Heart defects and hemodynamics in rheumatic fever
Rheumatic fever is characterized by predominant involvement of the valve apparatus, most commonly leading to stenosis of the left atrioventricular orifice (mitral stenosis). This defect triggers a clear pathogenetic chain of hemodynamic disturbances.
First, progressive dilatation of the left atrium occurs as it attempts to force blood through the narrowed orifice. Then, venous congestion develops in the pulmonary circulation. Chronic blood flow impairment causes remodeling of the pulmonary parenchyma and vascular bed, resulting in brown induration of the lungs. In addition, due to slowed blood flow in the dilated left atrial cavity, thrombi begin to form.
The myocardium itself undergoes staged changes during the development of the defect:
- Stage of compensation: hypertrophy of the right ventricle and concentric myocardial hypertrophy are observed.
- Stage of decompensation: due to myogenic dilatation (enlargement) of the heart chambers, hypertrophy is replaced by eccentric hypertrophy.
Morphological forms of rheumatic myocarditis
Myocarditis (inflammation of the myocardium) in rheumatic fever occurs in three main morphological forms, differing in severity and prognosis.
- Nodular (granulomatous) myocarditis. Its main characteristic is the formation of specific rheumatic granulomas in the perivascular tissue of the stroma. These granulomas can be in different phases of their development. The surrounding cardiomyocytes undergo protein or fatty dystrophy, up to the appearance of micro-necrosis. The outcome of this form is diffuse microfocal cardiosclerosis, in which small oval or spindle-shaped perivascular scars remain in the myocardium.
- Diffuse interstitial exudative myocarditis. This form is of significant epidemiological importance because it frequently develops in children. Clinically, it manifests as severe cardiovascular failure. Macroscopically, the heart is altered: the chambers are markedly dilated, and the myocardium itself becomes flabby and dull. The microscopic picture demonstrates marked vascular congestion. The entire interstitium is soaked with serous exudate and densely infiltrated with cells: lymphocytes, histiocytes, and band neutrophils. Muscle fibers dissociate, showing marked dystrophic changes and foci of necrosis. The process terminates in diffuse cardiosclerosis—a continuous proliferation of connective tissue in the form of thin layers between groups of muscle fibers.
- Focal interstitial exudative myocarditis. This form is usually encountered in the latent (asymptomatic) course of rheumatic fever. It is characterized by only minor foci of lymphohistiocytic infiltration with a small admixture of band neutrophils in the interstitium. Dystrophy and necrosis of cardiomyocytes are also focal in nature. The regular outcome is the formation of focal cardiosclerosis.
Rheumatic pericarditis
Pericarditis is inflammation of the outer membrane of the heart. In rheumatic fever, the inflammatory process can proceed according to three types: serous, serous-fibrinous, or fibrinous.
The most striking macroscopic picture is seen in fibrinous inflammation. Massive fibrin strands are deposited on the epicardial surface, giving the heart a specific shaggy appearance—the so-called "hairy heart".
Subsequent evolution of the process is associated with the organization of the deposited exudate. Fibrin strands are invaded by connective tissue, leading to the formation of adhesions (synechiae) between the pericardial layers. In severe cases, complete obliteration of the pericardial cavity occurs. Ultimately, the connective tissue undergoes calcification (calcium salt deposition), forming a rigid, non-distensible framework around the myocardium, leading to the development of an "armor heart".
To easily recall the forms of myocarditis, use the acronym UDO: Nodular (granulomas, scars), Diffuse (children, severe failure), Focal (latent course).
Class and exam questions
How does the myocardium change in the stage of heart defect decompensation?
In the stage of decompensation, myogenic dilatation of the heart chambers occurs, causing concentric hypertrophy to be replaced by eccentric hypertrophy.
Which form of myocarditis is most typical for childhood?
Diffuse interstitial exudative myocarditis most commonly develops in children and clinically presents with severe cardiovascular failure.
What is an "armor heart"?
This is the outcome of rheumatic pericarditis characterized by organization of the exudate, complete obliteration of the pericardial cavity, and subsequent calcification of the connective tissue.
What else to study on this topic
- Pathogenesis of brown induration of the lungs in mitral stenosis
- Cellular composition and stages of development of the rheumatic granuloma
- Differences between concentric and eccentric myocardial hypertrophy
- Mechanisms of myogenic dilatation of heart chambers
- Morphological differences between serous and fibrinous inflammation
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