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Relationship between birthweight and arterial elasticity in childhood.

Authors
  • Rondó, Patricia H C
  • Lemos, Jesuana O
  • Pereira, Joilane A
  • Oliveira, Julicristie M
  • Innocente, Luiz Roberto
Type
Published Article
Journal
Clinical Science
Publisher
Portland Press
Publication Date
Nov 01, 2008
Volume
115
Issue
10
Pages
317–326
Identifiers
DOI: 10.1042/CS20070420
PMID: 18393941
Source
Medline
License
Unknown

Abstract

There is a considerable debate about the potential influence of 'fetal programming' on cardiovascular diseases in adulthood. In the present prospective epidemiological cohort study, the relationship between birthweight and arterial elasticity in 472 children between 5 and 8 years of age was assessed. LAEI (large artery elasticity index), SAEI (small artery elasticity index) and BP (blood pressure) were assessed using the HDI/PulseWave CR-2000 CardioVascular Profiling System. Blood concentrations of glucose, total cholesterol and its fractions [LDL (low-density lipoprotein)-cholesterol and HDL (high-density lipoprotein)-cholesterol] and triacylglycerols (triglycerides) were determined by automated enzymatic methods. Insulin was assessed by a chemiluminescent method, insulin resistance by HOMA (homoeostasis model assessment) and CRP (C-reactive protein) by immunonephelometry. Two linear regression models were applied to investigate the relationship between the outcomes, LAEI and SAEI, and the following variables: birthweight, gestational age, glucose, LDL-cholesterol, HDL-cholesterol, triacylglycerols, insulin, CRP, HOMA, age, gender, waist circumference, per capita income, SBP (systolic BP) and DBP (diastolic BP). LAEI was positively associated with birthweight (P=0.036), waist circumference (P<0.001) and age (P<0.001), and negatively associated with CRP (P=0.024) and SBP (P<0.001). SAEI was positively associated with birthweight (P=0.04), waist circumference (P=0.001) and age (P<0.001), and negatively associated with DBP (P<0.001). Arterial elasticity was decreased in apparently healthy children who had lower birthweights, indicating an earlier atherogenetic susceptibility to cardiovascular diseases in adolescence and adult life. Possible explanations for the results include changes in angiogenesis during critical phases of intrauterine life caused by periods of fetal growth inhibition and local haemodynamic anomalies as a way of adaptation to abnormal pressure and flow.

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