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INTRODUCTION

Early recognition and immediate treatment of acute MI are essential; diagnosis is based on characteristic history, ECG, and serum cardiac markers.

Symptoms

Chest pain similar to angina (Chap. 37) 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.

Physical Examination

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.

ECG

ST elevation, followed (if acute reperfusion is not achieved) by T-wave inversion, then Q-wave development over several hours (see Figs. 120-3 and 120-4).

Non-ST Elevation MI, or NSTEMI

ST depression followed by persistent ST-T-wave changes without Q-wave development. Comparison with old ECG helpful (see Chap. 129).

Cardiac Biomarkers

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. Total CK (but not CK-MB) rises (two- to threefold) after IM injection, vigorous exercise, or other skeletal muscle trauma. A ratio of CK-MB mass: CK activity ≥2.5 suggests acute MI. CK-MB peaks earlier (about 8 h) following acute reperfusion therapy (see below). 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. Myocardial perfusion imaging (thallium 201 or technetium 99m-sestamibi) is sensitive for regions of decreased perfusion, but is not specific for acute MI. MRI with delayed gadolinium enhancement accurately indicates regions of infarction, but is technically difficult to obtain in acutely ill pts.

TREATMENT STEMI INITIAL THERAPY

Initial goals are to (1) quickly identify if pt is candidate for reperfusion therapy, (2) relieve pain, and (3) prevent/treat arrhythmias and mechanical complications.

  • Aspirin should be administered immediately (162–325 mg chewed at presentation, then 162–325 mg PO qd), unless pt is aspirin-intolerant.

  • Perform targeted history, exam, and ECG to identify STEMI (>1 mm ST elevation in two contiguous limb leads, ≥2 mm ST elevation in two contiguous precordial leads, or new LBBB) and appropriateness of reperfusion therapy [percutaneous coronary intervention (PCI) or IV fibrinolytic agent], which reduces infarct size, LV dysfunction, and mortality.

  • Primary PCI is generally ...

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