Skip Navigation

Cardiovascular Research 1997 36(3):445-452; doi:10.1016/S0008-6363(97)00199-5
© 1997 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Stroes, E.
Right arrow Articles by Rabelink, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Stroes, E.
Right arrow Articles by Rabelink, T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1997, European Society of Cardiology

NO activity in familial combined hyperlipidemia: potential role of cholesterol remnants

Erik Stroesa, Tjerk de Bruinb, Harold de Valkb, Willem Erkelensb, Jan-Dirk Bangab, Herman van Rijnc, Hein Koomansa and Ton Rabelinka,*

aDepartment of Nephrology and Hypertension, Room F 03.226, University Hospital Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands
bDepartment of Internal Medicine and Lipid Research, University Hospital Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands
cDepartment of Clinical Chemistry, University Hospital Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands

* Corresponding author. Tel.: (+31-30) 2507375; Fax: (+31-30) 2543492.

Objective: Patients with familial combined hyperlipidemia (FCH) have an increased cardiovascular mortality despite only moderate elevations of LDL-cholesterol. Since endothelial NO release is intimately involved in the anti-atherosclerotic effects of the endothelium, we studied the effect of short-term lipid-lowering therapy on NO-mediated vasodilatation in patients with FCH. In view of only moderate LDL elevations, we evaluated whether alterations in other lipid fractions upon therapy correlated to changes in NO-mediated vasodilatation. Methods: NO activity was assessed by serotonin-induced, nitric oxide-mediated increase in forearm blood flow (FBF). Measurements were performed 2 weeks off and 4 weeks on lipid-lowering therapy in 12 FCH patients using forearm venous occlusion plethysmography. Control experiments were performed in 12 healthy subjects. Results: Serotonin-induced vasodilatation was impaired in FCH patients (FBF (unit ml/100 ml forearm tissue/min) from 3.0 (0.3) to 4.8 (0.4)) compared to controls (FBF from 2.9 (0.3) to 6.5 (0.6); p<0.05 vs. FCH). FBF response to serotonin improved significantly upon lipid-lowering therapy (from 3.0 (0.3) to 5.7 (0.5); p<0.05 treated vs. untreated). The level of improvement in endothelial function was significantly correlated to the absolute reduction of intermediate density lipoproteins upon lipid-lowering therapy (r = –0.64; p<0.05), whereas it did not correlate to changes in VLDL- or LDL-cholesterol, nor to Lp(a). Conclusion: Patients with familial combined hyperlipidemia have impaired NO-mediated vasodilatation, that responds rapidly to lipid lowering medication, and may be related to changes in intermediate density lipoproteins.

KEYWORDS Endothelium; Nitric oxide; Familial combined hyperlipidemia; Human; Forearm; Lipid-lowering therapy


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Journal of Renin-Angiotensin-Aldosterone SystemHome page
J. R Chiong and A. B Miller
Review: Renin-angiotensin system antagonism and lipid-lowering therapy in cardiovascular risk management
Journal of Renin-Angiotensin-Aldosterone System, June 1, 2002; 3(2): 96 - 102.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.