Prothrombotic potential of NSAID in ischemic heart disease.
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.
Krötz
Florian
F
Institute of Cardiology, Medical Policlinic, Ludwig-Maximilians-University, Ziemssenstr.1, 80336 Munich, Germany. florian.kroetz@med.uni-muenchen.de
Hellwig
Nicole
N
Schiele
Thomas M
TM
Klauss
Volker
V
Sohn
Hae-Young
HY
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use; D016861:Cyclooxygenase Inhibitors / Q000627:therapeutic use; D006801:Humans; D017202:Myocardial Ischemia / Q000188:drug therapy*
D000894:Anti-Inflammatory Agents, Non-Steroidal; D016861:Cyclooxygenase Inhibitors; D001241:Aspirin