Plaque rupture and thrombus formation play a major role in the genesis of acute coronary occlusion. (See "The role of the vulnerable plaque in acute coronary syndromes".)
The introduction of fibrinolytic (thrombolytic) therapy was a major advance in the treatment of acute ST elevation (Q wave) myocardial infarction (STEMI). Primary percutaneous coronary intervention (PCI) is now preferred for most patients if it can be performed by an experienced operator with less than a two-hour delay from presentation to the emergency department. Due in part to limited availability of primary PCI, fibrinolytic therapy remains an important therapeutic modality. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome".)
In comparison, fibrinolytic therapy has largely not been effective in patients with a non-ST elevation MI (NSTEMI). Coronary arteriography, performed in the acute period following NSTEMI, demonstrates that the infarct-related artery is not occluded in 60 to 85 percent of cases. Since microvascular perfusion is often reduced in patients with NSTEMI, the ongoing mechanism of ischemia is more likely to be embolization than epicardial vessel occlusion .
Currently used fibrinolytic drugs are intravenously infused plasminogen activators that activate the blood fibrinolytic system. These agents have a high specificity for their substrate plasminogen, hydrolyzing a peptide bond to yield the active enzyme plasmin. Free plasmin is rapidly neutralized by the serine proteinase inhibitor alpha-antiplasmin, whereas fibrin-bound plasmin is protected from rapid inhibition, thereby promoting clot lysis. (See "Vascular endothelial function and fundamental mechanisms of fibrinolysis (thrombolysis)".)
The characteristics of the different fibrinolytic agents (table 1) and their efficacy in clinical trials of patients with STEMI will be reviewed here. The indications, contraindications, and adverse effects of these drugs are discussed separately. (See "Fibrinolytic therapy in acute ST elevation myocardial infarction: Initiation of therapy".)