ECG Stages of Myocardial Infarction

Bayley's concept of zones (ECG manifestations)

According to Bayley's theory, impaired normal blood supply to the heart muscle leads to the formation of three concentric zones around the area of cell death. Each of these regions generates specific ECG changes if the active electrode is positioned directly over the affected area.

1. Necrosis zone. Reflects irreversible cardiomyocyte death. The main marker is the appearance of a pathological Q wave lasting more than 30 milliseconds. Meanwhile, the amplitude of the R wave sharply decreases. In severe cases, a QS-type ventricular complex is registered, indicating extensive damage.
2. Ischemic injury zone. Surrounds the necrosis focus. On the tracing, it manifests as discordant RS–T segment displacement. If the injury involves the entire thickness of the wall (transmural), the segment elevates above the baseline. When the process is localized beneath the endocardium (subendocardially), the RS–T segment is depressed below the baseline.
3. Ischemia zone. The outer contour of the pathological focus. It is characterized by the formation of the so-called "coronary" T wave — it becomes symmetrical (isosceles) and acquires a pointed shape. The direction of the wave depends on the depth: in subendocardial localization, it is tall and positive, while in transmural localization, it is negative.

Hyperacute stage of myocardial infarction

The electrocardiographic picture is not static and transforms as the pathological process develops. The earliest phase is the hyperacute stage, which lasts up to two hours from the moment of critical coronary blood flow disruption.

In the first minutes after vessel occlusion, a pattern of subendocardial ischemia forms. On the ECG, this is expressed by the appearance of tall "coronary" T waves combined with RS–T segment depression (displacement below the baseline). It is important to note that in practice, capturing these changes is extremely rare due to their short duration.

Soon, the ischemic injury zone expands, reaching the epicardium. Transmural ischemic injury develops, accompanied by a characteristic elevation of the RS–T segment above the baseline.

Myocardial infarction as a complication of congenital heart disease (CHD)

Myocardial infarction can act not only as an independent disease but also as a severe specific complication of congenital heart defects. This occurs against the background of pronounced hemodynamic shifts and chronic tissue oxygen starvation.

The course of CHD has a strict stadiation. By the second or third year of the child's life, the phase of relative compensation is established. During this period, the clinical condition stabilizes due to the activation of powerful adaptive mechanisms — myocardial hypertrophy and hyperfunction. This phase can last for many years.

However, over time, the terminal (irreversible) phase ensues. It is caused by the complete depletion of the body's compensatory reserves. The morphological basis of this stage includes profound myocardial dystrophy, massive development of cardiosclerosis, and a critical drop in coronary blood flow. It is against this background, along with cerebrovascular disorders (hemorrhages) and the onset of infective endocarditis, that acute infarction develops.

ECG and comprehensive diagnostics in heart defects

Since infarction can develop against the background of heart defects, it is important to understand the principles of their instrumental diagnostics. The evaluation aims to assess the degree of hypoxia, visualize the anatomical defect, and identify chamber overload.

• Electrocardiography (ECG). Reflects hypertrophy and hemodynamic overload. There is a clear pattern: cyanotic ("blue") defects cause right heart overload, while "pale" defects cause left heart overload.
• Echocardiography (EchoCG). The key imaging method. Demonstrates the anatomical substrate (septal defects, diameters of great vessels) and intracardiac hemodynamics (direction and distribution of blood flows).
• Phonocardiography (PCG). Allows for the objectification of the auscultatory picture by precisely recording the phase, shape, duration, and amplitude of systolic and diastolic murmurs.
• Chest X-ray. Reveals cardiomegaly and changes in the pulmonary pattern (its enhancement is a marker of pulmonary hypervolemia and pulmonary hypertension). The shape of the cardiac silhouette is strictly specific: mitral configuration (smoothed "waist") is typical for patent ductus arteriosus, and aortic configuration ("boot-shaped heart") is typical for Tetralogy of Fallot. Alteration of the vascular bundle (narrow in the frontal plane, wide in the sagittal plane) is characteristic of transposition of the great vessels.
• Laboratory findings. In cyanotic defects, the complete blood count and acid-base balance (ABB) show signs of chronic hypoxia: decreased partial pressure of oxygen (paO2), hypercapnia (paCO2), and compensatory erythrocytosis (elevated hemoglobin, red blood cells, and hematocrit).

Clinical presentation and differential diagnosis

The clinical diagnosis of CHD is based on the early onset of symptoms (from birth or in the first 2–3 years). General manifestations include cyanosis, dyspnea, and easy fatigability. Local findings include cardiomegaly, chest deformity ("cardiac hump"), and systolic or diastolic thrills upon palpation. Auscultation reveals an intense, harsh murmur radiating to the back. A mandatory procedure is blood pressure measurement in the upper and lower extremities to rule out coarctation of the aorta.

Differential diagnosis depends on age:

• In the neonatal and early age periods, heart defects are differentiated from early and late congenital carditis.
• In children older than three years, the spectrum expands to rule out rheumatic fever, bacterial endocarditis, non-rheumatic carditis, and cardiomyopathies.
• Functional murmurs are often caused by connective tissue dysplasia, which manifests as minor cardiac anomalies (MCA) — mitral valve prolapse, accessory chordae, or papillary muscle anomalies.

Class and exam questions

What else to study on this topic

• Mechanisms of myocardial hypertrophy and hyperfunction formation in the CHD compensation phase
• Pathogenesis of infective endocarditis as a specific complication
• Minor cardiac anomalies (MCA): mitral valve prolapse and accessory chordae
• Intragroup differential diagnosis of various types of congenital heart defects
• Interpretation of acid-base balance (ABB) parameters in cyanotic defects

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