Antithrombotic therapy in acute coronary syndromesBMJ 2002; 325 doi: https://doi.org/10.1136/bmj.325.7376.1348 (Published 07 December 2002) Cite this as: BMJ 2002;325:1348
- Robert D S Watson,
- Bernard S P Chin,
- Gregory Y H Lip
The use of antithrombotic therapy in acute coronary syndromes has reduced the incidence of death and Q wave myocardial infarction dramatically in recent years. Antithrombotic drugs in routine use include antiplatelet drugs (aspirin, clopidogrel, and glycoprotein IIb/IIIa receptor antagonists) and anticoagulants (unfractionated and low molecular weight heparin, warfarin, and direct thrombin inhibitors).
Thrombosis is the basic pathophysiological process underlying the acute coronary syndromes. Thus, antithrombotic therapy is the cornerstone of management, and the appropriate choice of antithrombotic drugs to reduce platelet aggregation or interfere with the clotting process can be critical.
Rupture of the fibrous cap of an atheromatous plaque exposes the lipid core, which is highly thrombogenic and contains an abundance of procoagulant tissue factor. Plaque rupture (exposing surface binding glycoproteins) allows platelets to adhere to the plaque, become activated, and release thromboxane A2, which causes further platelet aggregation and vasoconstriction. As the platelets aggregate around the ruptured plaque, membrane glycoprotein IIb/IIIa receptors undergo a configuration change to bind fibrinogen and form a complex platelet linkage. Further incorporation of fibrin and red blood cells within this platelet-rich thrombus results in a partial or total occlusion of the coronary artery. Alternatively, thrombus may break off from a ruptured plaque and occlude a downstream vessel. Occlusion may also follow from trapping of circulating thrombi formed elsewhere in the circulation.
Aspirin has been in use for more than 150 years and is cheap and effective. It has been shown to reduce the risk of fatal and non-fatal myocardial infarction by at least 50% in patients with unstable angina. Aspirin blocks cyclo-oxygenase and formation of thromboxane A2, thus …
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