Which of the following best describes the pathogenesis of mitral valve prolapse (MVP) at the molecular level?
- A Myxomatous degeneration with accumulation of proteoglycans and fragmentation of collagen/elastin in the fibrosa layer ✓
- B Calcification of the mitral annulus due to hypercalcemia
- C Inflammation-mediated fibrosis of the mitral leaflets from rheumatic fever
- D Congenital bicuspid valve anatomy causing prolapse under systemic pressure
Correct answer: A. Myxomatous degeneration with accumulation of proteoglycans and fragmentation of collagen/elastin in the fibrosa layer
Explanation
Mitral valve prolapse results from myxomatous degeneration of the valve leaflets — accumulation of proteoglycans (dermatan sulfate, chondroitin sulfate) weakens the structural fibrosa layer by fragmenting collagen and elastin, causing the valve leaflets to become floppy, redundant, and to prolapse into the left atrium during systole. This can be familial (often associated with Marfan syndrome via FBN1 mutation or FLNB/DCHS1 mutations). Rheumatic fever causes commissural fusion and fibrosis, not myxoid change.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.