Abstract
Non-steroidal anti-inflammatory drugs (NSAID) target the enzyme cyclooxygenase (COX) thus affording relieve from pain, inflammation or fever. As COX-dependently formed prostanoids not only mediate signals involved in inflammation and pain, but also regulate important physiological cardiovascular functions, some NSAID have recently been reported to be associated with arterial thrombosis or hypertension. This is in contrast to the well-known antiplatelet effects of low-dose aspirin, but in coherence with the specific effects of some NSAID on prostanoid formation in the vasculature. A correlation between the intake of selective inhibitors of the cyclooxygenase 2 (COX-2) isoform and atherothrombotic events has recently been established. Large retrospective analyses of clinical data have repeatedly shown this effect and in some cases have also observed potential hazards for other, rather non-selective NSAID. This review evaluates potential prothrombotic effects of NSAID in vascular ischemic disease in comparison to low-dose aspirin and selective COX-2 inhibitors and discusses pathophysiological backgrounds for such observations.
Keywords: COX inhibitors, antithrombotic, cardiovascular events, prostaglandin, thromboxane
Mini-Reviews in Medicinal Chemistry
Title: Prothrombotic Potential of NSAID in Ischemic Heart Diesase
Volume: 6 Issue: 12
Author(s): Florian Krotz, Nicole Hellwig, Thomas M. Schiele, Volker Klauss and Hae-Young Sohn
Affiliation:
Keywords: COX inhibitors, antithrombotic, cardiovascular events, prostaglandin, thromboxane
Abstract: Non-steroidal anti-inflammatory drugs (NSAID) target the enzyme cyclooxygenase (COX) thus affording relieve from pain, inflammation or fever. As COX-dependently formed prostanoids not only mediate signals involved in inflammation and pain, but also regulate important physiological cardiovascular functions, some NSAID have recently been reported to be associated with arterial thrombosis or hypertension. This is in contrast to the well-known antiplatelet effects of low-dose aspirin, but in coherence with the specific effects of some NSAID on prostanoid formation in the vasculature. A correlation between the intake of selective inhibitors of the cyclooxygenase 2 (COX-2) isoform and atherothrombotic events has recently been established. Large retrospective analyses of clinical data have repeatedly shown this effect and in some cases have also observed potential hazards for other, rather non-selective NSAID. This review evaluates potential prothrombotic effects of NSAID in vascular ischemic disease in comparison to low-dose aspirin and selective COX-2 inhibitors and discusses pathophysiological backgrounds for such observations.
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Cite this article as:
Krotz Florian, Hellwig Nicole, Schiele M. Thomas, Klauss Volker and Sohn Hae-Young, Prothrombotic Potential of NSAID in Ischemic Heart Diesase, Mini-Reviews in Medicinal Chemistry 2006; 6 (12) . https://dx.doi.org/10.2174/138955706778993030
DOI https://dx.doi.org/10.2174/138955706778993030 |
Print ISSN 1389-5575 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5607 |
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