Copyright © 2003 by the European Society of Cardiology.
Myocardial damage, inflammation and thrombin inhibition in unstable coronary artery disease
a Department of Medical Sciences, Cardiology, University Hospital, Uppsala, Sweden
b Department of Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden
c Department of Cardiology, Karolinska Hospital, Stockholm, Sweden
d Department of Medicine and Cardiology, Aarhus University Hospital, Aarhus, Denmark
e Clinical Chemistry, University Hospital, Uppsala, Sweden
revised April 20, 2003; accepted April 24, 2003 * Correspondence: Jonas Oldgren, MD, Department of Medical Sciences, Cardiology, Uppsala University Hospital, SE-751 85 Uppsala, Sweden
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.
Key Words: Unstable coronary artery disease • inflammation • fibrinogen • C-reactive protein • troponin
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