Antiplatelet Therapy 
BMS3021 – Research Topic: Aspirin
TOPIC SUMMARY
Aspirin is able to inhibit the synthesis of the Thromboxane A2 precursor, by irreversibly binding to the COX-1 enzyme
Lack of Thromboxane A2 means that there is no signalling for platelet aggregation so there is no blood clot formation, leading to its ability to act as a ‘blood thinner‘
SALT found that in a low-dose of 75mg of Aspirin a day, secondary prophylaxis of new cardiovascular events were reduced by 16-20%
By decreasing the daily dose to 75mg instead of 300mg or higher, there was also a significant decrease in the frequency of gastrointestinal side-effects
POWERPOINT
The role of Thromboxane in Heart Attacks and Strokes
What is Thromboxane – normal role in the body
What is its role in causing heart attacks and stroke
Aspirin as a Blood Thinner
How does Aspirin inhibit thromboxane production, therefore reducing coagulation
RCT – in Secondary Prevention
Aim, Method, Results, Outcome – evaluate findings of the study
WRITTEN REPORT
Thromboxanes are a group of eicosanoids derived from Arachidonic Acid. They are synthesised through the cyclooxygenase pathway, and are derivatives of the prostaglandin intermediate, PGH2. In platelets, thromboxane synthase is the enzyme responsible for the conversion of Thromboxane into its active form, Thromboxane A2 (TXA2). In the event of vascular injury, platelets release Adenosine diphosphate (ADP) and TXA2. ADP is responsible for the activation of other platelets, while TXA2 primarily causes platelet aggregation and vasoconstriction. As platelets lack nuclei, they are unable to produce the inducible COX-2 enzyme, meaning that only the COX-1 isoform is present. Build-up of plaque in the arteries supplying blood to the heart or brain is the major cause of heart attacks and strokes. In some cases, accumulation of plaque can lead to rupture of the artery walls, resulting in platelet, and subsequent TXA2 activation. A combination of arterial stenosis and thrombus formation
TOPIC SUMMARY
Aspirin is able to inhibit the synthesis of the Thromboxane A2 precursor, by irreversibly binding to the COX-1 enzyme
Lack of Thromboxane A2 means that there is no signalling for platelet aggregation so there is no blood clot formation, leading to its ability to act as a ‘blood thinner‘
SALT found that in a low-dose of 75mg of Aspirin a day, secondary prophylaxis of new cardiovascular events were reduced by 16-20%
By decreasing the daily dose to 75mg instead of 300mg or higher, there was also a significant decrease in the frequency of gastrointestinal side-effects
POWERPOINT
The role of Thromboxane in Heart Attacks and Strokes
What is Thromboxane – normal role in the body
What is its role in causing heart attacks and stroke
Aspirin as a Blood Thinner
How does Aspirin inhibit thromboxane production, therefore reducing coagulation
RCT – in Secondary Prevention
Aim, Method, Results, Outcome – evaluate findings of the study
WRITTEN REPORT
Thromboxanes are a group of eicosanoids derived from Arachidonic Acid. They are synthesised through the cyclooxygenase pathway, and are derivatives of the prostaglandin intermediate, PGH2. In platelets, thromboxane synthase is the enzyme responsible for the conversion of Thromboxane into its active form, Thromboxane A2 (TXA2). In the event of vascular injury, platelets release Adenosine diphosphate (ADP) and TXA2. ADP is responsible for the activation of other platelets, while TXA2 primarily causes platelet aggregation and vasoconstriction. As platelets lack nuclei, they are unable to produce the inducible COX-2 enzyme, meaning that only the COX-1 isoform is present. Build-up of plaque in the arteries supplying blood to the heart or brain is the major cause of heart attacks and strokes. In some cases, accumulation of plaque can lead to rupture of the artery walls, resulting in platelet, and subsequent TXA2 activation. A combination of arterial stenosis and thrombus formation