Antiplatelets
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Antiplatelet agents is a group of medicines which works by decreasing platelets aggregation and preventing the formation of blood clots. When blood vessels are damaged platelets arrive on the affected area and form blood clots. This helps to stop bleedings. However, in the case of blood vessels injury (inner surface) platelets can aggregate and form blood clots inside the blood vessels. Besides platelets blood clots consist of cholesterol and calcium salts. Blood clots can detach from the blood vessels wall and then plug up the smaller vessels. This usually leads to heart attacks and strokes.
Antiplatelet drugs help to reduce the formation of platelets and usually are prescribed for patients with peripheral artery disease, strokes, stenocardia (chest pain), heart attacks, coronary artery disease. Antiplatelet agents can also be prescribed in conditions after stent placement, angioplasty and bypass surgery as well as prevention of blood clots in patients with arterial fibrillation.
Antiplatelets drugs include the following group of drugs:
- COX (cyclooxygenase) inhibitors: acid acetyl salicylic)
- ADP receptor inhibitors: (clopidogrel and ticlopidine)
- PDE (phosphodiesterase) inhibitors: cilostazol
- Glycoprotein IIB/IIIA inhibitors : Defibrotide, Terofiban, Eptifibatide, Abciximab
- Adenosine reuptake inhibitors: (dipyridamole)
COX inhibitors works by inhibiting the enzyme called cyclooxygenase and thromboxane A2 which are responsible for the formation of platelets
ADP receptor inhibitors act on ADP receptors. They selectively inhibit the activation of GPIIb/IIIa under the action of ADP. This leads to inhibiting ADP induced platelets aggregation.
ADP inhibitors work by inhibiting the enzyme called phosphodiesterase type 3. By inhibiting this enzyme the drugs increase the amount of cAMP and causes the increase of Protein Kinase A. This closely relates to platelets aggregation.
Glycoprotein IIb/IIIa receptor antagonists. Action mechanism of this group of medicines is associated with blocking the platelets receptors in fibrinogen which is structural protein in the platelets.
Adenosine reuptake inhibitors works by increasing the blood levels of ADP. The increased amount of ADP prevents platelets for clumping together.
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