How is the diagnosis of acute myocardial infarction made?

The diagnosis of myocardial infarction is made on the basis of clinical presentation, electrocardiographic (ECG) findings, and elevated serum enzymes. Classic ECG findings of acute Q-wave myocardial infarction initially include hyperacute T waves and ST-segment elevation. T-wave inversion and the development of Q waves follow over hours to days. In nontransmural infarction, ECG findings are less specific and include T-wave inversion and ST-segment depression. It is important to note that the ECG is normal in 20% of acute myocardial infarctions. Right ventricular infarction can be diagnosed using right-sided precordial ECG leads. ST elevation of 0.5 mm or more in V3R-V6R is diagnostic. Precordial lead V4R is the most sensitive. Right-sided ECG leads should be obtained routinely in the setting of inferior ischemia.

Creatinine kinase (CK), lactate dehydrogenase (LDH), and serum glutamic oxaloacetic transferase (AST, SGOT) are enzymes used in making the diagnosis of infarction. CK rises within 6-8 hours of infarction, peaks at 24 hours, and normalizes by 48-96 hours. CK-MB is an isoenzyme of CK found almost exclusively in myocardium and is the cornerstone of enzymatic diagnosis. Elevations in CK-MB have also been reported with myocarditis, cardiac defibrillation, cardiac surgery, cardiac contusions, and prolonged ischemia without infarction. It may be falsely elevated in renal failure and hypothyroidism. LDH and its isoenzymes also rise in myocardial infarction, beginning at 24-48 hours, peaking in 3-5 days, and normalizing in 7-10 days. A ratio of isoenzymes LDH[/LDH2 of 1.0 is sensitive for myocardial infarction. SGOT levels usually peak in 48-72 hours, although this enzyme is not specific for myocardial infarction and has been replaced by CK measurements.

Echocardiography may have a limited role in the diagnosis of myocardial infarction by demonstrating new wall-motion abnormalities when the ECG is nondiagnostic. This tool is essential in diagnosing mechanical complications and will be discussed later.

What are the differences between Q-wave and non-Q-wave myocardial infarction?

Q-wave infarction (once called transmural infarction) represents 60-70% of all acute myocardial infarctions and generally occurs when the ECG initially shows ST elevation and there is no intervention. Non-Q-wave infarction (once referred to as subendocardial infarction) represents 30-40% of all acute infarctions. Pathologically, non-Q-wave infarctions may exhibit complete transmural involvement. Thus, the terms transmural and subendocardial infarction have been replaced by the terms Q-wave and non-Q-wave infarction as defined by the development of Q waves postinfarction.

The 3-year mortality is the same in the two groups. Up to 60% of patients with non-Q-wave myocardial infarction have significant two- or three-vessel coronary artery disease. In light of this, many physicians suggest early angiography to stratify the risk in these patients. Calcium channel blockers may affect the short-term reinfarction rate in non-Q-wave infarction but have not been shown to improve mortality. In non-Q-wave infarction, the benefit of routine acute therapy with thrombolytic agents or percutaneous transluminal angioplasty has not been definitively proven.

How is the diagnosis of acute myocardial infarction made? Photo Gallery

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