The PLATO trial demonstrated superior outcomes with ticagrelor over clopidogrel in ACS patients. The mechanism by which ticagrelor differs from clopidogrel is:

• A Ticagrelor is a prodrug requiring hepatic activation whereas clopidogrel is active directly
• B Ticagrelor blocks the GPIIb/IIIa receptor
• C Ticagrelor irreversibly inhibits P2Y12 with faster onset than clopidogrel
• D Ticagrelor reversibly blocks P2Y12 receptor directly without requiring metabolic activation ✓

Explanation

Ticagrelor is a cyclopentyl-triazolopyrimidine that binds P2Y12 receptor directly and reversibly without requiring hepatic biotransformation. Clopidogrel is a thienopyridine prodrug requiring CYP2C19 activation to its active metabolite, which irreversibly binds P2Y12. Ticagrelor's direct, reversible binding gives more predictable and rapid platelet inhibition. This distinction explains why ticagrelor outperformed clopidogrel in the PLATO trial for reducing MACE in ACS.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.