Antiplatelets

Antiplatelets reduce platelet activation and aggregation, making them especially useful against platelet-rich thrombi in diseased arteries. Their major clinical settings are acute coronary syndrome (ACS), coronary stenting, non-cardioembolic ischemic stroke or TIA, and symptomatic peripheral arterial disease. They do not replace anticoagulation when the dominant problem is a cardioembolic or venous clotting mechanism. The benefit and hazard are inseparable: suppressing platelet function lowers infarction and stent-thrombosis risk but makes bleeding more likely. Aspirin is often paired with a P2Y12 inhibitor as dual antiplatelet therapy (DAPT) during a period of heightened ischemic risk, then treatment is reduced when the bleeding risk begins to outweigh additional protection. The correct plan is therefore not simply to choose the strongest drug; it is to match the drug, combination, and duration to the indication, the procedure, the patient's bleeding risk, and any need for anticoagulation or surgery. For Canadian practice, routine aspirin initiation for primary cardiovascular prevention is no longer the default. A patient without established atherosclerotic disease needs an individualized benefit–harm discussion rather than automatic low-dose aspirin.