Blood clotting is a complex process involving both circulating proteins and platelet activation. When blood vessels sustain damage, platelets bind to exposed collagen and von Willebrand factor, leading to further platelet activation and the formation of a plug. This plug is solidified by a fibrin meshwork. Central to this mechanism are platelet activators like adenosine diphosphate (ADP), serotonin, and thromboxane A2, with thromboxane A2 being synthesized mainly by the COX enzymes, especially COX-1.
Antiplatelet drugs such as aspirin counter platelet aggregation by targeting COX enzymes and P2Y12 ADP receptors. Others, like abciximab, eptifibatide, and tirofiban, inhibit GP IIb/IIIa receptors, preventing the binding of fibrinogen to platelets. Additionally, phosphodiesterase inhibitors like dipyridamole and cilostazol increase cAMP and disrupt platelet function, resulting in arterial dilation.
Aspirin impedes platelet aggregation by inhibiting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), reducing the synthesis of thromboxanes, especially thromboxane A2 (TXA2)‚Äîa potent promoter of platelet aggregation. clopidogrel and prasugrel, classified as P2Y12 inhibitors, inhibit the ADP-dependent activation of the GP IIb/IIIa complex, a pivotal glycoprotein involved in platelet aggregation. By inhibiting these processes, these agents effectively diminish platelet aggregation and subsequent thrombus formation.
Coagulation factors orchestrate a series of reactions culminating in the creation of fibrin strands, which solidify the initial platelet plug at an injury site. Thrombin, derived from prothrombin, plays a cardinal role in coagulation by transforming soluble fibrinogen into insoluble fibrin. This fibrin meshwork consolidates and reinforces the initial platelet plug, resulting in a resilient thrombus.
Antiplatelet agents are crucial in managing cardiovascular disorders. They are vital in the treatment of acute myocardial infarction and in preventing recurrent events in coronary artery disease. Additionally, they are routinely prescribed for ischemic stroke prevention following a transient ischemic attack and in patients with peripheral arterial disease.
Eftifibatide and tirofiban are GP IIb/IIIa inhibitors that prevent platelet aggregation by blocking fibrinogen from binding to platelets. They show pronounced efficacy in acute coronary situations and during coronary procedures. A notable side effect of both drugs is thrombocytopenia, elevating the risk of bleeding.