Subendocardial ischemia on ECG

Bayley zones concept

According to classical Bayley concepts, impaired coronary circulation in myocardial infarction forms three concentric zones of pathological changes around the necrosis area. From center to periphery, these are: the necrosis zone, ischemic injury zone, and ischemia zone.

Each zone produces its own graphic changes on the ECG if the active electrode is located directly over the affected area. Subendocardial ischemia reflects a situation where the pathological process affects only the inner layer of the heart muscle, without penetrating through the entire thickness of the ventricle to the epicardium.

What subendocardial ischemia looks like on an ECG

The graphic display of subendocardial disorders is based on the analysis of the terminal part of the ventricular complex — the ST segment and the T wave.

• The ischemia zone forms the so-called "coronary" T wave. With subendocardial localization of the process, it becomes tall, positive, symmetrical, and acquires a pointed shape.
• The ischemic injury zone manifests on the cardiogram as a displacement of the RS–T segment below the baseline.
• Absence of the necrosis zone: unlike extensive transmural lesions, in subendocardial (nontransmural, microfocal) myocardial infarction, a pathological Q wave does not form. The QRS complex does not transform into QS because the necrosis is limited.

Dynamics in the hyperacute stage

The electrocardiographic picture directly depends on the stage of myocardial infarction. Subendocardial ischemia manifests most vividly in the hyperacute stage, which lasts up to two hours from the onset of the clinical event.

1. In the first minutes after the complete cessation of coronary blood flow, the subendocardial layer suffers most. Tall coronary T waves combined with a displacement of the RS–T segment below the baseline are recorded on the tracing.
2. Capturing such changes is extremely rare, as patients rarely undergo an ECG in the first minutes of the attack.
3. If blood flow is not restored, the ischemic injury zone spreads to the epicardium. Transmural injury occurs, and the RS–T segment shifts above the baseline (elevation).

Morphological picture and MRI diagnostics

If subendocardial ischemia progresses to infarction, nontransmural (microfocal) necrosis develops. At the cellular level, electron microscopy records mitochondrial destruction, sarcolemmal damage, sarcoplasmic edema, swelling of the sarcoplasmic reticulum, and separation of intercalated discs. Over time, this leads to post-infarction remodeling: wall thinning and left ventricular cavity dilation.

To accurately visualize the volume of the lesion, cardiac MRI (CMR) with late gadolinium enhancement (LGE) is used:

• Gadolinium chelates are administered intravenously and distribute within the extracellular space.
• The maximum volume of contrast accumulates in the necrotic tissue, shortening the T1 relaxation time compared to the intact myocardium.
• The zone of contrast accumulation in such an infarction is typically located subendocardially and strictly corresponds to the basin of the affected artery.
• Dark areas within the bright zone of infarction indicate microvascular obstruction (absence of tissue perfusion).

Class and exam questions

What else to study on this topic

• ECG criteria for transmural myocardial infarction and formation of the QS complex.
• Myocardial Salvage Index and aborted infarction.
• Microvascular obstruction on ECG and MRI.
• Post-infarction remodeling: mechanisms of left ventricular dilation.
• Organ-specific features of infarctions: kidney, lung, and brain.

Other topics in the "Additional Topics" section

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.