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Selective COX-2 Inhibitors, NSAIDs, Aspirin, and Myocardial Infarction
Arch Intern Med. 2002;162:1091-1092.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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NONSTEROIDAL ANTI-INFLAMMATORY drugs (NSAIDs) are among the most widely
used medications in the world.1 NSAIDs inhibit
cyclooxygenase-1 (COX-1) and COX-2 isoenzymes. Inhibition of COX-1 isoenzymes
inhibits the production of thromboxane and thus inhibits platelet aggregation.
In addition, inhibition of COX-1 isoenzymes compromises the gastrointestinal
mucosa. As a result, the major limitation of NSAIDs is gastrointestinal toxicity,
resulting in upper gastrointestinal events in 2% to 4% of patients per year.1
Selective COX-2 inhibitors do not inhibit COX-1 isoenzymes, and as a
result they produce an analgesic and anti-inflammatory effect without gastric
toxicity. Since their introduction in 1999, they have become enormously popular,
with US sales in the billions of dollars.2
Unlike nonselective NSAIDs, COX-2 inhibitors do not inhibit platelet aggregation.
As a result, COX-2 inhibitors could adversely affect the hemostatic balance
and favor thrombosis.
The concerns that COX-2 inhibitors might predispose to cardiovascular
thrombotic events came to center stage with publication . . . [Full Text of this Article]
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