Antiplaquettaires

Antiplaquettaires, in medical terminology, are drugs that inhibit platelet aggregation to reduce the formation of arterial thrombi. They are distinct from anticoagulants, which target the coagulation cascade, and from antiplatelet agents used for venous thromboembolism prevention. The term is used in French-language literature to describe this class of medications.

The mechanisms of antiplaquettaires vary by subclass. Aspirin inhibits cyclooxygenase-1, lowering thromboxane A2 production and thereby reducing platelet activation. P2Y12 receptor inhibitors, such as clopidogrel, prasugrel, and ticagrelor, block ADP-induced platelet activation. Other agents include dipyridamole, which elevates cyclic AMP by inhibiting phosphodiesterase and increasing extracellular adenosine, and glycoprotein IIb/IIIa inhibitors (eptifibatide, abciximab, tirofiban), which prevent final common pathways of platelet aggregation. Cilostazol, a phosphodiesterase-3 inhibitor, has both antiplatelet and vasodilatory effects. Some regimens combine different antiplaquettaire drugs to enhance protection against thrombotic events.

Clinical use focuses on the prevention of arterial thrombosis in conditions such as acute coronary syndrome, post-percutaneous coronary intervention with stent placement, and secondary prevention after ischemic stroke or transient ischemic attack. Therapy must balance thrombotic risk against bleeding risk, with careful consideration of patient factors and potential drug interactions, especially with nonsteroidal anti-inflammatory drugs, anticoagulants, and certain antidepressants. Discontinuation around surgical procedures requires coordinated planning to minimize bleeding or thrombotic complications.

In summary, antiplaquettaires are a key class of antithrombotic agents whose primary role is to prevent platelet-driven clot formation in high-risk cardiovascular settings.