Antiplatelet drug

Platelet aggregation inhibitors or antiplatelet drugs, short TAH, drugs that inhibit the aggregation of platelets ( platelet aggregation) are ( inhibition of platelet aggregation ). They are used in medicine to prevent the growth of blood clots (thrombi ) particularly in the arteries ( arteries). For example, they are prescribed in the prevention and treatment of strokes, heart attacks and other circulatory disorders. Colloquially, antiplatelet agents are often (as well as anticoagulants ) incorrectly referred to as a blood thinner.

Therapeutic Application

Antiplatelet agents used in the therapy are:

  • Abciximab
  • Acetylsalicylic acid ( ASA for short )
  • A combination of acetylsalicylic acid (see above) and dipyridamole
  • Clopidogrel
  • Eptifibatide
  • Ilomedin ( prostacyclin analogue): Prostacyclin is the most potent endogenous inhibitor of platelet aggregation
  • Prasugrel
  • Ticagrelor
  • Ticlopidine
  • Tirofiban

Different mechanisms are responsible for its antiplatelet effect. Aspirin is an irreversible inhibitor of cyclo-oxygenase and thus inhibits platelet aggregation enhancing the thromboxane pathway of platelets. Clopidogrel, ticlopidine, and prasugrel are P2Y - receptor antagonists and inhibit adenosine diphosphate - dependent mechanisms of platelet activation. Ticagrelor reversibly blocked the platelet P2Y12 adenosine receptor. Platelet aggregation inhibition is comparable pronounced as prasugrel, but stronger and faster than with clopidogrel. Dipyridamole as an adenosine reuptake inhibitor with antiplatelet effect of endogenous adenosine. While these mechanisms to inhibit the activation of the platelets, a blockade of Glycoprotein-GPIIb/IIIa-Rezeptoren on the platelet surface by means of drugs, abciximab, tirofiban or eptifibatide leads to a direct inhibition of platelet aggregation.

Because the effect of these drugs for every person is individually somewhat different, the strength of inhibition can be determined for example by means of platelet aggregometry in the laboratory. Particularly in the case of clopidogrel this is the currently preferred method. Depending on the result can then be either reduced or increased the dose to ( too high dose) (at low dose) to set the best possible effect between bleeding and thrombosis.

The dual platelet inhibition, also known as "dual platelet inhibition ," mostly aspirin ( irreversible COX ) inhibitors and clopidogrel served the utilization of two modes of action for the inhibition of platelet aggregation ( irreversible ADP receptor antagonist). This combination is aimed at preventing a closure obligate after stenting in an arterial vessel.

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