Choice of agents to limit the coagulation cascade in acute coronary syndromes.

Arterial thrombosis, the predominant event in acute coronary syndromes (ACS), is the end-result of endothelial cell dysfunction, impaired vascular thromboresistance, and sudden atheromatous plaque disruption, each occurring amid a backdrop of inflammation and inflammatory mediators. Because the contribution of individual coagulation proteins to coronary arterial thrombosis varies from modest to marked, selective pharmacologic targeting is both pathobiologically sound and clinically preferred. The development of second-generation anticoagulants with broadened therapeutic windows represents an advance in the management of ACS.