Among 111 patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), 14% also had mitral valve prolapse (MVP), with 83% of these dual-condition patients carrying PKP2 gene variants compared to 64% in the broader ARVC cohort. Patients with both conditions showed higher left ventricular mass (93 vs 75 g/m²) and more frequent left heart wall motion abnormalities than those with ARVC alone. This genetic overlap challenges the traditional view of ARVC as purely a right-sided heart disease. The PKP2 gene encodes plakophilin-2, a protein crucial for cell-to-cell adhesion in heart muscle, suggesting a shared molecular pathway between these seemingly distinct conditions. Importantly, MVP in ARVC patients differed from typical arrhythmic MVP—lacking the dangerous features like bileaflet involvement and annular disjunction that usually predict sudden cardiac death. However, cardiac arrest rates were slightly higher in the MVP group (20% vs 16%). This preprint awaits peer review, and the findings need validation in larger cohorts. The research represents an incremental but important advance in understanding how genetic cardiomyopathies may manifest across multiple heart structures rather than in isolation.