Fibrinolytics: current indications and treatment modalities in the absence of mechanical reperfusion
Fibrinolytic therapy and reperfusion Acute MI is generally caused by rupture of an atherosclerotic plaque, triggering the formation of an occlusive coronary thrombus. Coronary artery occlusion sets off a wave front of myocardial necrosis spreading from endocardium to epicardium, with an inverse relation between the time to perfusion and the ultimate size and extent of transmurality of the infarct. To rescue myocardial muscle at risk from undergoing necrosis, rapid restoration of coronary blood flow is essential. In the absence of access to immediate primary PCI, clot lysis can be achieved by activating the endogenous fibrinolytic
system using plasminogen-activating agents. These agents convert plasminogen to plasmin, which then degrades fibrin, a major constituent of clots ( Figure 19.1 ).