Celecoxib, a selective COX-2 inhibitor, has increased cardiovascular risk compared to non-selective NSAIDs because:

• A It inhibits COX-1 in renal tubules, causing sodium retention and hypertension
• B It directly activates platelet aggregation via thromboxane receptor stimulation
• C It has a higher affinity for cardiac COX-1, reducing myocardial prostacyclin production
• D It blocks COX-2-derived prostacyclin (PGI2) in endothelium without affecting COX-1-derived thromboxane A2 in platelets ✓

Explanation

COX-2 is the predominant isoform in vascular endothelium and generates anti-aggregatory, vasodilatory prostacyclin (PGI2). Selective COX-2 inhibitors suppress endothelial PGI2 without affecting platelet COX-1-derived TXA2 (which promotes aggregation and vasoconstriction), tipping the prostaglandin balance toward a pro-thrombotic, pro-vasoconstrictive state and increasing cardiovascular events (rofecoxib was withdrawn for this reason).

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

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