Category:Antiplatelet drugs: Difference between revisions
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[[Category:Cardiovascular Drug]] | [[Category:Cardiovascular Drug]] | ||
'''Antiplatelet drugs''' | |||
Platelet aggregation is important in haemostasis and is also involved in thrombus formation, particularly in the arterial circulation. Antiplatelet drugs reduce platelet aggregation and are used to prevent further thromboembolic events in patients who have suffered myocardial infarction, ischaemic stroke or transient ischaemic attacks, or unstable angina, and for primary prevention of a thromboembolic event in patients at risk. | Platelet aggregation is important in haemostasis and is also involved in thrombus formation, particularly in the arterial circulation. Antiplatelet drugs reduce platelet aggregation and are used to prevent further thromboembolic events in patients who have suffered myocardial infarction, ischaemic stroke or transient ischaemic attacks, or unstable angina, and for primary prevention of a thromboembolic event in patients at risk. | ||
Antiplatelet drugs act through a wide range of mechanisms. Aspirin is the most widely used. It acts by irreversibly inhibiting platelet cyclo-oxygenase and thus preventing synthesis of thromboxane A2. | Antiplatelet drugs act through a wide range of mechanisms. Aspirin is the most widely used. It acts by irreversibly inhibiting platelet cyclo-oxygenase and thus preventing synthesis of thromboxane A2. | ||
Revision as of 03:59, 5 August 2022
Antiplatelet drugs
Platelet aggregation is important in haemostasis and is also involved in thrombus formation, particularly in the arterial circulation. Antiplatelet drugs reduce platelet aggregation and are used to prevent further thromboembolic events in patients who have suffered myocardial infarction, ischaemic stroke or transient ischaemic attacks, or unstable angina, and for primary prevention of a thromboembolic event in patients at risk.
Antiplatelet drugs act through a wide range of mechanisms. Aspirin is the most widely used. It acts by irreversibly inhibiting platelet cyclo-oxygenase and thus preventing synthesis of thromboxane A2.
