Chronic Mitral Valve Fibrosis in Rheumatic Heart Disease: From Immune Trigger to Inflammatory and Mechanical Progression

Figures

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  Figure 1. Gross and histological comparison between normal and rheumatic mitral valves. Upper, a normal mitral valve obtained from a heart transplant recipient; lower, a severely fibrotic rheumatic mitral valve from a patient undergoing surgery for RHD. Longitudinal full‐thickness sections were stained with HE and Masson’s trichrome stain to assess tissue structure and collagen deposition. HE indicates hematoxylin–eosin stain; Masson, Masson’s trichrome stain; and RHD, rheumatic heart disease.

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  Figure 2. Multiplanar cardiac CT reconstruction of mitral valve leaflet thickness in normal individuals and patients with RHD. Representative CT images illustrate mitral valve leaflet morphology and thickness measurements. N, N‐1, N‐2, and N‐3 show normal leaflet thickness in healthy individuals. R, R‐1, R‐2, and R‐3 demonstrate significantly thickened mitral leaflets in patients with RHD. Dashed lines indicate the measurement of maximum leaflet thickness in each case. CT indicates computed tomography; and RHD, rheumatic heart disease.

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  Figure 3. Echocardiography imaging of the mitral valve in normal individuals and patients with RHD. A and B, normal mitral valve imaging; C and D, findings in RHD. A and C are 2‐dimensional short‐axis views of the mitral valve; B and D, 3‐dimensional reconstructions of the mitral valve. RHD indicates rheumatic heart disease.

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  Figure 4. Mechanistic diagram of the ongoing progression of rheumatic mitral valve fibrosis. This diagram illustrates the key cellular and molecular drivers underlying the persistent progression of rheumatic mitral valve fibrosis, highlighting the dynamic interplay between acute and chronic phases. Leukotrienes have been implicated in inflammatory processes across multiple cardiovascular pathologies and may potentially contribute to valvular inflammation in RHD; however, their specific role in rheumatic mitral valve fibrosis remains unproven and requires additional experimental and clinical investigation. ECM indicates extracellular matrix; IL‐1β, interleukin‐1 beta; MMP, matrix metalloproteinase; RHD, rheumatic heart disease; and TNF‐α, tumor necrosis factor‐alpha.

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  Figure 5. Schematic of the imaging—based assessment model for predicting rheumatic mitral valve repair success. This figure presents the preoperative CT—based assessment model. It includes representative CT imaging findings (calcification quality score, symmetry measurements, the thinnest ALCZ, and calcification of the ALCZ), clinical parameters (CAD status, PAP), and a nomogram for predicting the EGMR—related repair success rate. The model integrates multiple CT—derived and clinical variables to calculate the probability of a successful mitral valve repair. For detailed modeling methodology and assessment procedures, please refer to our previously published article. 97 ALCZ indicates anterior mitral leaflet clean zone; CA, calcification; CAD, coronary artery disease; CT, computed tomography; EGMR, early good mitral valve repair; and PAP, pulmonary artery pressure.