INTRODUCTION

Mechanisms of thrombogenesis are closely linked, with activation of both the coagulation and platelet aggregation pathways being responsible for thrombus formation.

Thrombin, a key clotting enzyme generated by blood coagulation, is a very potent platelet activator. At the same time, activated platelets provide a platform for the coagulation process. Therefore combination therapy with antiplatelet agents and anticoagulants should be effective in the prevention and treatment of arterial and venous thrombosis. Conversely, considering the pathophysiology, antiplatelet therapy would be more effective in the case of arterial thrombosis, whereas anticoagulants would have superior efficacy in venous and cardiac thromboembolism (Fig. 21.1).

The real stand of antiplatelet therapy versus other antithrombotic strategies and their combination can be derived from studies assessing these treatment modalities in patients at risk or in those diagnosed with coronary artery disease (CAD), peripheral vascular disease, atrial fibrillation, stroke, deep venous thrombosis, and pulmonary embolism.

Antiplatelet therapy for arterial thrombosis in patients with CAD is constantly evolving. Essentially all patients with acute coronary syndrome (ACS) are currently recommended to receive dual antiplatelet therapy, including acetylsalicylic acid (ASA) and clopidogrel, with proven indications for triple antiplatelet therapy by adding GP IIb/IIIa inhibitors (GPIs) for patients with high-risk features. The search for additional benefits regarding mortality rate, cardiovascular events, bleeding, convenience, and cost of treatment is continuing.