We investigated whether structural variants, including copy number losses or gains, inversions, or insertions, affected genes that were highly mutated between pediatric and adult cardiomyopathy patients i.e., MYH7, MYL3, OBSCN, TTNT2, TTN, and VCL. This identified six additional predicted deleterious copy number deletions in OBSCN and TTN, none of which have been previously reported in the reference population. This evidence concerns the gene OBSCN and cardiomyopathy.