Early recognition and immediate treatment of acute ST-segment elevation myocardial infarction (STEMI) are essential; diagnosis is based on characteristic history, ECG, and serum cardiac markers.
Chest pain similar to angina (Chap. 31. Chest Pain) but more intense and persistent; not fully relieved by rest or nitroglycerin, often accompanied by nausea, sweating, apprehension. However, ~25% of MIs are clinically silent.
Pallor, diaphoresis, tachycardia, S4, dyskinetic cardiac impulse may be present. If CHF exists, rales and S3 are present. Jugular venous distention is common in right ventricular infarction.
ST elevation, followed (if acute reperfusion is not achieved) by T-wave inversion, then Q-wave development over several hours.
Cardiac-specific troponins T and I are highly specific for myocardial injury and are the preferred biochemical markers for diagnosis of acute MI. They remain elevated for 7-10 days. Creatine phosphokinase (CK) level rises within 4-8 h, peaks at 24 h, and returns to normal by 48-72 h. CK-MB isoenzyme is more specific for MI but may also be elevated with myocarditis or after electrical cardioversion. Serum cardiac markers should be measured at presentation, 6-9 h later, and then at 12-24 h.
Noninvasive Imaging Techniques 
Useful when diagnosis of MI is not clear. Echocardiography detects infarct-associated regional wall motion abnormalities (but cannot distinguish acute MI from a previous myocardial scar). Echo is also useful in detecting RV infarction, LV aneurysm, and LV thrombus. MRI with delayed gadolinium enhancement accurately indicates regions of infarction, but is technically difficult to obtain in acutely ill pts.
Treatment: STEMI |
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