*For medical professionals only
Recommended Favorites!
Antiplatelet drugs are widely used in the treatment of coronary heart disease, stroke and peripheral artery disease. Aspirin, clopidogrel, ticagrelor, sarpogrelate, and ozagrel are commonly used clinical antiplatelet drugs. What is the difference between these five drugs?
I. The process of platelet thrombosis
■1. Platelet adhesion
Under normal circumstances, prostacyclin (PGI2) produced by vascular endothelial cells can relax blood vessels and inhibit platelet aggregation.
When vascular endothelial cells are damaged, PGI2 production is reduced, and platelets can adhere to subendothelial tissue [collagen, von Willebrand factor (vWF), etc.].
Hypertension, hyperlipidemia, hyperglycemia, hyperhomocysteine, etc., can all cause vascular endothelial damage.
Note: Thromboxane A2 (TXA2), Serotonin (5-HT), Adenosine Diphosphate (ADP)
■2. Platelet aggregation
The adhesion of platelets to platelets is called “platelet aggregation.”
Under normal circumstances, the platelet membrane sugar monoprotein complex (GPIIb/IIIa) on the platelet membrane cannot bind to fibrinogen.
When GPIIb/IIIa is activated, it can combine with fibrinogen and connect with adjacent platelets through fibrinogen, so that platelets aggregate and form early thrombus.
ADP, 5-HT and TXA2 are the common pathways of platelet aggregation that activate GPIIb/IIIa.
■3. Vasoconstriction
Platelets adhering to the injury release vasoconstrictor substances such as 5-HT and TXA2, which can cause vasoconstriction and facilitate thrombosis.
Second, the mechanism of action of commonly used antiplatelet drugs
■1, TXA2 synthesis inhibitor
TXA2 promotes platelet aggregation.
Aspirin irreversibly inhibits cyclooxygenase (COX-1), and indobufen reversibly inhibits COX-1.
■2. Cyclic adenosine monophosphate (cAMP) degradation inhibitor
cAMP inhibits platelet aggregation and dilates blood vessels.
Cilostazol inhibits phosphodiesterase III, inhibits the degradation of cAMP, increases the concentration of cAMP in platelets, inhibits platelet aggregation, and dilates blood vessels.
■3. GPⅡb/Ⅲa receptor antagonists
Tirofiban and eptifibatide directly prevent the binding of GPIIb/IIIa to fibrinogen and inhibit platelet aggregation.
■4. ADP receptor antagonists
ADP can indirectly activate GPIIb/IIIa after binding to P2Y12 receptor.
The active metabolite of clopidogrel irreversibly inhibits P2Y12 receptor andADP binding, ticagrelor and its active metabolite reversibly inhibit P2Y12 receptor binding to ADP.
■5,5-HT receptor antagonists
Sapogrelate inhibits 5-HT-induced vascular smooth muscle contraction and platelet aggregation.
III. Clinical application
Cilostazol: Phosphodiesterase III inhibitor, inhibits cAMP degradation, inhibits platelet aggregation and dilates blood vessels.
Sapogrelate: 5-HT receptor antagonist, inhibits platelet aggregation and dilates blood vessels.
Cilostazol and sarpogrelate can be used to improve ischemic symptoms such as ulcers, pain and coldness caused by chronic arterial occlusive disease.
Source of this article: Center for Drug Evaluation
This article was written by Gcplive
Editor in charge: Yuan Xueqing, Zhang Li
Copyright Notice