Novel SCN5A Variant in a Patient With Dilated Cardiomyopathy Complicated by Conduction Disorders and Recurrent Ventricular Arrhythmias

Background Although sodium voltage-gated channel alpha subunit 5 (*SCN5A*) was traditionally linked to electrophysiological disorders, growing evidence underscores its significant involvement in structural abnormalities. Case Summary A young dilated cardiomyopathy patient presented with a distinctive electro-structural dual phenotype, characterized by progressive left ventricular systolic dysfunction, conduction disorders, and concomitant severe ventricular arrhythmias. Comorbidities included coronary artery disease, chronic kidney disease, obesity, and obstructive sleep apnea. Genetic testing identified a de novo heterozygous nonsense variant in the *SCN5A* gene. Comprehensive management included guideline-directed medical therapy for heart failure, antiarrhythmic agents, along with comorbidities management and risk factor modification. Conclusions This case highlights the diagnostic complexity of dilated cardiomyopathy in young patients with multiple overlapping etiologies—genetic, ischemic, metabolic. A de novo *SCN5A* variant may contribute to the arrhythmic phenotype and progressive cardiomyopathy. Take-Home Messages Beyond its classical electrophysiological role, *SCN5A* is increasingly implicated in structural remodeling. This case emphasizes the complexity of genotype-phenotype correlation and gene-environment interaction.