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  • Oldgren, JonasUppsala universitet,Kardiologi (författare)

Myocardial Damage, Inflammation and Thrombin Inhibition in Unstable Coronary Artery Disease

  • Artikel/kapitelEngelska2003

Förlag, utgivningsår, omfång ...

  • 2003
  • printrdacarrier

Nummerbeteckningar

  • LIBRIS-ID:oai:DiVA.org:uu-89549
  • https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-89549URI
  • https://doi.org/10.1016/S0195-668X(02)00312-3DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • 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.

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Wallentin, LarsUppsala universitet,Kardiologi(Swepub:uu)larswall (författare)
  • Grip, L (författare)
  • Linder, R (författare)
  • Nørgaard, B (författare)
  • Siegbahn, AgnetaUppsala universitet,Klinisk kemi(Swepub:uu)agsie424 (författare)
  • Uppsala universitetKardiologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:European Heart Journal24:1, s. 86-930195-668X1522-9645

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