Repolarization Abnormalities on ECG

Characteristics of repolarization abnormalities

On the electrocardiogram, the electrical recovery processes of cardiomyocytes are represented by the ST–T complex. Electrocardiography (ECG) is the primary screening tool when myocardial injury is suspected. In inflammatory, infectious, or toxic myocardial damage, the following typical deviations occur:

• ST segment shift: its deviation from the isoelectric line directly indicates hypoxic tissue changes or tissue injury.
• T wave changes: against the background of a pathological process, flattening or inversion of the T wave is registered (it becomes negative).

Such ECG shifts are often non-specific and accompanied by sinus tachycardia. In severe forms, such as toxic myocarditis, in addition to repolarization abnormalities, prolongation of the PR interval is detected, along with severe rhythm and conduction disturbances (atrioventricular blocks of varying degrees).

When analyzing a pediatric electrocardiogram, it is critically important to consider the age-standard normal values. The presence of sinus arrhythmia or isolated incomplete right bundle branch block on a standard ECG is not considered pathological. These findings in isolation should not be interpreted as signs of an inflammatory process.

Repolarization shifts as a manifestation of carditis

Repolarization abnormalities often become the first objective instrumental sign of cardiac involvement in acute rheumatic fever. Rheumatic carditis is accompanied by damage to various layers of the heart, with myocardial involvement being the primary determinant of the severity of the clinical picture.

Patients present with complaints of dyspnea, palpitations, various types of chest pain, and reduced exercise tolerance. The main clinical consequence of myocardial layer inflammation is the progression of heart failure symptoms. The development of diffuse myocarditis with hemodynamic decompensation is a powerful predictor of an unfavorable prognosis.

In addition, the infectious-immune process can spread to the pericardium. Such combined involvement (pancarditis) indicates an extremely high degree of severity and systemic inflammation.

Differential diagnosis and valvular lesions

The detection of altered ST–T complexes requires careful exclusion of valvular apparatus involvement, as rheumatic fever most specifically affects the endocardium. Valvulitis most commonly affects the mitral valve (in about 65–70% of cases) or causes combined mitral and aortic valve involvement (25%). The tricuspid valve is affected significantly less often, and pulmonary valve involvement is exceedingly rare.

Morphologically, the process can present as diffuse, acute verrucous, recurrent verrucous, or fibroplastic endocarditis. The outcome of such inflammation is the formation of a heart valve defect due to sclerosis and hyalinosis. The valve leaflets thicken, shorten, and may become deformed. The anterior and posterior mitral leaflets often fuse into a dense fibrous "funnel" with a narrow slit-like or sickle-shaped orifice, while the chordae tendineae thicken and fuse.

Classically, a distinction is made between primary rheumatic carditis (developing during the first attack and often leaving no residual valvular defect) and recurrent rheumatic carditis (arising against the background of already deformed valves and much more frequently leading to progressive valvular disease and persistent decompensation).

Instrumental and laboratory confirmation of the diagnosis

Because isolated repolarization abnormalities are non-specific, an expanded set of investigations is used to reliably diagnose inflammatory myocardial injury:

1. Laboratory markers. A dynamic increase in cardiospecific biomarkers (troponins I and T, CK-MB) confirms acute cardiomyocyte injury regardless of its etiology (ischemic or non-ischemic). In toxic damage, AST plays an important role, with its serum level directly correlating with the severity of myonecrosis.
2. Echocardiography (EchoCG). Allows for the assessment of myocardial contractility and differentiation of chamber dilatation from fluid accumulation in the pericardial cavity. In infectious valvular involvement, the visualization of vegetations is a pathognomonic sign (sensitivity >50%). Cardiac remodeling and destruction of the valvular apparatus (chordal rupture, leaflet perforation) indirectly indicate inflammation.
3. Magnetic resonance imaging (MRI). Diagnostic specificity increases significantly when late gadolinium enhancement (LGE) techniques are used. T2-weighted images (T2-WI) and early gadolinium enhancement (EGE) reveal areas of edema typical of the active phase of inflammation. As the condition transitions to a chronic course, the sensitivity of MRI noticeably decreases.
4. Endomyocardial biopsy. Right ventricular tissue sampling is used for histological verification of active myocarditis when clinical and instrumental data are insufficient.

Class and exam questions

What else to study on this topic

• Morphological types of rheumatic endocarditis (acute verrucous, diffuse, fibroplastic).
• The process of rheumatic heart defect formation and mitral valve deformation ("funnel").
• The diagnostic role of transesophageal echocardiography (TEE) in searching for valve vegetations.
• Features of cardiac MRI with contrast enhancement (LGE, EGE) in active myocarditis.
• Prognostic factors in the course of rheumatic carditis and the risk of developing chronic rheumatic heart disease (CRHD).

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