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Mechanism of increased CVD risk associated with NSAIDs

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

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  • selective COX-2 inhibitors and non-selective NSAIDs both inhibit prostacyclin production to a similar degree
    • prostacyclin is vasculoprotective - it plays an inhibitory role in platelet aggregation, hypertension and atherogenesis
    • aspirin protects against vascular events by irreversibly inhibiting COX-1 in platelets - however the COX-1 inhibition by NSAIDs is generally insufficient to produce a similar effect (1)
      • in vivo studies have shown that 95% suppression of platelet COX-1 activity is required to inhibit thromboxane A2-dependent platelet aggregation (2)
        • low-dose aspirin use achieves this degree of inhibition. However other nonselective NSAIDs produce variable COX inhibition ranging from 50% to 95% in a reversible time-dependent fashion (2)
        • hypothesised that this inhibitory pattern may be insufficient to provide cardioprotection throughout the dosing interval and may explain the greater cardiovascular protection provided by aspirin
      • hence the net effect of NSAIDs, whether COX-2 specific or otherwise, is to reduce the vasculoprotective effects of prostacyclin
        • the only possible exception is naproxen which, because of its long duration of action, may inhibit platelet activity at high doses in some individuals, which may explain why naproxen appears to confer least cardiovascular risk (1)


  • it has been postulated that co-prescription of aspirin with NSAIDs may mitigate adverse cardiovascular effects, albeit at increased risk of gastrointestinal side effects (1)


  1. BHF Factfile (3/07). Non steroidal anti-inflammator drugs (NSAIDs) and Cardiovascular Disease.
  2. Reilly IA, Fitzgerald GA (1987). Inhibition of thromboxane formation in vivo and ex vivo: Implications for therapy with platelet inhibitory drugs. Blood; 69:. 180–186.

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