Differentiation of Myocardial Lesions
In clinical practice, it is important to distinguish myocarditis (an inflammatory lesion) from other pathologies of the heart muscle:
- Myocardial dystrophy: an early and reversible stage of metabolic disorders in known diseases (anemia, thyrotoxicosis, alcoholism). With adequate treatment of the underlying pathology, the changes regress completely.
- Cardiomyopathies (CMP): severe, progressive lesions (hypertrophic, dilated, and restrictive forms). Therapy provides only a symptomatic effect. CMPs also include severe myocardial dysfunctions in coronary artery disease (CAD) or hypertension, if the degree of muscle damage is disproportionately greater than the usual presentation of the disease.
- Postmyocarditic cardiosclerosis: the outcome of a previous infectious inflammation. Characterized by stable, slowly progressive changes that are usually detected only on the ECG.
Etiology and Nature of the Lesion
Inflammation of the heart muscle is caused by three main groups of factors:
- Infectious: influenza viruses, adenoviruses, Coxsackie B viruses.
- Toxic: reaction to medications (paracetamol, lithium preparations).
- Systemic: lesions associated with connective tissue diseases.
Symptoms directly depend on the extent of the inflammation:
- Focal myocarditis: clinical manifestations are dictated by localization. Even a tiny lesion in the conduction system will cause severe blocks.
- Diffuse myocarditis: the leading mechanism is a drop in contractility, which leads to dilation of the heart chambers and the development of heart failure (HF).
Depending on the course, acute (up to 3 months), subacute (up to 6 months), and chronic (with relapses) variants are distinguished.
Clinical presentation
The disease often debuts after the febrile period of an infection, masking as prolonged influenza or acute respiratory viral infection (ARVI). Severe forms (idiopathic or viral) are accompanied by cardiomegaly, life-threatening arrhythmias, and a high risk of mural thrombus formation with systemic embolism.
Patient complaints:
- General infectious: marked weakness, sweating, myalgia, and arthralgia. In 35–55% of patients, low-grade fever persists (37.5–38 °C).
- Cardiac: prolonged chest pain, shortness of breath, palpitations, and decreased exercise tolerance.
Physical examination findings:
- Pulse: tachycardia is recorded in 55–80% of patients. Bradycardia and extrasystoles are less common.
- Percussion: in diffuse processes, the borders of relative cardiac dullness are expanded.
- Auscultation: heart sounds are muffled. A gallop rhythm is characteristic: in the early stages due to the presystolic 4th heart sound, and in the later stages due to the protodiastolic 3rd heart sound. A systolic murmur occurs due to chamber dilation (relative mitral regurgitation). In concomitant pericarditis, a friction rub can be heard.
Diagnostics
During the examination, it is important to remember the pseudo-infarction course, where pain, a spike in enzymes, and the ECG picture completely mimic myocardial infarction.
- Laboratory markers: elevated ESR, leukocytosis, increased levels of $\alpha_2$- and $\gamma$-globulins, and changes in precipitation tests. In some patients, necrosis markers (troponins, CK-MB fraction) increase in the acute phase.
- ECG: repolarization disorders (ST-segment displacement, flattened or inverted T wave), decreased voltage of QRS complexes. Sinus tachycardia, supraventricular/ventricular arrhythmias, AV blocks, and bundle branch blocks are frequently observed.
- Echocardiography: in diffuse lesions, the chambers are dilated, and the picture may resemble dilated cardiomyopathy.
Principles of treatment
Treatment tactics are built around the cause, inflammatory activity, and presence of complications. Basic management requires a sparing regimen and restriction of physical activity.
- Glucocorticoids (prednisolone) are indicated for proven inflammatory activity, as well as for allergic or drug-induced etiologies. Restriction: in suspected viral etiology, they may provoke enhanced replication of the pathogen.
- NSAIDs are used for focal forms if there is no pronounced cavity dilation and signs of heart failure.
- Symptomatic therapy includes diuretics and vasodilators to correct heart failure.
Briefly: answers to topical questions
What signs of myocarditis are detected on cardiac MRI with contrast?
On cardiac MRI, signs of myocarditis are evaluated based on the Lake Louise criteria. The main findings include:
- Myocardial edema — determined on T2-weighted STIR images; in acute myocarditis, a subepicardial hyperintense zone may be detected. T2 mapping provides non-contrast quantitative assessment of edema, and native T1 values in myocarditis are significantly elevated.
- Late gadolinium enhancement (LGE) — reveals fibrosis/contrast accumulation in a non-ischemic pattern: in acute myocarditis, subepicardially within the edema zone; in myocarditis, intramyocardial or mid-wall patterns are also typical.
- Early gadolinium enhancement (EGE) — used as an additional technique to detect inflammation.
- Extracellular volume (ECV) expansion — in acute myocarditis, it reflects myocardial edema, myocyte necrosis, and subsequent fibrosis; the combination of ECV with LGE increases diagnostic accuracy.
MRI also allows for the assessment of biventricular global and regional systolic function and helps detect concomitant pericardial effusion in myopericarditis.
Class and exam questions
How does myocarditis differ from myocardial dystrophy?
Myocarditis is of an inflammatory nature, whereas myocardial dystrophy results from metabolic disorders (in thyrotoxicosis, anemia). The latter is reversible when the underlying disease is eliminated.
Why does a systolic murmur occur in myocarditis?
The murmur is associated with relative mitral regurgitation. Due to diffuse inflammation, the heart chambers and the valve annulus dilate, causing the leaflets to no longer close tightly.
In which cases can glucocorticoids be harmful in myocarditis?
In viral etiology, the use of hormones is questionable from a safety standpoint, as they may provoke enhanced viral replication.
What else to study on this topic
- Pathogenesis of immunological inflammation in viral invasion
- Mechanisms of mural thrombus formation in severe disease
- Differential diagnosis with acute myocardial infarction (pseudo-infarction course)
- Hemodynamic significance of presystolic (IV) and protodiastolic (III) gallop rhythms
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