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Pathophysiology · Additional topics

Subendocardial ischemia ECG

Ischaemia subendocardialis

Subendocardial ischemia is a pathological condition characterized by impaired blood circulation in the distal areas of the heart muscle adjacent to the endocardium. On the ECG, it manifests as ST-segment depression and specific T-wave changes, indicating the development of acute coronary syndrome (ACS) or a small-focal lesion.

ST segmentDisplacement below the isoelectric line (depression) in contiguous leads
T waveTall positive, symmetrical and peaked
ACS criterionST depression ≥1 mm (standard leads) or ≥2 mm (chest leads)
Affected areaConfined to the subendocardium, without a pathological Q wave
3 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Concept of pathological change zones

According to classical Bayley concepts, when coronary blood flow is disrupted, specific zones form around the necrosis area. Each of them has distinct ECG manifestations in leads where the active electrode is positioned over the infarction area:

  • Zone of ischemia manifests as the so-called "coronary" T wave—symmetrical and peaked. In subendocardial injury, it becomes tall and positive, whereas in transmural injury, it becomes negative.
  • Zone of ischemic injury is characterized by RS–T segment displacement. If the injury affects only the subendocardial layers, the segment shifts below the isoelectric line (depression). In transmural injury, it elevates above the isoelectric line.
  • Zone of necrosis is reflected on the ECG by the formation of a pathological Q wave (duration >30 ms) and a sharp decrease in R-wave amplitude, or the appearance of a QS complex. In isolated subendocardial ischemia, this zone is absent.

ECG changes in the hyperacute stage

The ECG picture changes dynamically depending on the stage of myocardial infarction. In the hyperacute stage, which lasts up to 2 hours from the onset of the attack, the earliest changes occur.

Within the very first minutes after the cessation of normal coronary blood flow, a zone of subendocardial ischemia forms. At this point, high coronary T waves combined with RS–T segment displacement below the isoelectric line can be recorded on the cardiogram. However, in practice, such early changes are registered extremely rarely. Subsequently, if the ischemic injury zone expands and reaches the epicardium, ST depression is replaced by ST elevation—indicating transmural ischemic injury.

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ECG diagnostics of non-ST-segment elevation ACS

Acute coronary syndrome without ST-segment elevation is directly associated with damage to the distal myocardial areas close to the endocardium. This condition may present with the following signs:

  1. Directly subendocardial ischemia.
  2. T-wave inversion: flattening or reversion (transition from negative to positive).
  3. ST-segment depression.

For ST depression to be considered a reliable diagnostic sign, it must be recorded in at least ≥2 contiguous leads. Furthermore, the depth of displacement must be ≥1 mm in standard leads and ≥2 mm in chest leads.

It is important to remember that such ECG changes may not be exclusively ischemic in origin. They occur in inflammatory, toxic, and traumatic lesions of the heart muscle. In all these cases, small-focal myocardial necrosis may develop, accompanied by the formation of negative T waves (e.g., in small-focal infarction of the anteroseptal, lateral, or apical regions of the left ventricle).

Morphological picture of non-transmural infarction

Macroscopically, myocardial infarction belongs to irregularly shaped infarctions. If necrosis is limited and localized predominantly subendocardially, a non-transmural (small-focal) infarction develops. Its key ECG feature is that changes affect only the ST segment and T wave; no pathological Q wave is formed.

At the microscopic level, profound structural disorders occur:

  • Light microscopy shows myofibrillar changes at the level of Z-discs.
  • Electron microscopy allows the registration of mitochondrial destruction, sarcolemma damage, pronounced sarcoplasmic edema, swelling of the sarcoplasmic reticulum, and separation of intercalated discs.

The outcome of this process triggers post-infarction remodeling. This includes wall thinning at the necrosis site, disproportionate stretching of the affected area, and subsequent dilation (enlargement) of the left ventricular cavity.

How to memorize

Ischemia near the endocardium pulls the ST segment "down" (depression) and makes the T wave tall and positive.

Class and exam questions

Does a Q wave form in subendocardial injury?

No, a pathological Q wave is characteristic of transmural necrosis. In subendocardial (small-focal) infarction, only the ST segment and T wave change on the ECG.

What does the T wave look like in subendocardial ischemia?

A "coronary" T wave is formed—tall, positive, symmetrical, and peaked.

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What else to study on this topic

  • ECG signs of transmural myocardial infarction
  • Formation of a pathological Q wave and QS complex
  • Left ventricular post-infarction remodeling
  • Ultrastructural changes in cardiomyocytes during necrosis
  • Differential diagnostics of non-ST-segment elevation ACS

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