Pathology · Cardiac Pathology (IHD, Myocardial Infarction, Valvular, Endocarditis)

Arrhythmogenic cardiomyopathy (ARVC/ACM), now classified as arrhythmogenic cardiomyopathy in WHO 2022, most commonly results from mutations in which molecular complex, and what is the mechanistic link between these mutations and the fibro-fatty replacement of the myocardium?

  • A Desmosomal protein mutations (plakophilin-2, desmoplakin, desmoglein-2) impair mechanical coupling at the intercalated discs; stressed cardiomyocytes lose desmoglein-mediated Wnt/β-catenin suppression of adipogenesis, transdifferentiating into adipocytes and fibroblasts
  • B Sarcomeric mutations (MYH7, MYBPC3) disrupt mechanical coupling, causing myocyte death and fibro-fatty infiltration similar to dilated cardiomyopathy
  • C Lamin A/C nuclear envelope mutations cause cardiomyocyte loss preferentially in the right ventricle due to lower wall stress in the right compared to left ventricle
  • D SCN5A sodium channel mutations cause ventricular arrhythmias, and repeated ischemia from arrhythmia-mediated hemodynamic compromise leads to fibro-fatty scar formation
Correct answer: A. Desmosomal protein mutations (plakophilin-2, desmoplakin, desmoglein-2) impair mechanical coupling at the intercalated discs; stressed cardiomyocytes lose desmoglein-mediated Wnt/β-catenin suppression of adipogenesis, transdifferentiating into adipocytes and fibroblasts

Explanation

ARVC is predominantly caused by mutations in desmosomal proteins: plakophilin-2 (PKP2, most common in European populations), desmoplakin (DSP), desmoglein-2 (DSG2), desmocollin-2 (DSC2), and junction plakoglobin (JUP). The mechanistic link to fibro-fatty replacement involves two pathways: (1) impaired mechanical coupling at intercalated discs leading to cardiomyocyte death under hemodynamic stress; (2) loss of desmosomal junction plakoglobin disrupts its inhibitory signalling on β-catenin nuclear translocation (Wnt pathway), releasing nuclear β-catenin-mediated transcriptional programs that activate adipogenic transcription factors (PPARγ) — causing cardiomyocyte-to-adipocyte transdifferentiation. Sarcomeric mutations cause HCM/DCM not ARVC. Lamin mutations cause ARVC-DCM overlap but are not the primary mechanism.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.

Sponsored

Want to test yourself?

Create a free account for timed mock tests, mistake tracking, and FSRS spaced-repetition revision across 23,000+ MCQs.

Start free → Log in

More Cardiac Pathology (IHD, Myocardial Infarction, Valvular, Endocarditis) MCQs

See all Cardiac Pathology (IHD, Myocardial Infarction, Valvular, Endocarditis) MCQs →