Antiplatelet drug

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An antiplatelet drug (antiaggregant) is a member of a class of pharmaceuticals that decrease platelet aggregation [1] and inhibit thrombus formation. They are effective in the arterial circulation, where anticoagulants have little effect.[citation needed]

They are widely used in primary and secondary prevention of thrombotic cerebrovascular or cardiovascular disease.

Antiplatelet drug decreases the ability of blood clot to form by interfering with platelet activation process in primary haemostasis.[2] Antiplatelet drugs can reversibly or irreversibly inhibit the process involved in platelet activation resulting in decreased tendency of platelets to adhere to one another and to damaged blood vessels endothelium.[2]

Choice of antiplatelet drug[edit]

A 2006 review [3] states: "...low-dose aspirin increases the risk of major bleeding 2-fold compared with placebo. However, the annual incidence of major bleeding due to low-dose aspirin is modest—only 1.3 patients per thousand higher than what is observed with placebo treatment. Treatment of approximately 800 patients with low-dose aspirin annually for cardiovascular prophylaxis will result in only 1 additional major bleeding episode."


The class of antiplatelet drugs include:


Prevention and treatment of arterial thrombosis

Prevention and treatment of arterial thrombosis is essential in patients with certain medical conditions whereby the risk of thrombosis or thromboembolism may result in disastrous consequences such as heart attack, pulmonary embolism or stroke.[2] Patients who require the use of antiplatelet drugs are: stroke with or without atrial fibrillation, any heart surgery (especially prosthetic replacement heart valve), Coronary Heart Disease such as stable angina, unstable angina and heart attack, patients with coronary stent, Peripheral Vascular Disease/Peripheral Arterial Disease and apical/ventricular/mural thrombus.[2]

Treatment of established arterial thrombosis includes the use of antiplatelet drugs and thrombolytic therapy. Antiplatelet drugs alter the platelet activation at the site of vascular damage crucial to the development of arterial thrombosis.

  • Aspirin and Triflusal irreversibly inhibits the enzyme COX, resulting in reduced platelet production of TXA2 (thromboxane - powerful vasoconstrictor that lowers cyclic AMP and initiates the platelet release reaction).
  • Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic AMP with potentiation of the action of PGI2 – opposes actions of TXA2
  • Clopidogrel affects the ADP-dependent activation of IIb/IIIa complex
  • Glycoprotein IIb/IIIa receptor antagonists block a receptor on the platelet for fibrinogen and von Willebrand factor. 3 classes:
    • Murine-human chimeric antibodies (e.g., abciximab)
    • Synthetic peptides (e.g., eptifibatide)
    • Synthetic non-peptides (e.g., tirofiban)
  • Epoprostenol is a prostacyclin that is used to inhibit platelet aggregation during renal dialysis (with or without heparin) and is also used in primary pulmonary hypertension.

Thrombolytic therapy is used in myocardial infarction, cerebral infarction, and, on occasion, in massive pulmonary embolism. The main risk is bleeding. Treatment should not be given to patients having had recent bleeding, uncontrolled hypertension or a hemorrhagic stroke, or surgery or other invasive procedures within the previous 10 days.

  • Streptokinase forms a complex with plasminogen, resulting in a conformational change that activates other plasminogen molecules to form plasmin.
  • Plasminogen activators (PA), tissue-type plasminogen activators (alteplase, tenecteplase) are produced by recombinant technology.

Drug toxicity[edit]

Drug toxicity may be increased when multiple antiplatelet drugs are used. Gastrointestinal bleeding is a common adverse event seen in many patients.[4]

See also[edit]