Summary
Acute coronary syndrome (ACS) is a medical emergency. Patients who survive the initial
event remain at risk of recurrent cardiovascular events. In most cases, ACS is triggered
by thrombosis after rupture of an atherosclerotic plaque. Key to thrombus formation
at this site is the generation of thrombin, which not only converts fibrinogen to
fibrin but also serves as a potent platelet agonist and induces platelet aggregation
at the site of vascular injury. Although dual antiplatelet therapy is more effective
for the prevention of recurrent events than aspirin alone after ACS, there remains
an approximately 10 % risk of recurrent ischaemic events at one year. Recent studies
have evaluated whether the addition of an anticoagulant to antiplatelet therapy reduces
the risk of recurrent ischaemia after an ACS event. Rivaroxaban, an oral factor Xa
inhibitor, attenuates thrombin generation. When used in conjunction with dual antiplatelet
therapy in patients with stabilised ACS, rivaroxaban 2.5 mg twice daily significantly
reduced the risk of the composite endpoint of cardiovascular death, myocardial infarction
and stroke compared with placebo. Although it increased the risk of bleeding, rivaroxaban
was associated with a reduction in mortality; a finding that supports the use of a
dual-pathway approach that combines anticoagulant and antiplatelet therapy. This review
explores the pathophysiology of ACS to provide perspective on the results of recent
clinical trials with novel oral anticoagulants for ACS and to identify their potential
role in this setting.
Keywords
Acute coronary syndrome - thrombin - thrombosis - factor Xa - rivaroxaban
