The non-coding part of the genome accounts for the majority of our DNA. In inherited cardiac diseases, where a pathogenic variant is often found in a particular gene, the high variability in disease expression and reduced penetrance points at other players besides the gene with the pathogenic variant. Genome-wide association studies (GWAS) have revealed that the majority of common variants associated with disease traits lay in non-coding regions of the genome, which indicates that non-coding DNA functionality could explain part of the disease variability. In this thesis, we aimed to uncover new mechanisms of gene regulation in inherited cardiac diseases focusing on the non-coding part of the genome. The first part of this thesis focuses on LQT1 and how the fine-tuned regulation of KCNQ1 expression in the presence of a heterozygous pathogenic variant determines disease severity. We identified a regulatory region in intron 1 of KCNQ1 that regulates KCNQ1 expression in an allele-specific manner and contains common variants that affect QTc duration in an allele and sex-dependent manner in LQT1 patients. Furthermore, we use synthetic non-coding RNAs to suppress the mutant KCNQ1 allele by targeting common variants in KCNQ1 as a versatile strategy to treat LQT1. In the second part of this thesis, we investigate the role of a new class of non-coding RNAs, circular RNAs (circRNAs), in cardiac homeostasis and disease. We focus on circRNAs derived from TTN, which is the most commonly mutated gene in inherited cardiac diseases. We revealed the importance of TTN-derived circRNAs in regulating the proper expression and splicing of key cardiac genes in vitro and in vivo. This thesis contributes to broadening our knowledge of the functions of the non-coding genome in inherited cardiac diseases.