Introduction Offspring of hypertensive pregnancies have higher blood pressure (BP) in later life. Whether this is accompanied by impaired vascular function and worse cardiovascular risk profiles suggesting mediation by intrauterine exposure to vascular toxins and long term programming, or is restricted to hypertension consistent with a genetic predisposition, is unknown. Specificity of association would be a useful test of these alternatives.
Methods We examined the associations of maternal gestational hypertension and preeclampsia with offspring vascular outcomes (endothelial dysfunction assessed by radial artery flow-mediated dilatation, arterial stiffness assessed by carotid to radial pulse wave velocity, brachial artery distensibility and BP) and with markers of inflammation (C reactive protein and Interluekin-6), lipids (triglycerides, high density lipoprotein cholesterol, non-HDLc) and apolipoproteins A1 and B assessed at age 9–12 years in a UK cohort (N=3127–4624).
Results We confirmed previous associations of both preeclampsia and gestational hypertension with offspring systolic BP (confounder adjusted mean differences: 2.37 mm Hg (95% CI 1.66 to 3.08) and 2.17 mm Hg (95% CI 0.39 to 3.95) comparing offspring of women with gestational hypertension and preeclampsia, respectively, with normotensive women) and diastolic BP (1.31 mm Hg (95% CI 0.69 to 1.92) and 1.40 mm Hg (95% CI −0.14 to 2.95)). However, we found no associations of either preeclampsia or gestational hypertension with endothelial dysfunction, any of the other vascular outcomes, inflammatory markers, lipids or apolipoproteins.
Conclusion The specific association of both preeclampsia and gestational hypertension with higher BP in offspring supports the underlying mechanism being due to genetic variants related to higher BP, rather than intrauterine mechanisms related to inflammation and endothelial dysfunction.
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