Infarct ECG: Patterns, Leads, and Clinical Interpretation

Recognizing Infarct on ECG: The Core Patterns

An infarct ECG reflects the electrical consequences of myocardial cell death. When coronary occlusion leads to ischemia and necrosis, the heart's electrical vectors change in ways the 12-lead ECG can detect. The classic triad of ST-segment elevation, pathological Q waves, and T-wave inversion marks different phases of infarction evolution. Recognizing these patterns promptly is essential because time-sensitive interventions directly affect outcomes.

ST elevation indicates acute injury current flowing between the infarct zone and surrounding viable tissue. Pathological Q waves suggest completed necrosis with loss of electrical forces in that region. T-wave inversion often signals the subacute or healing phase. Not every infarct displays all three simultaneously, and the specific ECG appearance depends on the coronary territory involved and the timing of presentation.

The ECG does not capture all infarcts. A posterior infarct, for instance, may show tall R waves and ST depression in V1 to V3 rather than the expected ST elevation. Right ventricular infarction often accompanies inferior wall damage and requires right-sided leads (V3R to V6R) for detection. These patterns are easy to miss without a systematic approach.

Infarct ECG by Coronary Territory

Each coronary artery supplies a distinct region of the heart, and occlusion produces recognizable patterns across specific leads:

• Left anterior descending (LAD): Anterior septal and anterior wall infarcts show ST elevation in V1 to V4. LAD occlusion affecting the apex can produce anterior-lateral patterns.
• Right coronary artery (RCA): Inferior infarcts display ST elevation in II, III, and aVF. RCA occlusion may also cause right ventricular infarction, with ST elevation in V3R and V4R, and posterior infarction with ST depression in V1 to V3.
• Left circumflex (LCx): Lateral infarcts show ST elevation in I, aVL, V5, and V6. Posterior lateral patterns can be subtle, often requiring posterior leads V7 to V9 for confirmation.
• Left main: Widespread changes across multiple territories, often with severe hemodynamic compromise and a high-risk ECG profile.

Evolution of ECG Changes Over Time

The infarct ECG evolves through stages that help clinicians estimate the timing of the event. Hyperacute T waves — tall, broad, and symmetrical — appear within minutes of occlusion. ST elevation follows within hours as injury current develops. Peak T-wave inversion occurs during the subacute phase, while pathological Q waves emerge over days to weeks as necrosis becomes established.

In some cases, ST elevation resolves without Q wave formation, indicating a myocardial infarction without Q waves (NSTEMI equivalent), often called a non-Q-wave infarct. This pattern typically reflects subendocardial injury, which may not be fully captured by standard surface ECG and can require serial biomarker correlation.

Differential Diagnoses That Mimic Infarct ECG

Several conditions produce ST elevation or Q waves that can be mistaken for acute infarct:

• Pericarditis produces diffuse, concave ST elevation across multiple leads, often with PR depression, rather than the regional, convex ST elevation seen in infarct.
• Left bundle branch block can mask infarct patterns or create pseudo-infarct Q waves in lateral leads.
• Left ventricular hypertrophy with strain patterns may mimic ischemic changes in precordial leads.
• Early repolarization, a common benign variant, can cause concave ST elevation that must be distinguished from infarct-related elevation.
• Pulmonary embolism can cause right heart strain patterns, S1Q3T3 configuration, and anterior T-wave inversions that mimic infarct.

Clinical Approach to the Infarct ECG

When the infarct ECG is identified, the clinical context determines urgency. ST elevation myocardial infarction (STEMI) requires immediate reperfusion, either through primary PCI or fibrinolysis, depending on available resources and time to treatment. The ECG helps identify the culprit vessel and guides reperfusion strategy.

For non-ST elevation presentations, the ECG still provides critical risk stratification. New ST depression, T-wave inversions, or dynamic changes in serial tracings raise suspicion for unstable angina or NSTEMI and prompt early invasive strategy in high-risk patients. Serial ECGs, taken 15 to 30 minutes apart, can reveal evolving changes that a single tracing might miss.

Understanding the infarct ECG remains a foundational clinical skill. Recognizing patterns, knowing which leads correspond to which territories, and interpreting changes in context allow clinicians to act decisively when myocardial injury is present.