5 Antiplatelet Drugs

How antiplatelet drugs work

Antiplatelet drugs reduce platelet activation and aggregation. They help prevent platelet-rich arterial clots, but they also increase bleeding risk. They are not anticoagulants.

Aspirin irreversibly inhibits platelet cyclooxygenase-1 (COX-1), reducing formation of thromboxane A₂. P2Y₁₂ inhibitors—including clopidogrel, prasugrel, and ticagrelor—block a platelet receptor for ADP. Both approaches reduce platelet aggregation, but they do so through different mechanisms.

Use after acute coronary syndrome and stenting

Antiplatelet treatment is used in conditions including acute coronary syndrome and after coronary stenting. For some patients, treatment combines aspirin with a P2Y₁₂ inhibitor; this is called dual antiplatelet therapy (DAPT). The combination reduces recurrent ischemic events and stent-related thrombosis.

For acute coronary syndrome, DAPT is the default strategy for at least 12 months when bleeding risk is not high. Individualized alternatives may be appropriate. Drug choice and treatment duration depend on the clinical situation and the patient’s ischemic and bleeding risks. Patients should not stop either medicine without consulting their treating clinician.

Use in stroke prevention

Antiplatelet therapy is commonly used to prevent recurrence after a noncardioembolic ischemic stroke or TIA. A stroke related to atrial fibrillation often calls for a different prevention strategy.

DAPT is appropriate only for selected patients and generally for a limited period. Long-term DAPT is not routine therapy for all stroke survivors.

Bleeding risks and drug-specific precautions

The main shared hazard of antiplatelet drugs is bleeding. Patients should promptly report unusual or prolonged bleeding, black or bloody stools, blood in the urine, or extensive unexplained bruising. They should tell clinicians and dentists that they take an antiplatelet drug, and check before starting other medicines or supplements that may increase bleeding.

Aspirin can cause dyspepsia, peptic ulcers, and gastrointestinal or other bleeding. Allergy or aspirin-sensitive asthma requires clinical review. Aspirin should not be given to children or teenagers with viral infections unless specifically directed by a clinician, because of the risk of Reye syndrome. Patients should check with a healthcare professional before adding nonprescription NSAIDs, which can increase bleeding risk.

Prasugrel is contraindicated in patients with a prior stroke or TIA. It is generally not recommended for adults aged 75 years or older, except in selected high-risk situations, and it increases bleeding risk. Ticagrelor can cause dyspnea and is contraindicated with active pathological bleeding or a history of intracranial hemorrhage. Patients should report unexpected or troublesome symptoms rather than stopping treatment on their own.

Interactions and monitoring

Clopidogrel is a prodrug that partly depends on CYP2C19 for activation. Omeprazole and esomeprazole can reduce formation of clopidogrel’s active metabolite and lessen its antiplatelet effect. Patients should ask the prescriber or pharmacist to review this combination and possible alternatives; they should not change either medicine independently.

PT/INR is not a routine measure of aspirin’s or clopidogrel’s antiplatelet effect.