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(Stroke. 2004;35:e26.)
© 2004 American Heart Association, Inc.

Letters to the Editor

Both Thrombotic and Nonthrombotic Cardiovascular and Cerebrovascular Side Effects of Nonsteroidal Anti-Inflammatory Drugs Should Be Considered

2nd Medical Department

Josef Finsterer, MD

Neurological Department, Krankenanstalt Rudolfstiftung, Wien, Austria

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Selective cyclooxygenase (COX)-2 inhibitors are increasingly used instead of "conventional" nonsteroidal anti-inflammatory drugs (NSAIDs). This is because they are just as effective as NSAIDs in relieving pain and less gastrotoxic.^1–3 The cardiovascular safety of selective COX-2 inhibitors, however, has been questioned because they selectively reduce prostacyclin (PGI₂) production without concomitant inhibition of platelet thromboxane A₂ (TXA₂), thus disrupting the normal homeostatic balance and promoting a prothrombotic state. This theory is supported by secondary analyses of clinical trials, which found an increased rate of thrombotic cardiovascular events (like myocardial infarction, unstable angina, ischemic stroke and transient ischemic attacks) in patients randomized to COX-2 inhibitors compared with conventional NSAIDs.^1,4 On the contrary, emerging data from animal, experimental, and clinical studies suggest that COX-2 is atherogenic and thrombogenic and that selective COX-2 inhibitors may be cardioprotective, possibly due to their ability to improve endothelial function.^5,6

Facing these controversies and uncertainties about COX-2 inhibitors, it has to be stressed that both conventional NSAIDs and COX-2 inhibitors share many side effects that may render them dangerous, especially to patients with cardiovascular or cerebrovascular diseases. All NSAIDs have cardiovascular, hematological, renal, central nervous system, and dermatological side effects. They may lead to uncontrolled hypertension and aggravation of heart failure by neurohumoral mechanisms and by attenuation of the effects of cardiac medications like ACE-inhibitors, AT-2 blockers, beta-blockers, and diuretics.^7–9 They potentiate the effect of oral anticoagulants, thus leading to a higher bleeding risk.¹⁰ Whether these side effects occur as frequently during COX-2 . . . [Full Text of this Article]