Rheumatic Endocarditis

Localization and Frequency of Involvement

Inflammation can affect various structures of the inner lining of the heart. Three main localizations are distinguished:

• Valvular endocarditis — occurs most frequently, affecting the cusps and leaflets.
• Chordal endocarditis — inflammation extends to the tendinous cords.
• Mural (parietal) endocarditis — involves the endocardium of the atrial or ventricular walls.

Valve involvement frequency is unevenly distributed. The absolute leader is the mitral valve (65–70% of cases). In second place is combined involvement of the mitral and aortic valves (about 25%). Isolated aortic valve involvement is less common, tricuspid involvement is significantly rarer, and pulmonary valve involvement is considered a casuistry.

Initial Forms: From Valvulitis to Thrombosis

Morphological changes in rheumatic fever represent a unified, interconnected process that goes through several stages.

1. Diffuse endocarditis (valvulitis). This is an early stage where the endothelium remains intact, therefore thrombotic vegetations are absent. Macroscopically, the leaflets appear unevenly thickened, grayish, and translucent along the line of closure. Microscopic examination reveals mucoid swelling, moderate fibrinoid changes, and lymphohistiocytic infiltration. Specific rheumatic granulomas may form deep within the tissue. With timely treatment, this process is completely reversible.
2. Acute verrucous endocarditis. If the process progresses, fibrinoid changes intensify, and endothelial necrosis occurs. Small thrombi measuring 1–2 mm («vegetations») deposit on the damaged areas (along the closing margin of the leaflets). Initially gray and translucent, they subsequently become turbid and yellowish-gray. These thrombotic masses are easily detached. Outside the zone of "vegetations," the valve tissue appears unchanged.

Progressive Forms: Sclerosis and Recurrence

1. Fibroplastic endocarditis. This is a consequence of the first two forms. Active sclerosis processes come to the fore. The valve tissue thickens, acquiring a gray, translucent appearance, but its density does not yet reach its maximum. Microscopic examination shows connective tissue disorganization and inflammatory infiltration. Fresh thrombi may appear, with no temporal gap between old and new changes.
2. Recurrent verrucous endocarditis. Occurs during repeated rheumatic attacks. The process unfolds against the background of already altered, sclerosed, and deformed valves. Inflammation and disorganization involve both the intact stroma and old scar tissues. The endothelium is damaged anew on the sclerosed masses, and fresh portions of fibrin are deposited, which also undergo sclerosis when the process subsides.

Complications and Outcomes

Verrucous forms (acute and recurrent) are characterized by a formidable complication — thromboembolism of the systemic circulation. Detached thrombotic masses lead to infarctions of the spleen, kidneys, brain, myocardium, and retina. In some cases, intestinal or lower limb gangrene develops.

A regular outcome of the inflammation is the development of a valvular heart defect. Valve tissue undergoes sclerosis and hyalinosis. The leaflets thicken, shorten, and deform.

• Semilunar cusps (aorta, pulmonary trunk) curl along their free edges and may fuse with the vessel wall.
• The mitral valve undergoes profound changes: the anterior and posterior leaflets fuse, blurring the boundaries between them. A dense fibrous funnel forms, and the orifice itself narrows into a narrow slit or crescent. The chordae tendineae also thicken, shorten, and fuse together.
• Functionally, these changes manifest as stenosis (narrowing of the orifice), insufficiency (incomplete closure), or their combination, which is most common.