Abstract 330: Ethnic Variability in the Association of Pulse Pressure with Adhesion Pathway Proteins: The Multi-Ethnic Study of Atherosclerosis (MESA) Study

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Cecilia Berardi ◽  
Michael Tsai ◽  
James S Pankow ◽  
Michele Sale ◽  
Mariza de Andrade ◽  
...  
Keyword(s):  
African Americans ◽  
Arterial Stiffness ◽  
Pulse Pressure ◽  
Matrix Remodeling ◽  
Large Artery ◽  
Adhesion Protein ◽  
Ethnic Study ◽  
Artery Stiffness ◽  
Ethnic Variability ◽  
The Difference

Pulse pressure (PP), defined as the difference between systolic and diastolic blood pressure, is considered a marker of large artery stiffness and has been shown to independently predict cardiovascular disease. Differences among ethnicities with regard to PP have been previously described, yet the underlying biological mechanisms are poorly understood. In addition, biomarkers of inflammation and matrix remodeling have been shown to be involved in the development of arterial stiffness. The aim of this study was to investigate the role of adhesion pathway components in the development of arterial stiffness measured by PP among four ethnicities. E-cadherin, HGF, L-selectin, P-selectin, 6-Ckine, MMP1, MMP2, RANTES, SDF1, SLPI, TGFβ1, TIMP2 and VCAM were measured in a random sample of 2402 participants (579 African Americans, 619 Caucasians, 600 Chinese and 604 Hispanics) in the Multi-Ethnic Study of Atherosclerosis (MESA) study at Exam 2. PP was measured concurrently and its association with each adhesion protein level was assessed via linear regression in each ethnicity. All analyses were adjusted for age, sex, and traditional cardiovascular risk factors. Mean PP was significantly different among ethnicities: 55.9±18.0 mmHg in African Americans, 52.1± 16.1 mmHg in Caucasians, 51.4±16.4 mmHg in Chinese, and 55.0±17.5 in Hispanics, p<0.001. MMP2 was positively associated with PP among African Americans (β=2.3 (0.6), p<0.001) and Caucasians (β=1.7 (0.5), p=0.001); TIMP2 among Caucasians (β=1.5 (0.5), p=0.002) and to a lesser extent among African Americans (β=1.2 (0.6) p=0.050) and Chinese (β=1.3 (0.6), p=0.034). SDF1 was associated to PP in African Americans (β=1.4 (0.6), p=0.017) and in Chinese (β=1.1 (0.5), p=0.042); finally an association existed between TGFβ1 and PP in C (β=1.1 (0.5), p=0.025). None of the studied proteins was associated with PP in Hispanics. In conclusion, components of the adhesion pathway were correlated to PP in this large multi-ethnic cohort, possibly giving new insight on the pathophysiology of arterial stiffness. In addition, heterogeneity by ethnicity suggests different mechanisms in the development of arterial stiffness.

scholarly journals Effects of pacing modality on noninvasive assessment of heart rate dependency of indices of large artery function

2016 ◽  
Vol 121 (3) ◽  
pp. 771-780 ◽  
Author(s):  
Isabella Tan ◽  
Hosen Kiat ◽  
Edward Barin ◽  
Mark Butlin ◽  
Alberto P. Avolio
Keyword(s):  
Heart Rate ◽  
Arterial Stiffness ◽  
Pulse Pressure ◽  
Wave Reflection ◽  
Pulse Wave ◽  
Augmentation Index ◽  
Large Artery ◽  
Rate Dependency ◽  
Wave Reflections

Studies investigating the relationship between heart rate (HR) and arterial stiffness or wave reflections have commonly induced HR changes through in situ cardiac pacing. Although pacing produces consistent HR changes, hemodynamics can be different with different pacing modalities. Whether the differences affect the HR relationship with arterial stiffness or wave reflections is unknown. In the present study, 48 subjects [mean age, 78 ± 10 (SD), 9 women] with in situ cardiac pacemakers were paced at 60, 70, 80, 90, and 100 beats per min under atrial, atrioventricular, or ventricular pacing. At each paced HR, brachial cuff-based pulse wave analysis was used to determine central hemodynamic parameters, including ejection duration (ED) and augmentation index (AIx). Wave separation analysis was used to determine wave reflection magnitude (RM) and reflection index (RI). Arterial stiffness was assessed by carotid-femoral pulse wave velocity (cfPWV). Pacing modality was found to have significant effects on the HR relationship with ED ( P = 0.01), central aortic pulse pressure ( P = 0.01), augmentation pressure ( P < 0.0001), and magnitudes of both forward and reflected waves ( P = 0.05 and P = 0.003, respectively), but not cfPWV ( P = 0.57) or AIx ( P = 0.38). However, at a fixed HR, significant differences in pulse pressure amplification ( P < 0.001), AIx ( P < 0.0001), RM ( P = 0.03), and RI ( P = 0.03) were observed with different pacing modalities. These results demonstrate that although the HR relationships with arterial stiffness and systolic loading as measured by cfPWV and AIx were unaffected by pacing modality, it should still be taken into account for studies in which mixed pacing modalities are present, in particular, for wave reflection studies.

Abstract P253: Relation Between Microvascular Function and Large Artery Stiffness in African American Diabetic Patients

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Ajibola M Adedayo ◽  
Ayobami Eluwole ◽  
Fasika Tedla ◽  
Arye Kremer ◽  
Nicole Mastrogiovanni ◽  
...  
Keyword(s):  
African Americans ◽  
Glycemic Control ◽  
Vascular Complications ◽  
Microvascular Dysfunction ◽  
Microvascular Function ◽  
Reactivity Index ◽  
Entire Group ◽  
Diabetic Patients ◽  
Large Artery ◽  
Artery Stiffness

Rationale: Diabetes is highly prevalent among African Americans and poses a higher risk for vascular complications in this population. Although socioeconomic factors are well known to influence outcomes, true biologic differences in risk factor vulnerability have been suggested. Vascular complications have been traditionally viewed as either macrovascular (myocardial infarction and stroke) or microvascular (retinopathy, nephropathy, and neuropathy). Better glycemic control is known to improve microvascular but not macrovascular complications. In recent years, there has been a growing appreciation that microvascular dysfunction may promote large artery disease and vice versa. Given this notion of vascular “cross-talk” and since subclinical dysfunction is known to precede target organ damage, the objective of this study was to determine whether subclinical microvascular dysfunction is related to large artery stiffness. Methods: A total of 141 patients with type II diabetes were recruited from our outpatient clinics over a 6 month period. Medical information was obtained via patient interview and electronic medical record review including laboratory results. Microvascular function was assessed by the vascular reactivity index (VRI), which assesses changes in digital temperature before and after release of arterial cuff occlusion (VENDYS 5000BC DTM system Endothelix, Inc.). Large artery stiffness was assessed by carotid-femoral pulse wave velocity (PWV) using applanation tonometry (Sphygmocor, Atcor Inc.). Results: Mean age was 60 + 8 years, 64% were female. 80% had hypertension and 90% had dyslipidemia. 15% had chronic kidney disease. Mean HbA1C levels were 8.1 + 2.2%. For the entire group, VRI was significantly correlated with PWV (r=.27, p=.002). On multivariate analysis, VRI was independently associated with PWV (β=-1.0, p=.001) and a trend towards an association with HbA1c (β =.07, p=.09) after adjusting for traditional cardiovascular risk factors. Conclusions: Among African Americans with diabetes, subclinical microvascular dysfunction is significantly correlated to large artery stiffness and possibly to glycemic control. Further study is needed to clarify mediating factors of these relationships.

scholarly journals Race/Ethnicity-Specific Associations between Smoking, Serum Leptin, and Abdominal Fat: The Multi-Ethnic Study of Atherosclerosis

2018 ◽  
Vol 28 (4) ◽  
pp. 531-538
Author(s):  
Sina Kianoush ◽  
Andrew P. DeFilippis ◽  
Carlos J. Rodriguez ◽  
Mahmoud Al Rifai ◽  
Emelia J. Benjamin ◽  
...  
Keyword(s):  
African Americans ◽  
Abdominal Fat ◽  
Linear Regression Models ◽  
Serum Leptin ◽  
Ethnic Study ◽  
Outcomes Measures ◽  
Former Smokers ◽  
Race Ethnicity ◽  
The Difference ◽  
Never Smokers

Objective: Smoking is a well-known cardio­vascular risk factor associated with weight loss. We aimed to evaluate the association between smoking, serum leptin levels, and abdominal fat.Design: Cross-sectionalSetting: Data from examinations 2 or 3 (2002-2005) of the Multi-Ethnic Study of Atherosclerosis (MESA)Participants: 1,875 asymptomatic, commu­nity-dwelling adultsMain Outcomes Measures: We used multivariable linear regression models to assess the race/ethnicity-specific associations between smoking, serum loge-leptin levels, and computed tomography ascertained abdominal fat. Results were adjusted for de­mographic and relevant clinical covariates.Results: Participants (mean age 64.5±9.6 years; 50.6% women; 42.2% former, 11.4% current smokers) were White (40.1%), His­panic (25.8%), African American (21.1%), and Chinese (13.0%). Overall, median (25th – 75th percentile) leptin levels were signifi­cantly lower among current (11.14 ng/mL; 4.13 – 26.18) and former smokers (11.68 ng/mL; 4.72 – 27.57), as compared with never smokers (15.61 ng/mL; 3.05 – 30.12) (P<.001). The difference in median leptin levels between current and never smok­ers were significantly higher for Hispan­ics (Δ9.64 ng/mL) and African Americans (Δ8.81 ng/mL) than Whites (Δ2.10 ng/mL) and Chinese (Δ4.70 ng/mL) (P<.001). After adjustment for total abdominal fat, loge- leptin levels remained lower for former (-.14 [-.22 – -.07]) and current (-.17 [-.28 – -.05]) smokers, compared with never smokers. Results differed by race/ethnicity, with signif­icantly lower loge-leptin levels observed only among current and former African Ameri­cans and Hispanic smokers, compared with their never smoker counterparts. (Ps for interaction <.05)Conclusions: Among smokers, leptin levels significantly vary by race/ethnicity. Former and current smoking are associ­ated with lower leptin levels, although this may be restricted to Hispanics and African Americans. Ethn Dis. 2018;28(4):531-538; doi:10.18865/ed.28.4.531

scholarly journals Folic acid supplementation for 3 wk reduces pulse pressure and large artery stiffness independent of MTHFR genotype

2005 ◽  
Vol 82 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Carolyn Williams ◽  
Bronwyn A Kingwell ◽  
Kevin Burke ◽  
Jane McPherson ◽  
Anthony M Dart
Keyword(s):  
Folic Acid ◽  
Pulse Pressure ◽  
Folic Acid Supplementation ◽  
Large Artery ◽  
Acid Supplementation ◽  
Mthfr Genotype ◽  
Artery Stiffness

scholarly journals Folic acid supplementation for 3 wk reduces pulse pressure and large artery stiffness independent of MTHFR genotype

2005 ◽  
Vol 82 (1) ◽  
pp. 26-31 ◽  
Author(s):  
Carolyn Williams ◽  
Bronwyn A Kingwell ◽  
Kevin Burke ◽  
Jane McPherson ◽  
Anthony M Dart
Keyword(s):  
Folic Acid ◽  
Pulse Pressure ◽  
Folic Acid Supplementation ◽  
Large Artery ◽  
Acid Supplementation ◽  
Mthfr Genotype ◽  
Artery Stiffness

Carotid Artery Stiffness Mechanisms Associated With Cardiovascular Disease Events and Incident Hypertension: the MESA

Hypertension ◽  
2022 ◽  
Author(s):  
Ryan J. Pewowaruk ◽  
Claudia Korcarz ◽  
Yacob Tedla ◽  
Gregory Burke ◽  
Philip Greenland ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Elastic Modulus ◽  
Arterial Stiffness ◽  
The United States ◽  
Hazard Ratio ◽  
Structural Stiffness ◽  
Cox Models ◽  
Artery Stiffness ◽  
The Difference

Background: Elastic arteries stiffen via 2 main mechanisms: (1) load-dependent stiffening from higher blood pressure and (2) structural stiffening due to changes in the vessel wall. It is unknown how these different mechanisms contribute to incident cardiovascular disease (CVD) events. Methods: The MESA (Multi-Ethnic Study of Atherosclerosis) is a longitudinal study of 6814 men and women without CVD at enrollment, from 6 communities in the United States. MESA participants with B-mode carotid ultrasound and brachial blood pressure at baseline Exam in (2000–2002) and CVD surveillance (mean follow-up 14.3 years through 2018) were included (n=5873). Peterson’s elastic modulus was calculated to represent total arterial stiffness. Structural stiffness was calculated by adjusting Peterson’s elastic modulus to a standard blood pressure of 120/80 mm Hg with participant-specific models. Load-dependent stiffness was the difference between total and structural stiffness. Results: In Cox models adjusted for traditional risk factors, load-dependent stiffness was significantly associated with higher incidence of CVD events (hazard ratio/100 mm Hg, 1.21 [95% CI, 1.09–1.34] P <0.001) events while higher structural stiffness was not (hazard ratio, 1.03 [95% CI, 0.99–1.07] P =0.10). Analysis of participants who were normotensive (blood pressure <130/80, no antihypertensives) at baseline exam (n=2122) found higher load-dependent stiffness was also associated with significantly higher incidence of hypertension (hazard ratio, 1.53 [95% CI, 1.35–1.75] P <0.001) while higher structural stiffness was not (hazard ratio, 1.03 [95% CI, 0.99–1.07] P =0.16). Conclusions: These results provide valuable new insights into mechanisms underlying the association between arterial stiffness and CVD. Load-dependent stiffness was significantly associated with CVD events but structural stiffness was not.

Association of obesity with arterial stiffness: The Multi-Ethnic Study of Atherosclerosis (MESA)

2020 ◽  
Vol 25 (4) ◽  
pp. 309-318
Author(s):  
Jeongok G. Logan ◽  
Hyojung Kang ◽  
Soyoun Kim ◽  
Daniel Duprez ◽  
Younghoon Kwon ◽  
...  
Keyword(s):  
Risk Factors ◽  
Arterial Stiffness ◽  
Augmentation Index ◽  
Large Artery ◽  
Cvd Risk Factors ◽  
Small Artery ◽  
Cvd Risk ◽  
Ethnic Study ◽  
Interaction With Age ◽  
The Relationship

Arterial stiffness (AS) and obesity are recognized as important risk factors of cardiovascular disease (CVD). The purpose of this study was to investigate the relationship between AS and obesity. AS was defined as high augmentation index (AIx) and low elasticity (C1, large artery elasticity; C2, small artery elasticity) in participants enrolled in the Multi-Ethnic Study of Atherosclerosis at baseline. We compared AIx, C1, and C2 by body mass index (BMI) (< 25, 25–29.9, 30–39.9, ⩾ 40 kg/m2) and waist–hip ratio (WHR) (< 0.85, 0.85–0.99, ⩾ 1). The obesity–AS association was tested across 10-year age intervals. Among 6177 participants (62 ± 10 years old, 52% female), a significant inverse relationship was observed between obesity and AS. After adjustments for CVD risk factors, participants with a BMI > 40 kg/m2 had 5.4% lower AIx (mean difference [Δ] = −0.82%; 95% CI: –1.10, –0.53), 15.4% higher C1 (Δ = 1.66 mL/mmHg ×10; 95% CI: 1.00, 2.33), and 40.2% higher C2 (Δ = 1.49 mL/mmHg ×100; 95% CI: 1.15, 1.83) compared to those with a BMI < 25 kg/m2 (all p for trend < 0.001). Participants with a WHR ⩾ 1 had 5.6% higher C1 (∆ = 0.92 mL/mmHg ×10; 95% CI: 0.47, 1.37) compared to those with a WHR < 0.85. The WHR had a significant interaction with age on AIx and C2, but not with BMI; the inverse relationships of the WHR with AIx and C2 were observed only in participants < 55 years between the normal (WHR < 0.85) and the overweight (0.85 ⩽ WHR < 0.99) groups. Different associations of WHR and BMI with arterial stiffness among older adults should be further investigated.

scholarly journals Morning blood pressure surge is associated with arterial stiffness and sympathetic baroreflex sensitivity in hypertensive seniors

2013 ◽  
Vol 305 (6) ◽  
pp. H793-H802 ◽  
Author(s):  
Yoshiyuki Okada ◽  
M. Melyn Galbreath ◽  
Shigeki Shibata ◽  
Sara S. Jarvis ◽  
Tiffany B. Bivens ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Stiffness ◽  
Baroreflex Sensitivity ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Large Artery ◽  
Artery Stiffness ◽  
Morning Blood Pressure Surge ◽  
Morning Blood Pressure ◽  
Normotensive Subjects

Morning blood pressure (BP) surge is considered to be an independent risk factor for cardiovascular diseases. We tested the hypothesis that increased large-artery stiffness and impaired sympathetic baroreflex sensitivity (BRS) contribute to augmented morning surge in elderly hypertensive subjects. Morning surge was assessed as morning systolic BP averaged for 2 h just after waking up minus minimal sleeping systolic BP by using ambulatory BP monitoring (ABPM) in 40 untreated hypertensive [68 ± 1 (SE) yr] and 30 normotensive (68 ± 1 yr) subjects. Beat-by-beat finger BP and muscle sympathetic nerve activity (MSNA) were recorded in the supine position and at 60° upright tilt. We assessed arterial stiffness with carotid-to-femoral pulse wave velocity (cfPWV) and sympathetic BRS during spontaneous breathing. Awake and asleep ABPM-BPs and morning surge were higher in hypertensive than normotensive subjects (all P < 0.001). cfPWV was higher ( P = 0.002) and sympathetic BRS was lower ( P = 0.096) in hypertensive than normotensive subjects. Hypertensive subjects with morning surge ≥35 mmHg (median value) had higher cfPWV (11.9 ± 0.5 vs. 9.9 ± 0.4 m/s, P = 0.002) and lower sympathetic BRS (supine: −2.71 ± 0.25 vs. −3.73 ± 0.29, P = 0.011; upright: −2.62 ± 0.22 vs. −3.51 ± 0.35 bursts·100 beats−1·mmHg−1, P = 0.052) than those with morning surge <35 mmHg. MSNA indices were similar between groups (all P > 0.05), while upright total peripheral resistance was higher in hypertensive subjects with greater morning surge than those with lesser morning surge ( P = 0.050). Morning surge was correlated positively with cfPWV ( r = 0.59, P < 0.001) and negatively with sympathetic BRS ( r = 0.51, P < 0.001) in hypertensive subjects only. Thus, morning BP surge is associated with arterial stiffness and sympathetic BRS, as well as vasoreactivity during orthostasis in hypertensive seniors.

scholarly journals Effect of Estrogen Replacement Therapy on Insulin Sensitivity of Glucose Metabolism and Preresistance and Resistance Vessel Function in Healthy Postmenopausal Women1

2000 ◽  
Vol 85 (12) ◽  
pp. 4663-4670 ◽  
Author(s):  
Satu Vehkavaara ◽  
Jukka Westerbacka ◽  
Tiina Hakala-Ala-Pietilä ◽  
Antti Virkamäki ◽  
Outi Hovatta ◽  
...  
Keyword(s):  
Blood Flow ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Arterial Stiffness ◽  
Peripheral Blood ◽  
Whole Body ◽  
Peripheral Blood Flow ◽  
Large Artery ◽  
Before And After ◽  
Artery Stiffness

In the present study, we hypothesized that estradiol, via its ability to vasodilate in an endothelium-dependent manner, might enhance vascular effects of insulin. Basal and insulin-stimulated peripheral blood flow and resistance, arterial stiffness, and glucose metabolism were determined in 27 healthy postmenopausal women before and after 12 weeks of treatment with either transdermal or oral estradiol or corresponding placebo preparations. Whole body insulin sensitivity was determined using the euglycemic insulin clamp technique (rate of continuous insulin infusion 1 mU/kg·min), forearm blood flow with a strain-gauge plethysmography, and arterial stiffness using pulse wave analysis. Estradiol therapy increased basal peripheral blood flow (1.5 ± 0.1 vs. 1.9 ± 0.1 mL/dL·min, 0 vs. 12 weeks; P &lt; 0.01), decreased peripheral vascular resistance (65 ± 3 vs. 52± 3 mm Hg/mL/dL·min, respectively; P &lt; 0.01), and diastolic blood pressure (78 ± 2 vs. 75± 2 mm Hg, respectively; P &lt; 0.05) but had no effect on large artery stiffness. Infusion of insulin did not acutely alter peripheral blood flow but diminished large artery stiffness significantly both before and after the 12-week period of estradiol therapy. No measure of acute insulin action (glucose metabolism, blood flow, or large artery stiffness) was altered by estradiol or placebo treatment. These data demonstrate that insulin and estradiol have distinct hemodynamic effects. Physiological doses of estradiol increase peripheral blood flow but have no effects on large artery stiffness, whereas physiological concentrations of insulin acutely decrease stiffness without changing peripheral blood flow. Putative vasculoprotection by estradiol is, thus, not mediated via alterations in arterial stiffness or insulin sensitivity.

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