Respective Roles of Preterm Birth and Fetal Growth Restriction in Blood Pressure and Arterial Stiffness in Adolescence

Rossi, P.; Tauzin, Laurent; Marchand, Elise; Boussuges, Alain; Gaudart, Jean; Francès, Y.

doi:10.1016/j.jadohealth.2010.08.004

Cited by 73 publications

(55 citation statements)

References 10 publications

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“…In addition, in spontaneously hypertensive rat, interstitial fibrosis and LV hypertrophy accompany BP elevation at an adult age. Similar to spontaneously hypertensive rat, where cardiomyopathy progresses from concentric to eccentric LV hypertrophy later in life (≈18 months), with systolic dysfunction and LV chamber dilation, 18 in our model such transition occurs earlier at 12 weeks when dilated (eccentric) hypertrophy is accompanied by systolic and diastolic dysfunction.…”

Section: Discussionsupporting

confidence: 56%

Transient Neonatal High Oxygen Exposure Leads to Early Adult Cardiac Dysfunction, Remodeling, and Activation of the Renin–Angiotensin System

et al. 2014

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Abstract-Perinatal conditions (such as preterm birth) can affect adult health and disease, particularly the cardiovascular system. Transient neonatal high O 2 exposure in rat in adulthood (a model of preterm birth-related complications) leads to elevated blood pressure, vascular rigidity, and dysfunction with renin-angiotensin system activation. We postulate that neonatal hyperoxic stress also affects myocardial structure, function, and expression of renin-angiotensin system components. Sprague-Dawley pups were kept with their mother in 80% O 2 or in room air (control) from days 3 to 10 of life. Left ventricular function was assessed in 4-, 7-, 12-week-old (echocardiography) and in 16-week-old (intraventricular catheterization) male O 2 -exposed versus control rats. At 16 weeks, hearts from O 2 -exposed rats showed cardiomyocyte hypertrophy, enhanced fibrosis, and increased expression of transforming growth factor-β1, senescence-associated proteins p53 and Rb, upregulation of angiotensin II type 1 (AT1) receptor expression (protein and AT1a/b mRNA), and downregulation of AT2 receptors. At 4 weeks (before blood pressure increase), the expression of cardiomyocyte surface area, fibrosis, p53, and AT1b was significantly increased and AT2 decreased in O 2 -exposed animals. After 4 weeks of continuous angiotensin II infusion (starting at 12 weeks), O 2 -exposed rats developed severe heart failure, with impaired myocardial mechanical properties compared with saline-infused rats. Transient neonatal O 2 exposure in rats leads to left ventricular hypertrophy, fibrosis and dysfunction, and increased susceptibility to heart failure under pressure overload. These results are relevant to the growing population of individuals born preterm who may be at higher risk of cardiac dysfunction when faced with increased peripheral resistance associated with hypertension, vascular diseases, and In cardiovascular disease, RAS plays a major role in vascular dysfunction, cardiac hypertrophy, and fibrosis through Ang II acting predominantly on its type I receptor (AT1) 10,11 triggering downstream mechanisms such as the profibrotics transforming growth factor-β1 (TGF-β1) and hypoxic-inducible factor-1α (HIF-1α), 12 as well as senescence-associated pathways. 13Activation of the RAS in the kidneys, brain, and systemic vasculature plays a key role in the elevation and maintenance of BP in experimental models associated with deleterious perinatal conditions including transient neonatal high O 2 exposure. 6,14 However, the effect of neonatal pro-oxidant conditions on cardiac RAS components has not been reported. To determine whether neonatal hyperoxia exposure impaired cardiac development and predisposed to cardiac dysfunction, myocardial structure, and function, expression of cardiac RAS components, as well as TGF-β1, HIF-1α, and senescenceassociated proteins, was determined in young, 4-week-old, and adult, 16-week-old rats infused or not with Ang II. Materials and MethodsSprague-Dawley pups were kept with their mother in 80% O 2 using an oxyc...

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Section: Discussionsupporting

confidence: 56%

Transient Neonatal High Oxygen Exposure Leads to Early Adult Cardiac Dysfunction, Remodeling, and Activation of the Renin–Angiotensin System

et al. 2014

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“…Early impairment of arterial wall properties may permanently alter cardiovascular physiology and, thus, be considered a risk factor for CVD in later life in addition to smoking, diabetes mellitus, systemic hypertension, and hypercholesterolemia. 17,23,30,31 Actually, stiffening of the aorta may be a driven force for the excess risk of CVD related to preterm birth.…”

Section: Discussionmentioning

confidence: 99%

“…[7][8][9] Most of the studies investigating vascular function in preterm-born children included adolescents or young adults in whom conventional risk factors for CVD might already be present and do not permit straightforward attribution of vascular abnormality to prematurity. [10][11][12][13][14][15][16][17][18][19][20][21] Studies in young children would be best suitable, but are limited to 3 evaluations with small sample size. [22][23][24] Our study aims at investigating arterial wall properties in a comparatively large cohort of children at preschool age by means of a standardized, semiautomated, and noninvasive method.…”

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confidence: 99%

Aortic Elastic Properties in Preschool Children Born Preterm

Komazec

Posod

Schwienbacher

et al. 2016

ATVB

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Objective-Preterm birth predisposes children to the development of cardiovascular diseases in adulthood. The aim of this study was to characterize elastic properties of the aorta at preschool age and test the hypothesis that prematurity is associated with decreased aortic distensibility and increased stiffness, both of which are predictors of increased cardiovascular risk. Approach and Results-In an observational study of 76 five-to seven-year-old children born at a gestational age <32 weeks and 79 term-born controls, elastic parameters of the ascending and descending abdominal aorta were determined noninvasively by means of M mode echocardiographic tracings and calculated using computerized wall contour analysis. Compared with children born at term, the preterm group showed significantly reduced distensibility and increased stiffness of the descending abdominal aorta. These results remained significant under multivariable adjustment for birth weight z score, maternal smoking in pregnancy, maternal education, family history of cardiovascular disease, breastfeeding, childhood nutrition, and current body mass index z score (multivariable odds ratios and 95% confidence intervals 5.1, 1.7-15.9; P=0.005 and 2.8, 1.0-7.9; P=0.046, respectively). Further adjustment for intravenous lipid therapy attenuated the strength of association. Elastic properties of the ascending aorta did not differ between the 2 study groups. Conclusions-Children

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“…To date, studies have reported increased aortic stiffness in children as early as 7 to 14 years of age that were born moderately or very preterm. [29][30][31] In addition, adolescents and young adults born preterm were found to have smaller aortic, carotid, and brachial artery luminal diameters compared with controls born at term 18,32,33 ; aortic growth was shown to be impaired from the early neonatal period after preterm birth. 34 Furthermore, in a sheep model of moderate preterm birth, evidence of vascular injury to the ascending aorta was observed in animals examined at 11 weeks postnatal age.…”

Section: Vascularmentioning

confidence: 99%