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New antiplatelet agents
H D White1, J K French, C J Ellis
1Green Lane Hospital, Auckland, New Zealand.
Insights
Aspirin and newer antiplatelet agents target platelet aggregation pathways. Glycoprotein IIb/IIIa inhibitors show promise as adjunctive therapy for acute coronary syndromes and secondary prevention.
Area of Science:
- Cardiology
- Pharmacology
- Thrombosis
Background:
- Aspirin is a standard therapy for acute myocardial infarction (AMI) and unstable angina, and for secondary prevention in stable angina.
- Aspirin inhibits cyclooxygenase-1, reducing thromboxane A2 production and thus one pathway of platelet aggregation.
- Other antiplatelet agents like ticlopidine and clopidogrel inhibit adenosine diphosphate-mediated aggregation, affecting only one of many platelet activation pathways.
Purpose of the Study:
- To review the role of antiplatelet agents in managing acute coronary syndromes.
- To discuss the mechanisms of action of aspirin, ADP inhibitors, and glycoprotein IIb/IIIa inhibitors.
- To highlight the evolving role of glycoprotein IIb/IIIa inhibitors in angioplasty, unstable angina, and AMI.
Main Methods:
- Review of clinical trials evaluating antiplatelet agents.
- Discussion of the mechanisms of platelet aggregation and inhibition.
- Analysis of the characteristics and trial data for various antiplatelet drug classes.
Main Results:
- Aspirin inhibits a single pathway of platelet aggregation.
- Ticlopidine and clopidogrel target adenosine diphosphate-mediated aggregation.
- Glycoprotein IIb/IIIa inhibitors block the final common pathway of platelet aggregation and are used as adjunctive therapy.
Conclusions:
- Glycoprotein IIb/IIIa inhibitors have a significant role in adjunctive therapy for angioplasty and acute coronary syndromes.
- Ongoing trials are evaluating intravenous and oral glycoprotein IIb/IIIa inhibitors for broader clinical application.
- These agents are expected to be increasingly integrated into the management of patients with acute coronary syndromes.
Abstract:
Aspirin is an established therapy for the management of acute myocardial infarction (AMI) and unstable angina. Secondary prevention with chronic aspirin therapy is also indicated for patients with stable angina. Aspirin inhibits cyclo-oxygenase-I, a key enzyme in the biosynthetic pathway leading to the production of thromboxane A2. It therefore inhibits only one of the many activation pathways leading to platelet aggregation. Other antiplatelet agents that have also been evaluated in clinical trials include ticlopidine and clopidogrel, which inhibit adenosine diphosphate-mediated platelet aggregation, but these agents are known to be effective against only one of the 90 known agonists that stimulate platelet aggregation. The final common pathway for platelet aggregation involves the glycoprotein IIb/IIIa receptor combining with fibrinogen. Several inhibitors of the glycoprotein IIb/IIIa receptor have been developed and have an important role as adjunctive therapy in angioplasty. Recent trials have been performed in patients with unstable angina, and trials of adjunctive therapy are currently underway in patients receiving thrombolysis for AMI, and for secondary prevention. These drugs have various different features, including specificity for blockade of the glycoprotein IIb/IIIa receptor, half life, duration of the haemostatic effect and potential for antigenicity. Recently concluded and ongoing trials of both intravenous and oral agents are expected to provide further support for the introduction of these agents into clinical management of patients with acute coronary syndromes.