Etiology and pathogenesis
The formation of a defect is based on damage to the valves or vessels. Most often, the triggering mechanism is rheumatic fever. Less commonly, the pathology develops against the background of infective endocarditis, atherosclerosis, syphilis, or brucellosis. In recent years, an increase in lesions of the right side of the heart has been observed in drug users, which is associated with infective endocarditis.
Dynamics of development
The development of the defect goes through two key stages:
- Compensation stage: the heart adapts to the load due to concentric hypertrophy of the myocardium. Circulatory disorders at this stage are mild.
- Decompensation stage: myocardial reserves are depleted. Hypertrophy is replaced by eccentric hypertrophy with pronounced chamber dilation. This leads to blood congestion in both circulatory loops, the development of anasarca, and cavity effusion.
Morphological changes
In decompensated defects, the heart macroscopically appears flabby, its chambers are dilated, and thrombi are often found in the atrial appendages. The microscopic picture includes:
- Protein and fatty dystrophies of cardiomyocytes.
- Foci of damage: myocytolysis, contractures, and granular disintegration.
- Proliferation of connective tissue in the stroma and the presence of round-cell infiltrates.
Prognosis and Outcomes
The prognosis depends on the type of defect. The course of mitral and aortic valve insufficiency is considered the most favorable, whereas aortic valve stenosis has the worst prognosis. The main causes of death are cardiovascular failure, thromboembolic complications, and pneumonia.
Briefly: answers to topical questions
Which heart valves are most frequently affected in rheumatic fever?
In rheumatic fever, the mitral valve is most frequently affected: mitral regurgitation is most commonly formed, less often mitral stenosis. Aortic valve defects are less common and rank second in frequency after mitral defects. Combined mitral-aortic defects are possible.
What types of acquired heart defects are distinguished by morphological changes in the valves?
Based on morphological changes and functional disorders, three main types of acquired heart defects are distinguished.
- Stenosis — narrowing of the valve orifice lumen.
- Insufficiency — incomplete closure of the cusps, leading to the inability to prevent backflow of blood (regurgitation).
- Combined defect — a combination of stenosis and insufficiency on the same valve.
Also, mixed heart defects are distinguished, in which two or more valves are affected simultaneously.
What hemodynamic disorders and morphological changes occur in the pulmonary circulation in mitral stenosis?
In mitral stenosis, the outflow of blood from the pulmonary veins into the left atrium is impaired, leading to venous congestion and pulmonary hypertension.
Hemodynamic disorders include venous hyperemia, a significant increase in intracapillary pressure, and diapedesis of erythrocytes. Morphological changes are characterized by the development of brown induration of the lungs (induratio fusca pulmonum):
- Hemosiderosis — deposition of hemosiderin pigment in macrophages (siderophages).
- Sclerosis — diffuse proliferation of connective tissue in the interalveolar septa, around bronchi and blood vessels.
Macroscopically, the lungs acquire a brown color and dense consistency. In severe cases, plasma transudation into the alveoli and rupture of pulmonary-bronchial anastomoses occur.
C-E-D: Compensation (Concentric hypertrophy) → Eccentric hypertrophy → Dilation (decompensation).
Class and exam questions
How does concentric hypertrophy differ from eccentric hypertrophy?
In concentric hypertrophy, the ventricular walls thicken without significant chamber enlargement, which is characteristic of the compensation stage. Eccentric hypertrophy is accompanied by chamber dilation (enlargement), indicating exhaustion of the heart's reserves.
Why do thromboembolic complications frequently occur in heart defects?
In the decompensation stage, dilation of the heart chambers and slowing of blood flow occur, which promotes thrombus formation, especially in the atrial appendages.
What factors can accelerate the transition to the decompensation stage?
Decompensation is provoked by exacerbations of rheumatic fever, excessive physical or emotional stress, as well as concomitant infections and stress states.
What else to study on this topic
- Comparative characteristics of valve stenosis and insufficiency.
- Mechanisms of blood stasis development in the pulmonary and systemic circulations.
- Pathomorphology of thromboembolic complications in heart defects.
- Features of tricuspid valve involvement in septic processes.
- Cellular mechanisms of myocytolysis during myocardial overload.
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