Topographic diagnosis of myocardial lesions
Electrocardiography allows for precise determination of the anatomical lesion zone. Specific (direct) changes are recorded in those leads located directly above the necrosis zone. The following patterns are used to assess anterior localization and adjacent areas:
- Anteroseptal infarction: injury markers are recorded in leads I, aVL, and chest leads $V_1–V_4$.
- Extensive (anterolateral) infarction: the pathological process covers a significant area, with changes visible in I, II, aVL, and across all chest leads from $V_1$ to $V_6$.
- Isolated lateral infarction: direct signs are reflected in I, aVL, $V_4–V_6$.
- Inferior (diaphragmatic) infarction: the lesion is visible in standard and augmented limb leads — II, III, aVF.
- Inferolateral infarction: combines signs of inferior wall damage (II, III, aVF) and lateral wall damage (aVL, $V_5–V_6$).
When interpreting an ECG, it is critically important to consider the phenomenon of reciprocity (reciprocal changes). If ST-segment elevation is observed over the necrosis focus, a mirror-image depression (drop) will be recorded in the leads reflecting the opposite wall.
Stages of extensive anterolateral myocardial infarction
The pattern of transmural injury on ECG is not static. It undergoes predictable chronological stages of evolution, making it possible to estimate the age of the vascular event:
- Hyperacute stage (the first hour from the onset of chest pain): the earliest markers of ischemia are recorded. The main sign is acute ST elevation.
- Acute and subacute stages (about 24 hours): active formation of the necrosis focus begins.
- Scarring stage (approximately 10 days later): the process consolidates. The ST segment gradually returns to the isoelectric line, and a pathological Q wave is finally formed.
The appearance of a pathological Q wave is closely tied to cardiac anatomy. In lead $V_2$, it indicates tissue death in the interventricular septum, in $V_4$ — involvement of the left ventricular apex, and in $V_6$ — involvement of the lateral wall.
Microvascular obstruction on ECG and MRI
In clinical practice, there are cases where signs of injury persist on the ECG even after successful percutaneous coronary intervention (PCI) for anterior descending artery (LAD) occlusion. If a persistent QS complex (a marker of necrosis), maintained ST elevation, and positive T waves are recorded in leads $V_1–V_4$ several days later, this indicates a lack of tissue perfusion.
This clinical picture serves as an ECG marker of microvascular obstruction (microvascular obstruction). The diagnosis is verified using cardiac MRI (CMR) with late gadolinium enhancement. Gadolinium chelates have an extracellular distribution and accumulate maximally in the necrotic part of the myocardium, shortening the T1 relaxation time. In microvascular obstruction, dark areas of non-perfused tissue are visualized within the bright infarction zone on the tomogram.
Prognostic assessment: Myocardial Salvage Index
The contrast-enhancement zone during an acute event is typically located subendocardially and strictly corresponds to the basin of the affected artery (the degree of transmural spread may vary).
To assess treatment efficacy, the Myocardial Salvage Index (Myocardial Salvage Index) is calculated. The calculation principle is based on comparing the area of irreversible necrosis (where contrast has accumulated) with the total area of myocardial edema (the area at risk).
In situations where medical care is provided extremely quickly and necrosis does not develop, an aborted myocardial infarction (aborted myocardial infarction) is diagnosed. In this case, contrast does not accumulate, and the salvage index is 100%. Assessment of this parameter has the highest prognostic value for the patient's future life.
For quick memorization of chest lead topography: $V_2$ "looks" at the septum, $V_4$ points to the apex, and $V_6$ extends to the lateral wall of the left ventricle.
Class and exam questions
What does the hyperacute stage of an anterior infarction look like on an ECG?
In the first hour after pain onset, the main direct sign is pronounced ST-segment elevation in the corresponding chest leads, such as $V_1–V_4$.
What does the appearance of a QS complex in chest leads mean?
The formation of a QS complex is a reliable ECG sign of transmural necrosis development in the anterior wall of the left ventricle.
Why does ST depression occur in other leads during a myocardial infarction?
This is the phenomenon of reciprocity. Leads reflecting the healthy heart wall located opposite the infarction zone record changes in a mirror image relative to the direct signs.
What does the myocardial salvage index show on an MRI?
It reflects the proportion of preserved tissue within the area at risk. It is calculated by comparing the area of gadolinium enhancement (necrosis zone) with the total area of edema.
What else to study on this topic
- Topographic diagnosis of inferior and isolated lateral myocardial infarction
- Pathophysiology of microvascular obstruction with restored blood flow
- Rules for reading reciprocal changes on an ECG tracing
- Application of late gadolinium-enhanced MRI (LGE) in cardiology
- Criteria for aborted myocardial infarction (aborted myocardial infarction)
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