Skip Navigation


European Journal of Heart Failure Advance Access originally published online on March 10, 2009
European Journal of Heart Failure 2009 11(4):378-385; doi:10.1093/eurjhf/hfp031
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
11/4/378    most recent
hfp031v1
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 Tracchi, I.
Right arrow Articles by Brunelli, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tracchi, I.
Right arrow Articles by Brunelli, C.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Increased neutrophil lifespan in patients with congestive heart failure

Irene Tracchi1,{dagger}, Giorgio Ghigliotti1,{dagger},*, Marzia Mura1, Silvano Garibaldi1, Paolo Spallarossa1, Chiara Barisione1, Valentina Boasi1, Michele Brunelli1, Luca Corsiglia2, Antonio Barsotti1 and Claudio Brunelli1

1 Division of Cardiology, Department of Internal Medicine, Research Center of Cardiovascular Biology, University of Genova, Viale Benedetto XV/6, 16132 Genova, Italy
2 Casa Di Cura Istituto Cardiovascolare Camogli (ISC), Camogli, Italy

* Corresponding author. Tel: +103 537 545, Fax: +103 538 655, Email: gghiglio{at}unige.it


   Abstract

Aims: Congestive heart failure (CHF) can be thought of as a state of chronic immune activation. Polymorphonuclear neutrophil (PMN) apoptosis is one of the mechanisms responsible for the resolution of inflammation. A reduced PMN apoptotic rate in CHF patients may generate a persistent inflammatory response and hence mediate tissue damage in this group of patients. We aimed to measure levels of spontaneous apoptosis of circulating PMNs in CHF patients and in controls, and to examine whether NYHA class, left ventricular ejection fraction (LV-EF), and laboratory parameters of inflammation, endothelial damage, and of liver and renal function, could predict the rate of PMN apoptosis in CHF patients.

Methods and results: A total of 29 CHF patients and 26 controls were studied. Propidium iodide and flow cytometry were used to assess PMN apoptosis. Delay in PMN apoptosis was expressed as percentage (expressed as median, first and third quartiles) of surviving PMNs in the study subjects. We found an increased percentage of surviving PMNs [38(27.1–47.1)] in CHF patients compared with controls [19.4 (15.8–25.2)] (P < 0.05). The PMN survival rate in the CHF group was correlated to NYHA class, and plasma levels of C-reactive protein and alkaline phosphatase, while it was inversely correlated to LV-EF and protein levels. A positive relationship between PMN survival and increased ex vivo endothelial apoptosis was found.

Conclusion: Increased PMN lifespan in patients with worsening CHF could be used as a novel measurement of tissue and endothelial damage in this group of patients.

Key Words: Apoptosis • Neutrophils • Congestive heart failure • Neutrophil apoptosis • Endothelial apoptosis

Received February 5, 2009; Revised November 30, 2008; Accepted December 10, 2008


{dagger}The first two authors contributed equally to the study.


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.