitude of the backward pressure wave (Pb) and carotid augmentation index (cAIx), were recorded on admission and before discharge in Cohort A (n = 230, mean age 69.9 ±15.4 years), and long-term follow-up was performed in Cohort B (n = 2677, mean age 76.3 ± 33.4 years).ResultsIn Cohort A, patients with HFmrEF had persistently greater cf-PWV, cPP, Pb, and cAI than those with HFrEF, both on admission and before discharge. In contrast, patients with HFmrEF and HFpEF had similar pulsatile hemodynamic characteristics. In cohort B, patients with HFmrEF and HFrEF had similar three-year mortality rates and both were significantly higher than that in patients with HFpEF (both P values < 0.05).ConclusionsPatients with HFmrEF were characterized by a worse left ventricular systolic function than patients with HFpEF and excessive wave reflections than patients with HFrEF. Future studies are required to confirm that the unfavorable ventriculo-arterial coupling in HFmrEF might play a role in the pathogenesis of high long-term mortality in these patients.

THE RELATIONSHIP BETWEEN DIALYSIS MODALITY, ARTERIOVENOUS FISTULA AND HEMODYNAMIC PARAMETERS OF ARTERIAL RESERVOIR-WAVE ANALYSIS

Objective: Arterial reservoir-wave analysis (RWA) is a new model of arterial hemodynamics that separates the arterial wave into reservoir pressure (RP) and excess pressure (XSP). Whether RWA parameters are different in hemodialysis (HD), as compared to peritoneal dialysis (PD), and whether any differences are due to the presence of an arteriovenous fistula (AVF) remains unknown. The aims of the present study were to examine the differences in RWA 1) in HD versus PD patients and 2) in all dialysis patients (HD+PD) without AVF versus HD patients with AVF. Design and method: In a cross-sectional analysis of prevalent PD (n = 53) and HD (n = 208) patients, RWA was performed using pressure approach applied to the carotid pressure, which was calibrated with mean arterial pressure and used as a surrogate for central pressure. Among HD patients, 115 patients used AVF as vascular access. Results: In HD patients, diastolic blood pressure (BP) was lower (69 ± 14 vs 77 ± 10, mmHg, p < 0.001), while systolic BP was identical, resulting in increased carotid pulse pressure (PP) (58 ± 22 vs 50 ± 22 mm Hg, p = 0.036). Carotid RP and XSP integrals were higher in HD patients (2.11 ± 0.91 vs 1.89 ± 0.94, p = 0.027; 0.48 ± 0.30 vs 0.39 ± 0.27, p = 0.009). While there were no significant differences in BP medication between groups. HD patients were older and had a higher prevalence of clinical comorbidities such as diabetes and established cardiovascular disease. However, analysis of data according to AVF status resulted in homogenous groups in terms of age and comorbidities. In AVF group, dialysis vintage was higher (median 2.3 vs 1.1 years, p < 0.001), diastolic BP lower (68 ± 13 vs 72 ± 13 mm Hg, p = 0.003), PP higher (59 ± 22 vs 54 ± 22, p = 0.061), and RP and XSP integrals were higher (2.2 ± 0.9 vs 2.0 ± 0.9, p = 0.048; 0.5 ± 0.3 vs 0.4 ± 0.3, p = 0.078). After adjustment for dialysis vintage, XSP was significantly higher in AVF group (p = 0.034). Conclusions: In HD patients, RP and XSP integral were higher as compared to PD patients, but these differences were mainly due to the presence of AVF.

Early Wave Reflection and Pulse Wave Velocity Are Associated with Diastolic Dysfunction in Rheumatoid Arthritis.

Rheumatoid arthritis (RA) impacts arterial and diastolic function. This study examined whether arterial properties can determine diastolic function in RA. In 173 RA patients, arterial function measures including carotid femoral pulse wave velocity (PWV), central systolic and pulse pressure, pulse pressure amplification, and the magnitude and timing of the forward and reflected waves were measured using applanation tonometry. Diastolic function parameters including the ratio of early-to-late transmitral velocity (E/A) and ratio of E to the mean of the lateral and septal wall myocardial tissue lengthening (e') were measured using echocardiography. The timing of the reflected wave was associated with E/A; PWV was related to E/e'. The timing of the reflected wave, forward wave magnitude, and pulse pressure amplification were associated with impaired relaxation; PWV was related to increased left ventricular (LV) filling pressure. Early wave reflection and PWV are associated with LV-impaired relaxation and increased filling pressure, respectively, in RA.

Vascular Contributions to Intracranial Hemodynamic Pulsatility and Pulsatile Dampening in Adults

The brain is a high‐flow organ that requires continuous, non‐pulsatile blood flow. Intracranial blood flow pulsatility depends on the ability of the large elastic arteries and cerebrovasculature to dampen pulsatile hemodynamics transmitted from the heart. Aging is accompanied by large artery stiffening and reductions in cerebrovascular dampening, ultimately increasing intracranial pulsatility. It is unclear what hemodynamic forces may be responsible for these age‐related changes in the transmission and dampening of intracranial pulsatility across the lifespan. The purpose of this study was to explore hemodynamic contributors to intracranial pulsatility and pulsatile dampening in 244 adults between 35–85 yr (49% female, 56±12 yr, 27±4.2 kg/m2). Intracranial pulsatile dampening was calculated as the ratio between common carotid and middle cerebral artery (MCA) blood velocity pulsatility index (PI) measured via Doppler. Carotid ultrasound and wave intensity analysis were used to measure carotid diameter, forward compression wave energy (W1), wave reflection index (RIx), and forward traveling expansion wave (W2). Aortic (carotid‐femoral) and carotid pulse wave velocity (PWV) were assessed via tonometry and carotid ultrasound, respectively, and expressed as a ratio (aortic:carotid PWV). Carotid pulse pressure (PP) was measured via tonometry. Multiple regression was used to examine the contributions of 1) age, sex, BMI, aortic:carotid PWV, carotid diameter, PP, and W1 to intracranial pulsatility (MCA PI); and 2) age, sex, BMI, aortic:carotid PWV, carotid diameter, RIx, and W2 to intracranial pulsatile dampening. After entering all variables, significant predictors of MCA PI included age (β,0.44), aortic:carotid PWV (β,0.16), PP (β,0.29), and W1 (β,0.20; R2=0.50, p&lt;0.01). Significant predictors of intracranial pulsatile dampening included age (β,−0.47), sex (β,−0.43), and RIx (β,0.26; R2=0.53, p&lt;0.01). Our data confirms recent literature linking age, exaggerated stiffening of the aorta compared to carotid artery, and extracranial hemodynamics to intracranial pulsatility in the MCA. Moreover, our findings indicate age, sex, and wave reflections in the carotid artery impact the ability of the cerebrovasculature to dampen transmission of pulsatile hemodynamics. These data highlight the potential utility of the large extracranial arteries as therapeutic targets to reduce intracranial pulsatility and importance of carotid wave reflections in dampening intracranial pulsatility.Support or Funding InformationFunded in part by an ACSM Foundation Research Grant (WKL), AHA Predoctoral Fellowship (WKL), and Dairy Research Institute/Dairy management Inc. Grant 1154 (KSH).This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.