Elevated Blood Pressure in Adolescent Boys Predicts Endothelial Dysfunction: The Cardiovascular Risk in Young Finns Study

Hypertension is a major risk factor for atherosclerosis. It may cause or be a consequence of endothelial dysfunction. We studied whether systolic blood pressure measured in childhood and adolescence predicts endothelial-dependent brachial flow-mediated dilation (FMD) in adulthood. Brachial FMD was m...

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Published inHypertension (Dallas, Tex. 1979) Vol. 48; no. 3; pp. 424 - 430
Main Authors Juonala, Markus, Viikari, Jorma S.A., Rönnemaa, Tapani, Helenius, Hans, Taittonen, Leena, Raitakari, Olli T.
Format Journal Article
LanguageEnglish
Published Philadelphia, PA American Heart Association, Inc 01.09.2006
Hagerstown, MD Lippincott
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Summary:Hypertension is a major risk factor for atherosclerosis. It may cause or be a consequence of endothelial dysfunction. We studied whether systolic blood pressure measured in childhood and adolescence predicts endothelial-dependent brachial flow-mediated dilation (FMD) in adulthood. Brachial FMD was measured in 2109 white adults, aged 24 to 39 years, in the 21-year follow-up of the Cardiovascular Risk in Young Finns Study. These subjects have risk factor data available dating back to their childhood (baseline in 1980, ages 3 to 18 years). In male subjects, the level of systolic blood pressure measured in adolescence (at ages 12 to 18 years at baseline) was inversely related to adulthood FMD (P=0.004). This association was independent of brachial diameter and other childhood (P=0.003) and adulthood risk factors, including blood pressure (P=0.03). Childhood (age 3 to 9 years at baseline) systolic blood pressure did not correlate with adult FMD in men or in women (P always >0.2). In male subjects, elevated systolic blood pressure in adolescence predicts impaired brachial endothelial function 21 years later in adulthood. This association is independent of other childhood and adulthood cardiovascular risk factors suggesting that blood pressure elevation in adolescence may have an influence on biological processes that regulate endothelium-dependent flow-mediated vasodilatation capacity.
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ISSN:0194-911X
1524-4563
1524-4563
DOI:10.1161/01.HYP.0000237666.78217.47