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Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit the cyclooxygenase enzyme activity through differentmechanisms and prevent inflammation. But they all have different risks associated with them. Some are associated withgastrointestinal bleeding and some are strongly allied with the cardiovascular risks. Cyclooxygenase enzyme regulatesprostaglandin synthesis by converting arachidonic acid present at the sn-2 position of membrane phospholipids toprostaglandin H2. Prostaglandin H2 is the precursor of all prostaglandins. There are two isoforms of cyclooxygenaseenzyme, cyclooxygenase-1 and cyclooxygenase-2 which differ in their active site due to an isoleucine to valinesubstitution at amino acid 523 in cyclooxygenase-2. Cyclooxygenase-1 is constitutively expressed in plateletswhere it helps in the formation of thromboxane whereas cyclooxygenase-2 is inductive form and is expressed inthe endothelial cells due to shear stress and forms prostacyclins. Both thromboxanes and prostacyclins maintainthe homeostasis of the vascular wall. During vascular injury prostacyclin production decreases as a result of whichthromboxane synthesis increases in the platelets which leads to platelet aggregation. Although, being stronglyassociated with cardiovascular risks, NSAIDs are still prescribed to the patients to prevent pain according to theircondition. So this review aims to summarise the mechanism of cyclooxygenase pathway, possible mechanism ofaction of NSAIDs and the risks of cardiovascular events associated with the use of NSAIDs.

Role of Cyclooxygenase Pathway and Risk Associated with Non-Steroidal Anti-inflammatory Drugs Therapy in Cardiovascular Diseases