Most genetic determinants of inherited cardiomyopathies fall within coding regions and associate with variable penetrance and expressivity within families. Genetic testing helps identify pathogenic and likely pathogenic variants, but genetic testing often identifies variants of uncertain significance. Uncertain variants are rare but lack enough data to classify as either pathogenic or benign. We evaluated pathogenic and uncertain cardiomyopathy gene variants in a biobank and found clinical correlates of cardiomyopathy in the electronic health record. We also undertook efforts to evaluating the noncoding regions of cardiomyopathy genes by evaluating multiple independent approaches to identify regulatory regions. We superimposed epigenomic profiling from hearts and cardiomyocytes, including promoter-capture chromatin conformation information, to identify enhancers for two cardiomyopathy genes, MYH7 and LMNA. Enhancer function was validated in human cardiomyocytes derived from induced pluripotent stem cells. Multiple enhancers were identified and validated for LMNA and MYH7, including a key enhancer that regulates the switch from MYH6 expression to MYH7 expression. Deletion of this enhancer resulted in a dose-dependent increase in MYH6 and faster contractile rate in engineered heart tissues. We searched for genomic variation in enhancer sequences across the genome, with focus on nucleotide changes that create or interrupt transcription factor binding sites. We identified a variant that altered a TBX5 binding motif and mapped to an enhancer region 2KB from the transcriptional start site of MYH7. Gene editing to remove the enhancer harboring this variant markedly reduced MYH7 expression in human cardiomyocytes. Using biobank-derived data, this variant associated with longitudinal echocardiographic features with cardiomyopathy. In summary, we identified enhancers that regulate cardiomyopathy gene expression, and genomic variation within these enhancer regions that associates with cardiomyopathic progression over time. This integrated approach identified noncoding modifiers of cardiomyopathy and is applicable to other cardiac genes.