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Cyclooxygenase-2 inhibition and coagulation
Jan Steffel1, Thomas F Lüscher, Frank Ruschitzka
1Cardiovascular Research, Physiology Institute, University of Zürich, and Cardiology, Cardiovascular Center, University Hospital Zürich, Zürich, Switzerland.
Journal of Cardiovascular Pharmacology
|June 21, 2006
Summary
Selective COX-2 inhibitors may increase thrombotic risk by disrupting prostacyclin and thromboxane synthesis. Clinical data remains unclear, necessitating further research into their cardiovascular safety.
Area of Science:
- Pharmacology
- Cardiovascular Medicine
- Hematology
Background:
- Selective cyclooxygenase-2 (COX-2) inhibitors are under scrutiny for potential thrombotic risks.
- COX-2 inhibition may create a prothrombotic state by suppressing endothelial prostacyclin while sparing platelet thromboxane A2.
Purpose of the Study:
- To review the effect of COX-2 inhibition on the coagulation system.
- To discuss molecular mechanisms and summarize clinical trials regarding thrombotic complications associated with COX-2 inhibitors.
Main Methods:
- Review of in vitro studies on coxib effects on coagulation.
- Analysis of animal studies investigating COX-2 inhibition in atherosclerosis.
- Summary of clinical trials reporting thrombotic complications with coxibs.
Main Results:
- In vitro data on coxib effects on coagulation are variable; celecoxib may reduce tissue factor expression.
- Animal studies yield inconclusive results regarding the impact of COX-2 inhibition on atherosclerosis.
- Clinical trials have observed an increased frequency of thrombotic complications with coxibs.
Conclusions:
- The precise effect of COX-2 inhibition on coagulation and cardiovascular risk remains unclear.
- Further prospective, randomized, and adequately powered studies are needed to directly assess the cardiovascular safety of coxibs.