IMPAIRED FETAL GROWTH AND ATHEROSCLEROSIS OF CAROTID AND PERIPHERAL ARTERIES

Citation
Cn. Martyn et al., IMPAIRED FETAL GROWTH AND ATHEROSCLEROSIS OF CAROTID AND PERIPHERAL ARTERIES, Lancet, 352(9123), 1998, pp. 173-178
Citations number
23
Categorie Soggetti
Medicine, General & Internal
Journal title
LancetACNP
ISSN journal
01406736
Volume
352
Issue
9123
Year of publication
1998
Pages
173 - 178
Database
ISI
SICI code
0140-6736(1998)352:9123<173:IFGAAO>2.0.ZU;2-F
Abstract
Background Although epidemiological studies suggest that people with l ow birthweight are at higher risk of coronary heart disease and stroke in adult life than those of higher birthweight, the mechanisms underl ying this relation are unclear. We investigated whether impaired fetal growth leads to an increased risk of atherosclerosis by assessment of the carotid and lower-limb arteries in a group of people aged around 70 years for whom birthweight data were available. Methods 2232 single ton babies were born to married mothers at a maternity hospital in She ffield, UK, between 1922 and 1926, and had complete birth records. We traced 829 survivors and invited 395 who still lived in Sheffield to t ake part in this study. 322 agreed; they were interviewed at home and 181 underwent duplex ultrasonographic examination of the extracranial parts of the carotid arteries. Atherosclerosis in the arteries of the lower limb was assessed in 186 people by the ankle brachial-pressure i ndex (ABPI). Findings The prevalence and severity of carotid atheroscl erosis was greatest in those with the lowest recorded birthweight. The risk of carotid stenosis was greater for people who had weighed 6.5 l b or less at birth than for those who weighed over 7.5 lb (odds ratio 5.3 [95% CI 2.0-14.0]), after adjustment for cardiovascular risk facto rs and gestational age at birth. The odds ratio for atherosclerotic di sease in the lower limbs (low ABPI) was highest in people with the low est recorded birthweight, but this relation was not significant (odds ratio 2.3 [1.0-5.6]). Interpretation Increased atherogenesis may be on e mechanism mediating the observed epidemiological link between impair ed fetal growth and cardiovascular disease. Adaptations made by the fe tus in response to influences that retard its growth may have long-ter m consequences for the structure and metabolism of the vascular system .