Dyslipidemia is associated with sympathetic nervous activation and impaired endothelial function in young females.

Abstract:

BACKGROUND:Dyslipidemia is one the most well-established risk factors for cardiovascular disease development. Moreover, hypercholesterolemia and plasma cholesterol level in the high to normal range are established triggers for impairment in endothelial function. Evidence indicates that endothelial function is closely linked with sympathetic nervous activity in healthy individuals. We therefore investigated whether both endothelial and sympathetic functions may be impaired in young females with abnormal plasma cholesterol levels. METHODS:Baseline endothelial function (digital pulse amplitude) and muscle sympathetic nervous activity (microneurography) were retrospectively analyzed in 14 young healthy females with dyslipidemia as indicated by total cholesterol ≥197mg/dL, high-density lipoprotein ≤39mg/dL, or low-density lipoprotein >116mg/dL, and in 13 females with lipids in the healthy range. RESULTS:Subjects with dyslipidemia had significantly impaired endothelial function compared to those with a normal cholesterol profile (reactive hyperemia index; 1.61±0.10 vs. 2.32±0.14, P < 0.001), increased muscle sympathetic nervous activity (after adjusting for body mass and age, 36±3 vs. 27±3 bursts per 100 heartbeats, P = 0.049) and elevated high-sensitivity C-reactive protein (4.13±0.77 vs. 1.92±0.61mg/L, P = 0.03). DISCUSSION:Our results indicate that young healthy females with dyslipidemia present with a strong impairment of endothelial function and increased sympathetic drive. The sympathetic activation observed in the subjects with an elevated cholesterol profile may play a role in the development of cardiovascular disease development.

journal_name

Am J Hypertens

authors

Lambert E,Straznicky N,Sari CI,Eikelis N,Hering D,Head G,Dixon J,Esler M,Schlaich M,Lambert G

doi

10.1093/ajh/hps016

subject

Has Abstract

pub_date

2013-02-01 00:00:00

pages

250-6

issue

2

eissn

0895-7061

issn

1941-7225

pii

hps016

journal_volume

26

pub_type

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