Aortic wall thickness in newborns with intrauterine growth restriction

Skilton, Michael R.; Evans, Nick; Griffiths, Kalinda; Harmer, Jason A.; Celermajer, David S.

doi:10.1016/s0140-6736(05)66419-7

Cited by 263 publications

(231 citation statements)

References 6 publications

Supporting

Mentioning

203

Contrasting

Unclassified

Order By: Relevance

“…22 There could therefore be structural effect of HDP on neonatal blood vessels. 23 Another recent study with similar findings suggests that endothelial dysfunction in the offspring is either persistent after the preeclampsia in pregnancy or there is a heritable predisposition to endothelial dysfunction in both mother and child. 24 The elevated BP in the off- spring of preeclampsia pregnancies may also simply reflect a familial aggregation of this phenotype.…”

Section: Discussionmentioning

confidence: 82%

Does hypertensive disorder of pregnancy predict offspring blood pressure at 21 years? Evidence from a birth cohort study

et al. 2011

View full text Add to dashboard Cite

Although few studies found that the offspring of women who experienced preeclampsia have higher blood pressure (BP) at childhood and adolescence, no study has observed whether this association exists for adult offspring. To examine whether maternal hypertensive disorder of pregnancy (HDP) predicts adult offspring BP. We followed a sub-sample of 2608 mother-offspring pairs for 21 years from an original cohort of 7223 singleton infants whose mothers gave birth in Brisbane, Australia between 1981 and 1983. HDP was defined as diastolic BP (DBP) over 90 mm Hg on at least two occasions beyond 20 weeks gestation associated with proteinuria and/or excessive fluid retention. Adult offspring's systolic BP (SBP) and DBP were measured at 21 years. Multivariable regressions were used to examine the independent associations of HDP with offspring BP. Unadjusted regression analysis showed that offspring of women who experienced HDP have 3.46 mm Hg greater SBP and 3.02 mm Hg greater DBP at 21 years. This association remained consistent after adjusting for potential confounding and mediating factors including offspring gender, age, percentile birth weight for gestation, placenta weight and body mass index (BMI) at 21 year, maternal age, education, racial origin, and smoking during pregnancy and their pre-pregnancy BMI. Findings of this study suggest that maternal HDP predicts adult offspring BP. Keywords: hypertensive disorder of pregnancy; offspring blood pressure; young adults IntroductionWomen who develop hypertensive disorder of pregnancy (HDP) or preeclampsia are at an increased risk for high blood pressure (BP) and cardiovascular diseases later in life. 1 Also, men and women born after preeclampsia in pregnancies are likely to trigger severe preeclampsia in their own (or their partner's) pregnancy. 2 Recently, it has been observed that children exposed to preeclampsia are at an increased risk of a variety of diseases including endocrine, nutritional and metabolic diseases. 3 A recent study by Kajantie et al. 4 using the Helsinki Birth Cohort Study found that preeclampsia was associated with increased risk of stroke and severe preeclampsia was associated with hypertension in an adult offspring 60-70 years after their birth. Several other studies also reported that the offspring of women who developed preeclampsia have higher BP in childhood 5-7 and adolescence. [8][9][10][11] A recent meta-analysis also found that offspring of women with preeclampsia had higher levels of BP as compared with offspring from uneventful pregnancies. 12 Most of the studies have reported findings in children and adolescents but not in adults. Some studies have not adjusted for potential confounding or mediating factors such as maternal pre-pregnancy body mass index (BMI) 10 and maternal smoking during pregnancy. 8,11 It is unclear whether the observed associations are spurious or confounded with these factors. Using a long follow-up of a birth cohort study, we have the capacity to examine whether this association between HDP and offspring BP remai...

show abstract

Section: Discussionmentioning

confidence: 82%

Does hypertensive disorder of pregnancy predict offspring blood pressure at 21 years? Evidence from a birth cohort study

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Therefore, it is interesting that already at birth an increased intima media thickness can be shown in infants born with a low birth weight. 45 …”

Section: Mechanisms Of Perinatal Programming Of Hypertensionmentioning

confidence: 99%

Renal and extrarenal mechanisms of perinatal programming after intrauterine growth restriction

Dötsch

2009

Hypertens Res

View full text Add to dashboard Cite

The concept of fetal programming of disease in later life after intrauterine growth restriction (IUGR) has opened a potential new perspective on the treatment and prevention of arterial hypertension. Numerous large studies have recently confirmed the relationship between low birth weight and raised blood pressure. Hyperalimentation after birth appears to add to the risk of higher blood pressure later in life. However, there is still a controversy and clear intervention studies have not yet been possible. Therefore, the gain of knowledge about the underlying mechanisms of fetal programming is of utmost importance.Two major groups of mechanisms may be identified: renal and extrarenal mechanisms. Renal mechanisms include the reduction of nephron number, which is encountered in patients and animals with low birth weight. According to the so-called Brenner hypothesis, this may lead to increased arterial blood pressure. Another important renal system is the renin-angiotensin-aldosterone system, which appears to be more active on a number of levels in low birth weight individuals. Finally, there is the conversion of cortisol to inactive cortisone by the 11b-hydroxysteroid dehydrogenase in distal tubule cells, which is reduced after intrauterine growth restriction. This enables a more powerful activation of mineralocorticoid receptors by cortisol. Extrarenal mechanisms include alterations in vascular structure (primary and secondary), increased activity of the sympathetic nerve system, and maybe most interestingly, an impairment of endothelial function. The latter is at least partially caused by an inactivation of nitric oxide by an excess of free oxygen radicals. In summary, mechanisms of fetal programming are only in the process of being revealed, and research has to focus on finding the key mechanism that might allow for successful intervention.

show abstract

“…Both the earliest structural and functional changes of the vasculature consistent with early atherosclerosis are present in children with cardiovascular risk factors, including familial hypercholesterolaemia 8,9 and diabetes, 10,11 in addition to two intrauterine factors -maternal hypercholesterolaemia 7 and impaired fetal growth. 12,13 Vascular structure A key indicator of atherosclerosis progression is the thickness of conduit artery walls, which is due to both lipid deposits and smooth muscle cell proliferation. 14 High-resolution ultrasound has been used for many years to assess carotid artery intima-media thickness (IMT) in adults.…”

Section: Early Atherosclerosismentioning

confidence: 99%