The pathogenesis of ARVD involves apoptosis with fatty and fibro-fatty infiltration of the<unk>  ventricular free wall leading to heart failure and ventricular arrhythmias. Arrhythmogenic<unk>  ventricular cardiomyopathy is considered as a disease of the desmosome. Desmosomes are abundant in the skin and myocardium and their function is to contribute mechanical attachment between cells and work as an important mediator of the intracellular and intercellular signal transduction. Desmosomes are composed of plakoglobin, plakophilins, desmoplakin, desmogleins, and desmocollins. ARVC is usually caused by mutations in genes encoding for desmosomal proteins such as Plakoglobin (JUP), desmoplakin (DSP), plakophilin‐2 (PKP2), desmoglein‐2 (DSG2), and desmocollin‐2 (DSC2). A minority of cases is caused by mutations in nondesmosomal genes. Mode of transmission of Arrhythmogenic<unk>  ventricular cardiomyopathy is mostly an autosomal‐dominant trait. Autosomal‐recessive forms are rare, mostly in the cardiocutaneous syndromes such as Carvajal syndrome and Naxos disease. Studied have shown that multiple mutations with digenic heterozygosity are associated with earlier manifestation and more malignant phenotype.
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