I029 The regulation of large artery stiffness by the vascular endothelium includes the control of arterial wall viscosity

Older age is associated with elevated large elastic artery stiffness, a strong predictor of cardiovascular (CVD) risk in middle-age/older (MA/O) adults independent of blood pressure (BP). Greater 24-hour systolic BP variability (BPV) is also an independent risk factor for CVD and is linked to large artery stiffness in MA/O adults with hypertension and diabetes. However, its relation to age-related arterial stiffness in adults with low risk factor burden is unclear. We hypothesized that higher systolic BPV would be: 1) associated with advancing age, and 2) related to elevated aortic and carotid artery stiffness among healthy MA/O adults. To determine this, 98 healthy adults (ages 19-70 yrs) with measurements of systolic BPV (standard deviation of 24 hr systolic BP) via ambulatory BP monitoring, aortic stiffness (carotid-femoral pulse wave velocity, cfPWV), carotid artery stiffness (β-stiffness via carotid tonometry/B mode ultrasound) and circulating metabolic factors were included. In the entire cohort, greater systolic BPV was not associated with age, cfPWV, carotid β stiffness or circulating lipids/glucose (all P>0.05), but was correlated (age-adjusted) with 24 hr systolic BP (r= 0.41, P<0.001) and BMI (r= 0.21, P<0.05). In stepwise linear regression analyses that included age, sex, BMI, only 24 hr systolic BP was associated with systolic BPV (β= 0.14 ± 0.03, Model R 2 = 0.20, P< 0.001). Interestingly, there was no difference in 24 hr systolic BPV (11.4 ± 0.4 vs 11.4 ± 0.5 SD mmHg, P=0.99) in young (n=55; 29.0 ± 0.7 yrs) vs. MA/O (n= 43; 53.0 ± 1.2 yrs) adults despite higher cfPWV (594 ± 12 vs 913 ± 39 cm/sec, P<0.001), carotid β-stiffness (6.8 ± 0.6 vs 9.3 ±0.9 U, P=0.001) and 24 hr systolic BP (121 ± 1 vs 125 ± 2 mmHg, P<0.05). Systolic BPV was associated with BMI (r= 0.42, p< 0.01) and fasting blood glucose (r= 0.54, P= 0.001) in MA/O but not young adults. In a stepwise linear regression model among MA/O, 24 hr systolic BP (β= 0.18 ± 0.04, R 2 = 0.36, P<0.001) and fasting glucose (β= 0.10 ± 0.05, R 2 change= 0.07, P<0.001) were the only significant correlates of systolic BPV (Model R 2 = 0.43, P<0.001). In conclusion, 24 hr systolic BP and fasting blood glucose, but not age or large elastic artery stiffness, were the strongest determinants of higher systolic BPV in normotensive MA/O adults.

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

Hypertension ◽

10.1161/hyp.70.suppl_1.p253 ◽

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.

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Association of HIV-infection, antiretroviral treatment and metabolic syndrome with large artery stiffness: a cross-sectional study

BMC Infectious Diseases ◽

10.1186/s12879-018-3637-0 ◽

2018 ◽

Vol 18 (1) ◽

Cited By ~ 4

Author(s):

Titus F. Msoka ◽

Gary P. Van Guilder ◽

Yvo M. Smulders ◽

Marceline van Furth ◽

John A. Bartlett ◽

...

Keyword(s):

Metabolic Syndrome ◽

Hiv Infection ◽

Antiretroviral Treatment ◽

Cross Sectional Study ◽

Large Artery ◽

Sectional Study ◽

Cross Sectional ◽

Artery Stiffness

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Effect of chronic ANG I-converting enzyme inhibition on aging processes. II. Large arteries

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.267.1.r124 ◽

1994 ◽

Vol 267 (1) ◽

pp. R124-R135 ◽

Cited By ~ 19

Author(s):

J. B. Michel ◽

D. Heudes ◽

O. Michel ◽

P. Poitevin ◽

M. Philippe ◽

...

Keyword(s):

Blood Pressure ◽

Smooth Muscle ◽

Arterial Wall ◽

Left Ventricular ◽

Structure And Function ◽

Wall Structure ◽

Large Artery ◽

Converting Enzyme ◽

Wall Stiffness ◽

And Function

The consequences of hypertension and aging on cardiovascular structure and function are reputed to be similar, suggesting that blood pressure plays a role in the aging process. However, the exact relationship between aging, blood pressure, and the arterial structure-function relationship has not been demonstrated. To test the effects of aging, renin-angiotensin system, and pressure on the arterial wall, 20 normotensive male WAG/Rij rats were killed at 6, 12, 24, and 30 mo of age and compared with similar groups treated with an angiotensin (ANG)-converting enzyme inhibitor (ACEI), perindopril. Arterial function was determined by a systemic hemodynamic study and by in situ measurement of carotid compliance. Arterial wall structure was determined by histomorphometric and biochemical methods. Aging did not significantly modify blood pressure, but ACE inhibition decreased blood pressure significantly from 6 to 30 mo. Plasma renin activity decreased with age and increased with ACEI. Plasma atrial natriuretic factor increased with age and was significantly decreased with ACEI. Absolute and relative left ventricular weight increased with age, and ACEI delayed these increases. Arterial wall stiffness increased with age, as shown by a significant decrease in systemic and local arterial compliance and by an increase in aortic characteristic impedance. The increase in carotid wall compliance after poisoning of smooth muscle contractile function (KCN) was greater in young (6- and 12-mo old) than in old (24- and 30-mo old) rats. Chronic ACEI treatment increased basal carotid compliance values slightly and did not change KCN carotid compliance. The aortic and carotid luminal size increased regularly with age. Aging was associated without any change in absolute elastin content. In contrast, collagen content increased with aging. Aging was also associated with an increase in medial thickness. Medial thickening was mainly due to smooth muscle hypertrophy. Aging was associated with intimal proliferation, which became progressively thicker and collagen rich. ACEI treatment did not prevent aortic lumen enlargement but significantly postponed the increase in medial and intimal thickening. Biochemical determinations of the aortic wall components confirmed the morphometric data. In conclusion, the age-dependent large artery enlargement and stiffening were observed both in normotensive rats and in those rats whose blood pressure was lowered by ACEI. This suggests that aging and blood pressure affect arterial wall structure and function by different mechanisms.

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