Key result
COX-2 inhibitors and certain NSAIDs increase cardiovascular thrombotic risk by disrupting prostacyclin-thromboxane balance.
This narrative review highlights that because NSAIDs alter the balance between prothrombotic platelet thromboxane and vasoprotective endothelial prostacyclin, clinicians must carefully weigh individual cardiovascular and gastrointestinal risks and prescribe the lowest effective NSAID dose for the shortest duration.
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the cyclooxygenase enzyme activity through different mechanisms and prevent inflammation. But they all have different risks associated with them. Some are associated with gastrointestinal bleeding and some are strongly allied with the cardiovascular risks. Cyclooxygenase enzyme regulates prostaglandin synthesis by converting arachidonic acid present at the sn-2 position of membrane phospholipids to prostaglandin H2. Prostaglandin H2 is the precursor of all prostaglandins. There are two isoforms of cyclooxygenase enzyme, cyclooxygenase-1 and cyclooxygenase-2 which differ in their active site due to an isoleucine to valine substitution at amino acid 523 in cyclooxygenase-2. Cyclooxygenase-1 is constitutively expressed in platelets where it helps in the formation of thromboxane whereas cyclooxygenase-2 is inductive form and is expressed in the endothelial cells due to shear stress and forms prostacyclins. Both thromboxanes and prostacyclins maintain the homeostasis of the vascular wall. During vascular injury prostacyclin production decreases as a result of which thromboxane synthesis increases in the platelets which leads to platelet aggregation. Although, being strongly associated with cardiovascular risks, NSAIDs are still prescribed to the patients to prevent pain according to their condition. So this review aims to summarise the mechanism of cyclooxygenase pathway, possible mechanism of action of NSAIDs and the risks of cardiovascular events associated with the use of NSAIDs.
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Kumar et al. (2018) conducted a review in Cardiovascular diseases and pain/inflammation requiring NSAID therapy. Non-steroidal anti-inflammatory drugs (NSAIDs) was evaluated on Cardiovascular events (including acute myocardial infarction and stroke). Selective COX-2 inhibitors and certain non-selective NSAIDs increase cardiovascular thrombotic risk by disrupting vascular prostacyclin and platelet thromboxane homeostasis.
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