Diagnosis of myocardial infarction

Lore & Background

The diagnosis of myocardial infarction relies on integrating the patient's history of presenting illness and physical examination with electrocardiogram findings and cardiac markers (blood tests for heart muscle cell damage). A coronary angiogram allows visualization of narrowings or obstructions on the heart vessels, and therapeutic measures can follow immediately. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings. A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department.

Reader's Guide

The diagnostic process for myocardial infarction has evolved over time. According to the WHO criteria as revised in 2000, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic. Previous WHO criteria (1979) placed less emphasis on biomarkers, requiring two (probable) or three (definite) of: clinical history of ischemic chest pain lasting >20 minutes, changes in serial ECG tracings, and rise and fall of serum cardiac biomarkers. The ECG remains a primary tool to detect ischemia or acute coronary injury, but a normal ECG does not rule out infarction. Cardiac troponins T and I, released within 4–6 hours and remaining elevated for up to 2 weeks, are now the preferred markers due to their nearly complete tissue specificity. In difficult cases, coronary angiography can be performed, and histopathological examination at autopsy reveals coagulative necrosis with characteristic time-dependent changes.

Did You Know?

• A normal ECG does not rule out acute myocardial infarction.
• Cardiac troponins T and I are released within 4–6 hours of an attack and remain elevated for up to 2 weeks.
• Under a microscope, one of the earliest changes in myocardial infarction is so-called wavy fibers.
• The standard 12-lead ECG assesses the posterior and lateral walls well via leads V5, V6, I, and aVL; posterior involvement is inferred from reciprocal changes in V1-V3.