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Mechanisms underlying elevated SBP differ with adiposity in young adults: the Enigma study.


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Authors

Middlemiss, Jessica E 
Miles, Karen L 
McDonnell, Barry J 
Yasmin 
Maki-Petaja, Kaisa M 

Abstract

OBJECTIVES: The positive association between adiposity and hypertension is well recognized. However, not all overweight individuals have elevated blood pressure (BP). Moreover, different factors may be associated with high BP in normal-weight versus overweight individuals. The aim of the current study was to examine the influence of adiposity on the relationship between SBP and underlying haemodynamic mechanisms in young adults. METHOD: Data from 2502 patients were available from the Enigma study. Detailed demographic, biochemical, and haemodynamic data were obtained in all individuals. Data were analysed between lower and upper tertiles of BMI and SBP, separately for each sex. RESULTS: In normal-weight individuals, cardiac output (CO) was elevated in those with higher SBP, independently of body size. Moreover, higher CO was associated with an increased stroke volume in men (P < 0.001), but an increased heart rate in women (P = 0.002). In contrast, in overweight individuals, peripheral vascular resistance (PVR) was elevated in men with higher SBP (P = 0.02) and those with lower SBP had the lowest PVR of all groups. In linear regression analyses, there was a stronger association between SBP and CO in normal-weight individuals, but a stronger association between SBP and PVR in overweight individuals. CONCLUSION: Different haemodynamic mechanisms are associated with elevated SBP in young adults, depending on body size and sex. These data suggest the need for differential approaches to the identification and management of young adults with elevated BP.

Description

Keywords

Adiposity, Adult, Blood Pressure, Body Mass Index, Body Size, Female, Heart Rate, Humans, Hypertension, Male, Overweight, Sex Factors, Stroke Volume, Vascular Resistance, Young Adult

Journal Title

J Hypertens

Conference Name

Journal ISSN

0263-6352
1473-5598

Volume Title

34

Publisher

Ovid Technologies (Wolters Kluwer Health)
Sponsorship
British Heart Foundation (None)
This work was funded by the British Heart Foundation and the NIHR Cambridge Biomedical Research Centre