Cross-Talk Between Large Artery Stiffness and Retinal Microvasculature in Children: The ExAMIN Youth SA Study

Background: Cross-talk between the macro-and microvasculature is considered an important contributor to target organ damage. Previous findings were predominantly in adult populations and investigation into this mechanism in children may provide insight into the development of early adverse vascular changes. Whether any ethnic differences in cross-talk is evident, also remains to be determined.Objective: To determine whether retinal microvascular diameters are associated with large artery stiffness in young children and whether ethnic differences are evident.Materials and Methods: In this cross-sectional study, 730 black (n = 437) and white (n = 293) school children aged 5-9 years were included. Pulse wave velocity (PWV) was measured and the central retinal arteriolar equivalent (CRAE) and central retinal venular equivalent (CRVE) diameters were calculated from fundus images. The arterio-venous ratio (AVR) was subsequently calculated.Results: Pulse wave velocity was lower (p ≤ 0.001) in the black group when compared to the white group. The black group had a narrower CRAE, wider CRVE and lower AVR (all p < 0.001). Pulse wave velocity associated negatively with CRAE (r = –0.141, p = 0.003) and AVR (r = –0.185, p ≤ 0.001) in the black group only. A positive association between PWV and CRVE was seen in the black (r = 0.174, p ≤ 0.001) and white (r = 0.119, p = 0.043) group.Conclusion: Large artery stiffness is associated with retinal arterial narrowing and venular widening in children, suggesting cross-talk between the macro-and microvasculature. Ethnic differences in these associations are also evident. Our findings warrant further investigation into environmental and sociocultural risk factors contributing to premature cardiovascular disease development.

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Mechanisms and consequences of large artery rigidity

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y03-022 ◽

2003 ◽

Vol 81 (3) ◽

pp. 205-211 ◽

Cited By ~ 30

Author(s):

Karima Et-Taouil ◽

Michel Safar ◽

Gérard E Plante

Keyword(s):

Smooth Muscle ◽

Pulse Wave Velocity ◽

Smooth Muscle Cells ◽

Wave Velocity ◽

Pulse Wave ◽

Target Organ Damage ◽

Organ Damage ◽

Target Organ ◽

Vasa Vasorum ◽

Large Artery

In this review paper, the classical and more recently described mechanisms responsible for the structural and functional characteristics of large artery rigidity are described. Mostly important, these characteristics appear to be nonspecific to the primary disease process involved in arterial hypertension, diabetes mellitus, dyslipidemia, congestive heart failure, chronic uremia, and perhaps senescence, including vascular dementia. Nonspecific in terms of aetiology, the vasculopathy encountered in these diseases exhibits common structural and functional abnormalities. The identification of such abnormalities could well become the target of potent nonpharmacological and (or) pharmacological interventions capable of preventing or retarding morbidity and mortality. The structural characteristics responsible for large artery rigidity include smooth muscle cell hypertrophy, matrix collagen deposition, and recently described, dysfunction in proteoglycan metabolism. Functional abnormalities, such as bradykinin-dependent hyper-reactivity of smooth muscle cells and vasa vasorum microcirculation network disturbances, also appear to alter aortic wall rigidity. The physiopathology of target organ damage is then revisited, based on endothelial dysfunction, documented in large and resistance arteries, as well as in microcirculation networks, where altered permeability to macromolecules leads to interstitial matrix disorganization and cell damage. The clinical evaluation of large artery rigidity is described, and one of the noninvasive methods, evaluation of pulse-wave velocity, is validated in normal conditions and in disease processes. Finally, nonpharmacological and pharmacological therapeutic measures are presented, and includes physical exercise to reduce insulin resistance, and reninangiotensin-IIaldosterone modulators.Key words: large artery compliance, aortic structure, collagen, elastin, proteoglycans, vascular smooth muscle cells, vasa vasorum, target organ damage, pulse wave velocity, vascular pharmacology.

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Sympathetic neural modulation of arterial stiffness in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00734.2020 ◽

2020 ◽

Vol 319 (6) ◽

pp. H1338-H1346

Author(s):

Massimo Nardone ◽

John S. Floras ◽

Philip J. Millar

Keyword(s):

Arterial Stiffness ◽

Pulse Wave Velocity ◽

Wave Velocity ◽

Pulse Wave ◽

Augmentation Index ◽

Muscle Sympathetic Nerve Activity ◽

Experimental Studies ◽

Large Artery ◽

Cross Sectional ◽

Artery Stiffness

Elevated large-artery stiffness is recognized as an independent predictor of cardiovascular and all-cause mortality. The mechanisms responsible for such stiffening are incompletely understood. Several recent cross-sectional and acute experimental studies have examined whether sympathetic outflow, quantified by microneurographic measures of muscle sympathetic nerve activity (MSNA), can modulate large-artery stiffness in humans. A major methodological challenge of this research has been the capacity to evaluate the independent neural contribution without influencing the dynamic blood pressure dependence of arterial stiffness. The focus of this review is to summarize the evidence examining 1) the relationship between resting MSNA and large-artery stiffness, as determined by carotid-femoral pulse wave velocity or pulse wave reflection characteristics (i.e., augmentation index) in men and women; 2) the effects of acute sympathoexcitatory or sympathoinhibitory maneuvers on carotid-femoral pulse wave velocity and augmentation index; and 3) the influence of sustained increases or decreases in sympathetic neurotransmitter release or circulating catecholamines on large-artery stiffness. The present results highlight the growing evidence that the sympathetic nervous system is capable of modulating arterial stiffness independent of prevailing hemodynamics and vasomotor tone.

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P.055 COMMON CAROTID ARTERY STIFFNESS: MORE SENSITIVE TO AGE AND GENDER RELATED LARGE ARTERY STIFFENING THAN AORTIC PULSE WAVE VELOCITY?

Artery Research ◽

10.1016/j.artres.2007.07.112 ◽

2007 ◽

Vol 1 (2) ◽

pp. 65

Author(s):

S.J. Vermeersch ◽

E.R. Rietzschel ◽

M.L. De Buyzere ◽

D. De Bacquer ◽

G. De Backer ◽

...

Keyword(s):

Carotid Artery ◽

Pulse Wave Velocity ◽

Wave Velocity ◽

Common Carotid Artery ◽

Pulse Wave ◽

Aortic Pulse Wave Velocity ◽

Large Artery ◽

Age And Gender ◽

Artery Stiffness ◽

And Gender

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Decreased heritability and emergence of novel genetic effects on pulse wave velocity from youth to young adulthood

Scientific Reports ◽

10.1038/s41598-021-88490-3 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Yisong Huang ◽

Shaoyong Su ◽

Harold Snieder ◽

Frank Treiber ◽

Gaston Kapuku ◽

...

Keyword(s):

Environmental Factors ◽

Pulse Wave Velocity ◽

Wave Velocity ◽

Young Adulthood ◽

Ethnic Differences ◽

Genetic Factors ◽

Pulse Wave ◽

Environmental Influences ◽

Genetic Effects ◽

Over Time

AbstractIncreased arterial stiffness measured by pulse wave velocity (PWV) is an important parameter in the assessment of cardiovascular risk. Our previous longitudinal study has demonstrated that carotid-distal PWV showed reasonable stability throughout youth and young adulthood. This stability might be driven by genetic factors that are expressed consistently over time. We aimed to illustrate the relative contributions of genetic and environmental factors to the stability of carotid-distal PWV from youth to young adulthood. We also examined potential ethnic differences. For this purpose, carotid-distal PWV was measured twice in 497 European American (EA) and African American (AA) twins, with an average interval time of 3 years. Twin modelling on PWV showed that heritability decreased over time (62–35%), with the nonshared environmental influences becoming larger. There was no correlation between the nonshared environmental factors on PWV measured at visit 1 and visit 2, with the phenotypic tracking correlation (r = 0.32) completely explained by shared genetic factors over time. Novel genetic influences were identified accounting for a significant part of the variance (19%) at the second measurement occasion. There was no evidence for ethnic differences. In summary, novel genetic effects appear during development into young adulthood and account for a considerable part of the variation in PWV. Environmental influences become larger with age for PWV.

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66 Ethnic differences in carotid intimal medial thickness and carotid-femoral pulse wave velocity are present in UK children

Heart ◽

10.1136/heartjnl-2011-300198.66 ◽

2011 ◽

Vol 97 (Suppl 1) ◽

pp. A41-A41 ◽

Cited By ~ 1

Author(s):

P. H. Whincup ◽

C. M. Nightingale ◽

A. Rapala ◽

D. Joysurry ◽

M. Prescott ◽

...

Keyword(s):

Pulse Wave Velocity ◽

Wave Velocity ◽

Ethnic Differences ◽

Pulse Wave ◽

Intimal Medial Thickness ◽

Carotid Intimal Medial Thickness

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Abstract 545: Modification Over Time of Pulse Wave Velocity Parallel to Changes in Both Office and 24h-ambulatory Peripheral BP as well as Aortic BP

Hypertension ◽

10.1161/hyp.64.suppl_1.545 ◽

2014 ◽

Vol 64 (suppl_1) ◽

Author(s):

Anna Oliveras ◽

Julián Segura ◽

Carmen Suárez ◽

Luis García-Ortiz ◽

María Abad ◽

...

Keyword(s):

Pulse Wave Velocity ◽

Wave Velocity ◽

Pulse Wave ◽

Target Organ Damage ◽

Measurement Techniques ◽

Organ Damage ◽

Applanation Tonometry ◽

Target Organ ◽

Over Time

Aim: to assess the relationship of changes in pulse wave velocity (PWV), a marker of target organ damage, with the variation in BP over time, as assessed by three different methods of measurement: office and 24h-ambulatory peripheral BP as well as aortic BP. Methods: Observational prospective study in hypertensive subjects with impaired glucose metabolism consecutively recruited from Spanish Hypertension Units. Aortic BP and carotid-femoral PWV were evaluated by radial applanation tonometry (Sphygmocor®) at baseline ( b ) and after 12 months of follow-up ( fu ). Peripheral BP measurements were also recorded at baseline and at 12 months follow-up: office BP was obtained as the average of triplicate measurements taken at 1 min-intervals after 5 min of seated rest, using validated oscillometric devices; 24h-ambulatory BP recordings were taken with a validated device (Spacelabs®-90207) at 20-minute intervals throughout both the self-reported awake and asleep periods. Clinical and anthropometric features were also recorded. PWV variation (Δ) over time was calculated as follows: Δ PWV= [(PWV fu - PWV b ) / PWV b ] x 100. BP variation over time was calculated with the same formula applied to BP values obtained with the different measurement techniques. Correlations (Spearman “Rho”) of Δ PWV and Δ BP were calculated. Results: n=209 patients; mean age: 61.8 ± 11.2 y; 39% (81 of 209) were female; 80% (167 of 209) had type 2 diabetes. Other risk factors: hypertension: 100%; dyslipidemia: 69% (144 of 209); smokers: 13% (28 of 209); body mass index: 30.9 ± 4.4 Kg/m 2 . Baseline office systolic/diastolic BP (mmHg): oSBP = 143 ± 20; oDBP = 82 ± 12. Follow-up office systolic/diastolic BP (mmHg): oSBP = 136 ± 20; oDBP = 79 ± 12. Baseline PWV: 10.01 ± 3.5 m/s. Follow-up PWV: 10.19 ± 3.21 m/s. Δ PWV correlated with: Δ oSBP (Rho=0.212; p=0.002), Δ 24h-SBP (Rho=0.254; p<0.001), Δ daytime-BP (Rho=0.232; p=0.001), Δ nighttime-BP (Rho=0.320; p<0.001) and Δ aortic-SBP (Rho=0.320; p<0.001). Conclusion: Modification over time of PWV, a marker of target organ damage, parallel to changes in systolic BP, both office and 24h-ambulatory peripheral BP variation as well as aortic BP variation, at 12 months of follow-up. Among them, aortic SBP and nighttime peripheral SBP both showed the best correlation.

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