dc.contributor.author | Damås, Jan K | |
dc.contributor.author | Gullestad, Lars | |
dc.contributor.author | Aukrust, Pål | |
dc.date.accessioned | 2015-10-09T02:01:39Z | |
dc.date.available | 2015-10-09T02:01:39Z | |
dc.date.issued | 2001 | |
dc.identifier.citation | Current Controlled Trials in Cardiovascular Medicine. 2001 Oct 16;2(6):271 | |
dc.identifier.uri | http://hdl.handle.net/10852/46559 | |
dc.description.abstract | Inflammatory cytokines may negatively influence contractility and contribute to the remodelling process in the failing myocardium. Traditional cardiovascular drugs appear to have little influence on the overall cytokine network in chronic heart failure (CHF). Increased interest in anticytokine therapy has therefore evolved. Several small studies have used tumour necrosis factor (TNF)-α as a target, resulting in improved functional capacity and myocardial performance. Intravenous immunoglobulin (IVIG) represents another therapeutic approach in which the impact on myocardial performance appears to be correlated with anti-inflammatory effects. These studies demonstrate potential for immunomodulation as a therapy in addition to conventional cardiovascular treatment in CHF, but the most effective drugs in this regard have yet to be identified.
Published Open Access with springerlink.com | |
dc.language.iso | eng | |
dc.rights | Damås et al; licensee BioMed Central Ltd. | |
dc.title | Cytokines as new treatment targets in chronic heart failure | |
dc.type | Journal article | |
dc.date.updated | 2015-10-09T02:01:39Z | |
dc.creator.author | Damås, Jan K | |
dc.creator.author | Gullestad, Lars | |
dc.creator.author | Aukrust, Pål | |
dc.identifier.doi | http://dx.doi.org/10.1186/cvm-2-6-271 | |
dc.identifier.urn | URN:NBN:no-50713 | |
dc.type.document | Tidsskriftartikkel | |
dc.type.peerreviewed | Peer reviewed | |
dc.identifier.fulltext | Fulltext https://www.duo.uio.no/bitstream/handle/10852/46559/1/13063_2001_Article_84.pdf | |
dc.type.version | PublishedVersion | |
cristin.articleid | 271 | |