Skip Navigation

European Journal of Heart Failure 2006 8(4):361-365; doi:10.1016/j.ejheart.2005.10.008
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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 Kupari, M.
Right arrow Articles by Ylikorkala, O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kupari, M.
Right arrow Articles by Ylikorkala, O.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 2006 European Society of Cardiology

Vasoactive intestinal peptide—release from the heart and response in heart failure due to left ventricular pressure overload

Markku Kuparia,*, Tomi S. Mikkolab, Heikki Turtoa, Jyri Lommia and Olavi Ylikorkalab

a Division of Cardiology, Department of Medicine, Helsinki University Central Hospital 00029 Helsinki, Finland
b Department of Obstetrics and Gynecology, Helsinki University Central Hospital 00029 Helsinki, Finland

* Corresponding author. Tel.: +358 9 47172441; fax: +358 9 47174574. E-mail address: markku.kupari{at}hus.fi


  Abstract

Background: Vasoactive intestinal peptide (VIP) is a peptidergic neurotransmitter and a vasodilator with positive inotropic and chronotropic properties. Whether and how VIP contributes to the neuroendocrine response in heart failure (HF) is disputed, and there are no data on VIP in pressure overload-induced HF.

Methods: We studied 129 adults with isolated aortic valve stenosis (AS). Blood was sampled from the aortic root and, in a subset of 48 patients, also from the coronary sinus for determination of VIP by radioimmunoassay. HF was diagnosed according to the European Society of Cardiology criteria.

Results: Plasma VIP (mean±S.E.M.) was slightly higher in patients with HF (22.6±0.9 pmol/l, n=41) than in patients free of HF (21.1±0.5 pmol/l, n=88) or in 11 control patients without structural heart disease (20.0±1.3 pmol/l, n=11) (p=0.030 across the groups). VIP did not correlate with any measurement of cardiac structure or function in AS. The change in plasma VIP from aortic root to coronary sinus averaged +1.2±0.4 pmol/l in the 11 control patients (p=0.021), +1.2±0.2 pmol/l in 33 AS patients free of HF (p<0.001) and +0.8±0.3 pmol/l in 15 AS patients with HF (p=0.037).

Conclusions: Both structurally normal and diseased hearts release VIP into the coronary sinus. Although marginally elevated in the systemic circulation, VIP is unlikely to contribute significantly to the neuroendocrine activation in HF due to pressure overload.

Key Words: Heart failure • Aortic stenosis • Vasoactive intestinal peptide

Received March 13, 2005; Revised July 30, 2005; Accepted October 11, 2005


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




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.