Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most widely used medications worldwide for the treatment of postoperative pain, inflammatory conditions, and fever. They inhibit the conversion of arachadonic acid into prostaglandin H2 by cyclooxygenase (COX), decreasing the downstream synthesis of prostaglandins E2, D2, and F2, which are responsible for the symptom that NSAIDs are commonly used to treat. However, prostaglandin H2 is also metabolized into prostacyclin and thromboxane A2, 2 potent vasoactive prostanoids with directly opposing effects. Prostacyclin, primarily produced by endothelial cells, is a vasodilator and inhibits platelet aggregation, while thromboxane-A2, produced primarily by platelets, is a vasoconstrictor and promotes platelet aggregation.