Soluble aspirin (40–80 mg daily) and enteric-coated aspirin (80–100 mg daily) have a cumulative effect, so that platelet TXA 2 formation is maximally inhibited (by more than 95%) after 4–5 days. Thus, this dose (half 324 mg tablet) should be given as a loading dose if a rapid antiplatelet effect is required. When given as a single oral dose, at least 160 mg of soluble aspirin is required to maximally inhibit platelet function within 30 minutes. As, after stopping aspirin therapy, normal haemostasis may be regained when about 20% of platelets have normal cyclooxygenase activity, daily aspirin intake is recommended.ĭose and administration: Formulations of aspirin currently available in Australia include a 100 mg enteric-coated form as well as 300 mg and 324 mg soluble tablets.Īspirin is rapidly absorbed from the gastrointestinal (GI) tract, with peak concentrations achieved in 30–40 minutes. Because platelets are unable to regenerate cyclooxygenase, the immediate antithrombotic effect of aspirin remains for the lifespan of the platelet (8–10 days). 3 It is only the parent form, acetylsalicylic acid, which has any significant effect on platelet function. Mechanism of action: Aspirin (acetylsalicylic acid) irreversibly inhibits prostaglandin H synthase (cyclooxygenase-1) in platelets and megakaryocytes, and thereby blocks the formation of thromboxane A 2 (TXA 2 a potent vasoconstrictor and platelet aggregant). It is an appropriate alternative to aspirin for long-term secondary prevention in patients who cannot tolerate aspirin, have experienced a recurrent vascular event while taking aspirin, or are at very high risk of a vascular event (≥ 20% per year).Īddition of clopidogrel to aspirin reduces the risk of serious vascular events among patients with non-ST-segment elevation acute coronary syndromes by 20%, and patients undergoing percutaneous coronary intervention by 30%, compared with aspirin alone.Īddition of a glycoprotein IIb/IIIa receptor antagonist to aspirin reduces the risk of vascular events among patients with non-ST-segment elevation acute coronary syndromes by 10% and among patients undergoing percutaneous coronary intervention by 30%, compared with aspirin alone it appears to provide incremental benefit in patients also treated with clopidogrel.Īddition of dipyridamole to aspirin seems to be more effective than aspirin alone for preventing recurrent stroke, but its overall effect in preventing serious vascular events in patients with ischaemic stroke and transient ischaemic attack has not been determined. It is as safe as aspirin, but much more expensive. Statistics, epidemiology and research designĪntiplatelet drugs protect against myocardial infarction, stroke, cardiovascular death and other serious vascular events in patients with a history of previous vascular events or known risk factors for cardiovascular disease.Īspirin reduces the risk of serious vascular events in patients at high risk of such an event by about a quarter and is recommended as the first-line antiplatelet drug.Ĭlopidogrel reduces the risk of serious vascular events among high-risk patients by about 10% compared with aspirin.
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