WFRF:(Nørgaard Lars)
Sökning: WFRF:(Nørgaard Lars) > Myocardial Damage, ...
LIBRIS Formathandbok (Information om MARC21)
| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 03023naa a2200313 4500 | |
| 001 | oai:DiVA.org:uu-89549 | |
| 003 | SwePub | |
| 008 | 011115s2003 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-895492 URI |
| 024 | 7 | a https://doi.org/10.1016/S0195-668X(02)00312-32 DOI |
| 040 | a (SwePub)uu | |
| 041 | a engb eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Oldgren, Jonasu Uppsala universitet,Kardiologi4 aut0 (Swepub:uu)jonaoldg |
| 245 | 1 0 | a Myocardial Damage, Inflammation and Thrombin Inhibition in Unstable Coronary Artery Disease |
| 264 | 1 | c 2003 |
| 338 | a print2 rdacarrier | |
| 520 | a AIM:Unstable coronary artery disease (CAD) is a multifactorial disease involving both thrombotic and inflammatory processes. We have assessed the time-course and the influence of thrombin inhibitors on changes in fibrinogen and C-reactive protein levels, and their relation to myocardial ischaemia in unstable CAD.METHODS AND RESULTS:Three hundred and twenty patients were randomized to 72 h infusion with three different doses of inogatran, a direct thrombin inhibitor, or unfractionated heparin. There were no significant differences between the treatment groups in fibrinogen or C-reactive protein levels. Overall, the fibrinogen levels were significantly increased in the first 24-96 h and still elevated at 30 days. The C-reactive protein levels showed a more pronounced increase during the first 24-96 h, but then markedly decreased over 30 days. Troponin-positive compared to troponin-negative patients had higher fibrinogen and C-reactive protein levels up to 96 h, although there was an increase compared to pre-treatment levels in both groups. A high fibrinogen level (pre-treatment top tertile) was associated with an increased rate of death or myocardial (re-)infarction at 30 days, 13% vs 5.6%, P=0.03, and increased long-term mortality. A high C-reactive protein level was related to increased 30-day mortality, 4% vs 0%, P=0.01.CONCLUSION:Myocardial cell injury was related to a high degree of inflammation, only some of which is an acutephase response due to tissue damage. The rise in fibrinogen was sustained, which might reflect low grade inflammation with long-term risk of thrombosis. The transient elevation of C-reactive protein levels might indicate a propensity to a pronounced inflammatory response and is associated with increased mortality. | |
| 700 | 1 | a Wallentin, Larsu Uppsala universitet,Kardiologi4 aut0 (Swepub:uu)larswall |
| 700 | 1 | a Grip, L4 aut |
| 700 | 1 | a Linder, R4 aut |
| 700 | 1 | a Nørgaard, B4 aut |
| 700 | 1 | a Siegbahn, Agnetau Uppsala universitet,Klinisk kemi4 aut0 (Swepub:uu)agsie424 |
| 710 | 2 | a Uppsala universitetb Kardiologi4 org |
| 773 | 0 | t European Heart Journalg 24:1, s. 86-93q 24:1<86-93x 0195-668Xx 1522-9645 |
| 856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-89549 |
| 856 | 4 8 | u https://doi.org/10.1016/S0195-668X(02)00312-3 |
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- Oldgren, Jonas
- Wallentin, Lars
- Grip, L
- Linder, R
- Nørgaard, B
- Siegbahn, Agneta
- Artiklar i publikationen
- European Heart J ...
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- Uppsala universitet
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