ECG in Myocardial Infarction: Stages, Signs, and Localization

Analysis of ECG diagnostics in myocardial infarction: components of ischemia, injury, and necrosis, four developmental stages, signs of Q-wave and non-Q-wave infarctions, and topical diagnostics by leads.

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Components of the ECG pattern in myocardial infarction

Myocardial infarction on an ECG represents a combination of three processes: ischemia, injury, and necrosis. Each produces its own electrocardiographic equivalent, and their combination forms the characteristic pattern of infarction.

Stages of myocardial infarction

The classical Russian classification distinguishes four stages, differing in timing and combination of ECG signs. In practice, the stage is determined primarily by the medical history (duration of pain syndrome, time from disease onset), and the ECG serves as confirmation.

  1. Hyperacute stage (up to 3 days). An injury zone and a small necrosis zone are formed. The ECG registers ST-segment elevation and the beginning of a pathological Q wave formation. A tall "coronary" T wave often precedes the elevation.
  2. Acute stage (up to 3 weeks). The injury zone decreases, an ischemia zone appears at the periphery, and necrosis stabilizes. The ECG shows a pathological Q wave, persistent ST elevation, and a negative coronary T wave.
  3. Subacute stage (up to 3 months). Injury disappears, while necrosis and ischemia remain. The ST segment returns to the baseline, the pathological Q wave persists, and the coronary T wave reaches its maximum expression.
  4. Scar stage. The necrotic tissue is replaced by a connective tissue scar, which is electrically inactive. The ECG retains only the pathological Q wave (or QS) — a lifelong sign of prior myocardial infarction.

Non-Q-wave infarction and reciprocal changes

In non-Q-wave infarction, the focus of necrosis is located within the thickness of the myocardium, the surrounding tissue undergoes compensatory activation, and a pathological Q wave does not form. Diagnosis relies on clinical presentation (typical pain syndrome), elevated cardiospecific enzymes (troponins), and indirect ECG signs: ST elevation or depression, T-wave inversion, and decreased R-wave amplitude.

ST-segment depression during infarction is often a mirror (reciprocal) reflection of elevation in opposite leads. For example, depression in anterior leads corresponds to elevation in posterior leads (V7–V9).

Signs of myocardial infarction on ECG — Summary

Topical diagnostics: Localization of infarction

The localization of the infarction is determined by the leads in which ischemic-necrotic changes are recorded. Lead orientation corresponds to Einthoven's triangle and the chest lead system:

Typical localizations: anteroseptoapical infarction (V1–V4), posterobasal (V7–V9 with reciprocal depression in V1–V3), posterolateral and anterolateral (V5–V6 combined with I and aVL or II, III, aVF). Involvement of a large number of leads is referred to as extensive myocardial infarction.

Practical notes

The ECG picture of infarction is rarely "textbook": stages overlap, signs may be blunted, and bundle branch blocks mask typical changes. Therefore, diagnosis is always based on correlating the ECG, clinical presentation, and laboratory markers. Precise localization of infarction by ECG has limited practical value and requires significant experience in analyzing real tracings.

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