Acute coronary syndrome (ACS) is initiated by platelet accumulation at site of atheroma rupture. Thrombin plays a role in both platelet activation and subsequent fibrin formation. Antithrombotic therapy including antiplatelet and anticoagulant is a cornerstone of treatment for ACS and is essentially important for improving acute outcome and prevention of recurrence. Previous basic regimen of un-fractionated heparin, aspirin and clopidogrel may be replaced by newer agents in the future.

　　Platelet activation and aggregation are important pathophysiologic elements of ACS, making antiplatelet agents necessary components of the pharmacotherapeutic treatment paradigm for these patients. Clinical trials have demonstrated the usefulness of antiplatelet agents, percutaneous coronary intervention (PCI), and glycoprotein (GP) IIb/IIIa inhibitors in patients with ACS based on risk stratification. High-risk patients with ACS derive particular benefit from GP IIb/IIIa inhibitors and an early invasive strategy. Long-term oral antiplatelet therapy targeting specific platelet activation pathways has demonstrated significant long-term benefits, whereas antithrombin, such as bivalirudin use is limited to the acute setting. Bivalirudin has proven non-inferior to heparin in patients undergoing PCI. Enoxaparin is emerging as a safer and better alternative to un-fractionated heparin in invasively managed patients.

　　Despite proven efficacy of long-term dual oral antiplatelet therapy with aspirin and clopidogrel, residual morbidity and mortality is considerable. This may be partly due to incomplete inhibition of platelet activation with current agents and/or lack of long-term anticoagulant therapy. Improvements in patient outcomes could be achieved by developing new agents that inhibit other platelet activation pathways or by adding new anticoagulants such as oral anti-IIa or anti-Xa agents for a prolonged period of time after the acute event.
In conclusion, optimized antiplatelet and anticoagulant therapy may reduce the incidence of subclinical and clinical events in ACS patients.