Endogenous fibrinolysis inhibitors in acute coronary syndrome.

Patients with acute coronary syndrome have a high residual risk of ischemic events despite current treatment methods, both invasive and antithrombotic strategies. The strategy of very early revascularization although has been suggested to improve patient outcome, remains associated with a high residual risk of adverse events. Stenting of nonflow-limiting vulnerable plaques in addition to stenting of hemodynamically significant lesions in patients with acute coronary syndrome, has not shown a beneficial effect on major adverse cardiovascular events in early studies. Current antithrombotic therapy in acute coronary syndrome is focused mainly on antiplatelet agents, and to a lesser extent on oral anticoagulants. Besides thrombotic atherosclerotic plaque rupture and activated platelets, impaired fibrinolysis has gained attention as a strong independent risk factor for cardiovascular mortality and adverse outcome in patients with acute coronary syndrome. Various endogenous fibrinolysis inhibitors that act at different levels of the hemostatic process have been associated with the impaired fibrinolysis. This review presents available data for association of impaired fibrinolysis with major adverse cardiovascular outcome in acute coronary syndrome, and the potential role of endogenous fibrinolysis inhibitors in acute coronary syndrome. In addition, experimental evidence for modulation of impaired fibrinolytic state with profibrinolytic agents that target endogenous fibrinolysis inhibitors is summarized.