The gold standard for measuring reperfusion or coronary artery patency is coronary angiography. Bedside markers of reperfusion include the resolution of chest pain, reduction in ST-segment elevations, reperfusion arrhythmia, and early peaking creatine phosphokinase level. These markers, however, are extremely insensitive and lack specificity unless all occur together. Other available tests include early myoglobin peaking, thallium or sestamibi redistribution, improvement of wall motion abnormality on echocardiography, gated blood pool or magnetic resonance imaging, as well as signal average parameters and ultrasound tissue characterization.
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These tests have different availabilities, various advantages, and disadvantages. Their usefulness may depend on the institution as well as the clinical setting.
Does any thrombolytic agent confer improved survival benefit over the others?
Although tPA has higher patency rates than streptokinase or APSAC, there were no difference noted in survival until the recent GUSTO trial. This trial, using an accelerated tPA dosing schedule along with intravenous heparin, provided an approximately 14% survival benefit when compared to streptokinase combined with subcutaneous heparin, intravenous heparin, or tPA. An increased risk of intracerebral bleeding also was noted in the tPA group.
What adjunctive therapies are used to prevent reocclusion and potentiate thrombolysis?
Antiplatelet therapy with aspirin is an essential adjunct and has been recommended ever since ISIS II demonstrated its efficacy with or without a thrombolytic agent. Agents that bind or competitively inhibit glycoprotein receptors (glycoprotein IIB-IIIA) and prevent platelet cross-linking are under investigation. Inhibitors of the binding site for von Willebrand factor are also under investigation. Heparin accelerates the formation of antithrombin III complexes which, in turn, impede thrombin activity. Hirudin is a more specific direct inhibitor of thrombin and is currently being evaluated in the GUSTO II trial.