## Histopathology of Acute Rheumatic Carditis **Key Point:** Aschoff bodies (Aschoff granulomas) with central fibrinoid necrosis are the pathognomonic histological hallmark of acute rheumatic carditis and are the most characteristic finding in the acute phase of RHD. ### Aschoff Body: Pathognomonic Lesion **High-Yield:** Aschoff bodies are: - Granulomatous lesions with a central zone of fibrinoid necrosis - Surrounded by inflammatory cells (lymphocytes, plasma cells, and activated macrophages called Anitschkow cells) - Found in the myocardium, particularly in the perivascular connective tissue - Diagnostic of acute rheumatic fever (ARF) and acute rheumatic carditis ### Histological Progression in RHD | Phase | Timeline | Key Findings | |-------|----------|---------------| | **Acute** | Days–weeks | Aschoff bodies, fibrinoid necrosis, myocarditis | | **Subacute** | Weeks–months | Aschoff bodies persist, inflammation decreases | | **Chronic** | Months–years | Fibrosis, calcification, valve scarring, Aschoff bodies resolve | **Clinical Pearl:** Aschoff bodies are found in the myocardium during acute carditis but are NOT typically seen in the valve leaflets themselves. Valve damage occurs through inflammatory edema and necrosis of valve tissue during the acute phase, leading to chronic fibrosis and calcification later. **Mnemonic:** **ASCHOFF** — **A**ctive inflammation, **S**urrounded by inflammatory cells, **C**entral fibrinoid necrosis, **H**istologically diagnostic, **O**ccurs in myocardium, **F**ound in acute phase, **F**ibrosis follows. ### Why Aschoff Bodies Form? 1. **Post-streptococcal autoimmunity** — Molecular mimicry between Group A Streptococcus M protein and cardiac myosin triggers T-cell and B-cell autoimmunity. 2. **Type II hypersensitivity** — Autoantibodies cross-react with cardiac myosin, tropomyosin, and other cardiac proteins. 3. **Granulomatous response** — Activated macrophages (Anitschkow cells) aggregate around areas of fibrinoid necrosis.
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