Antiplatelet medications

This article has been translated from WikiSkripta; the formatting needs to be checked.

Antiplatelet medications (also antiaggregans) inhibit primary homeostasis and thus prevent the forming of primary platelet thrombus (platelet plug). They are mainly used as profylaxis for arterial thrombosis.

Common indications:

secondary prevention of myocardial infarction
secondary prevention of ischemic stroke and transitory ischemic attack (TIA)

Mechanism of action[edit | edit source]

We can classify antiplatelet drugs based on the mechanism of action:

irreversible inhibitors of COX on platelets and endothelial cells
inhibitors of platelet ADP receptors
inhibitors for fibrinogen (gpIIb-IIIa) receptors
inhibitors of platelet cyclic nucleotide phosphodiesterase

Irreversible inhibitors of COX on platelets and endothelial cells[edit | edit source]

Acetylsalicic acid (aspirin) is most commonly used antiplatelet medication. ASA irreversibly inactivates cyclooxygenase enzyme (COX-1) in platelets and thus stops the synthesis of prothrombic Thromboxane A2. By blocking COX-2 in endothelial cells it blocks the synthesis of vasodilating and antiplatelet PGI2 in endothelial cells. The therapy aims to block only the aggregating agent TXA2 while maintaining PGI2 secretion. This is achieved by administering low doses of ASA (100-300 mg/day), because of the different affinity of ASA to COX-2 and COX-2. At these doses, irreversible blockade of platelet cyclooxygenase occurs and lasts throughout the life of the platelet, approximately 7-8 days.

Inhibitors of platelet ADP receptors[edit | edit source]

These medications inhibit adenosine diphosphate induced (ADP-induced) platelet aggregation. They are administered to patients who do not tolerate the ASA for various reasons (eg. peptic ulcer) and to patients in whom we need dual antiplatelet therapy. This group includes: clopidogrelTemplate:HVLP, ticlopidine and new substances ticagrelorTemplate:HVLP a prasugrelTemplate:HVLP.

Ticlopidine is not used anymore because of potential hemotoxicity.
Ticagrelor and prasugrel in combination with ASA are used for antiplatelet therapy in arterial interventions (especially before and after percutaneous coronary artery interventions).

Inhibitors for fibrinogen (gpIIb-IIIa) receptors[edit | edit source]

Glycoproteins gpIIb-IIIa are fibrinogen receptors on the platelet surface. By blocking these receptors, we inhibit the final step of platelet activation. This group includes: abciximabTemplate:HVLP, tirofiban a eptifibatideTemplate:HVLP. Abciximab is a fragment of the chimeric monoclonal antibody and is indicated for patients who do not respond to conventional therapy and to prevent cardiac complications in percutaneous interventions. Tirofiban is a non-peptide antagonist that is indicated for unstable angina pectoris. The cyclic heptapeptide eptifibatide has similar indications. The importance of gpIIb-IIIa inhibitors decreased after the introduction of ticagrelor and prasugrel into clinical practice.

Inhibitors of platelet cyclic nucleotide phosphodiesterase[edit | edit source]

This group includes dipyridamole. It is a coronary vasodilator that does not show antiplatelet effects in vitro. It increases cAMP levels in platelets and reduces platelet adhesion to damaged endothelium. In therapy, it is most often used in combination with another antiplatelet agent.

Links[edit | edit source]

Literature[edit | edit source]

LINCOVÁ, Dagmar, et al. Základní a aplikovaná farmakologie. 1. edition. GALÉN, 2002. 601 pp. ISBN 80-7262-168-8.

HYNIE, Sixtus. Farmakologie v kostce. 2. edition. Praha : Triton, 2001. 520 pp. ISBN 80-7254-181-1.

WIVIOTT, Stephen D – STEG, Philippe Gabriel. Clinical evidence for oral antiplatelet therapy in acute coronary syndromes. Lancet [online]. 2015, vol. 386, no. 9990, p. 292-302, Available from <https://www.ncbi.nlm.nih.gov/pubmed/25777663>. ISSN 0140-6736 (print), 1474-547X.

IQBAL, Arshad Muhammad – LOPEZ, Richard A – HAI, Ofek. StatPearls : Antiplatelet Medications [online]. StatPearls Publishing, The last revision October 23, 2020, [cit. December 01, 2020]. <https://www.ncbi.nlm.nih.gov/books/NBK537062/>.