In rheumatic mitral stenosis, fibrosis of the mitral leaflets leads to a 'fish-mouth' or 'buttonhole' orifice. What is the primary microscopic change in the mitral valve in acute rheumatic carditis that leads to this chronic deformity?

• A Immune complex deposition in the valve stroma activating complement and causing direct fibrinogen precipitation
• B Fibrinous verrucae along the line of closure, Aschoff bodies (foci of fibrinoid necrosis with Aschoff cells/Anichkow cells) in the valve stroma, and subsequent progressive fibrosis and calcification ✓
• C Neutrophilic infiltration of valve leaflets forming micro-abscesses that heal by fibrosis
• D Myxomatous degeneration of the valve leaflets with glycosaminoglycan accumulation replacing fibrous tissue

Explanation

Acute rheumatic carditis produces (1) fibrinous verrucae (MacCallum plaques on the atrial wall posterior to the valve) along the line of valve closure — these are sterile fibrin deposits from valvular endothelial injury; and (2) Aschoff bodies — pathognomonic foci of fibrinoid necrosis surrounded by activated macrophages (Aschoff cells with 'caterpillar nuclei' / Anichkow cells) and lymphocytes in the myocardium and valve stroma. The T-cell molecular mimicry between streptococcal M-protein epitopes and cardiac valvular endothelial cells drives the initial injury. Repeated bouts of rheumatic fever cause progressive valvular fibrosis, commissural fusion, subvalvular chordal fusion, and calcification leading to the classic 'fish-mouth' mitral stenosis. Myxomatous degeneration characterises Barlow's disease/floppy mitral valve.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

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