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Acquired Valvular Heart Disease

*Vitium cordis acquisitum*

For medical students2 min readUpdated 2026-10-10

Acquired valvular heart disease encompasses pathological alterations of the heart valves and great vessels resulting from inflammatory or degenerative processes. These conditions are characterized by a staged progression, transitioning from compensatory myocardial hypertrophy to severe heart failure.

Main causesRheumatic fever, infective endocarditis, atherosclerosis, syphilis, and brucellosis.
Stages of developmentCompensation (concentric hypertrophy) and decompensation (chamber dilation).
Causes of deathCardiovascular failure, thromboembolism, and pneumonia.
MicroscopyCardiomyocyte dystrophy, myocytolysis, and connective tissue proliferation.

Etiology and Pathogenesis

The development of a valvular defect is based on damage to the valves or blood vessels. Rheumatic fever is most commonly the triggering mechanism. Less frequently, the pathology develops secondary to infective endocarditis, atherosclerosis, syphilis, or brucellosis. In recent years, there has been an increase in right-sided heart lesions among intravenous drug users, which is associated with infective endocarditis.

Dynamics of Development

The progression of a valvular defect goes through two key stages:

  1. Stage of compensation: the heart adapts to the workload via concentric hypertrophy of the myocardium. Circulatory disorders are mild at this stage.
  2. Stage of decompensation: myocardial reserves are exhausted. Hypertrophy gives way to eccentric hypertrophy with pronounced chamber dilation. This leads to blood congestion in both systemic and pulmonary circulations, anasarca, and serous cavity effusions.

Morphological Changes

In decompensated valvular disease, the gross appearance of the heart is flabby, its chambers are dilated, and thrombi are frequently found in the atrial appendages. Microscopic findings include:

Prognosis and Outcomes

The prognosis depends on the type of valvular defect. Mitral and aortic regurgitation (insufficiency) generally have a more favorable course, whereas aortic stenosis carries the poorest prognosis. The primary causes of mortality include cardiovascular failure, thromboembolic complications, and pneumonia.

Mnemonic

C-E-D: Compensation (Concentric hypertrophy) → Eccentric hypertrophy → Dilation (Decompensation).

Frequently asked questions

Which heart valves are most frequently affected in rheumatic fever?

The mitral valve is most frequently affected in rheumatic fever: mitral regurgitation (insufficiency) develops most commonly, followed less frequently by mitral stenosis. Aortic valve lesions are less common, ranking second in frequency after mitral disease. Combined mitral-aortic lesions can also occur.

What types of acquired valvular heart disease are distinguished based on morphological changes of the valves?

Based on morphological changes and functional disorders, three main types of acquired valvular heart disease are distinguished:

  • Stenosis — narrowing of the valvular orifice.
  • Insufficiency (regurgitation) — incomplete closure of the cusps, leading to the inability to prevent backflow of blood (regurgitation).
  • Combined defect — a combination of stenosis and insufficiency affecting the same valve.

Additionally, a multiple (complex) valvular defect is distinguished, in which two or more separate valves are affected simultaneously.

What hemodynamic disorders and morphological changes occur in the pulmonary circulation during 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 red blood cells. Morphological changes are characterized by the development of brown induration of the lungs (induratio fusca pulmonum):

  • Hemosiderosis — deposition of hemosiderin pigment in macrophages (siderophages / heart failure cells).
  • Sclerosis — diffuse proliferation of connective tissue in the interalveolar septa, around bronchi, and blood vessels.

Grossly, the lungs acquire a brownish color and a dense consistency. In severe cases, plasma transudation into the alveoli and rupture of pulmonary-bronchial anastomoses occur.

What is the difference between concentric and eccentric hypertrophy?

In concentric hypertrophy, ventricular walls thicken without significant chamber enlargement, which is typical for the compensation stage. Eccentric hypertrophy is accompanied by chamber dilation, indicating the exhaustion of the heart's functional reserves.

Why do thromboembolic complications frequently occur in valvular heart disease?

During the decompensation stage, dilation of the heart chambers and sluggish blood flow occur, which promotes thrombus formation, especially in the atrial appendages.

What factors can accelerate the transition to the decompensation stage?

Decompensation is triggered by recurrences of rheumatic fever, excessive physical or emotional stress, as well as concurrent infections and stressful conditions.

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