ABSTRACT
Rupture of a vulnerable atherosclerotic plaque is the most common trigger of thrombus formation in the coronary vasculature that results in an acute MI. The primary composition of thrombus consists of crosslinked fibrin with entrapped cellular elements. The body’s intrinsic fibrinolytic system utilizes plasmin, a nonspecific protease, to digest the meshwork of fibrin clot into fibrinogen degradation productions. In order to be active, plasmin needs to undergo a single peptide bond cleavage from plasminogen. Furthermore, once formed, plasmin catalyzes additional plasminogen conversion into plasmin. Currently available thrombolytic agents are serine protease plasminogen activators that directly or indirectly convert plasminogen to plasmin. These thrombolytic agents differ in fibrin selectivity and half-life duration.
