Dilated cardiomyopathy (DCM) is a heart muscle disease characterized by structural and functional myocardial abnormalities. Left ventricular or biventricular dilation results in impaired heart contraction. Up to 30% of DCMs are reported to have a monogenic etiology. Mutations in several genes can cause DCM, including genes encoding sarcomeric, nuclear envelope, or cytoskeletal proteins. As a result, decreased cardiac contractility and conduction defects occur, ultimately leading to arrhythmia, heart failure, and sudden cardiac death. To date, the only curative approach is heart transplant, and etiological treatments are lacking. Mutations in the LMNA gene are among the most prevalent candidates associated with severe genetic cardiomyopathy. We used prime editing (PE) to model and correct DCM-associated LMNA pathogenic variants in human cell lines and iPSC-derived cardiomyocytes. We compared different PE approaches to optimize editing frequencies, showing that the same pegRNAs can result in substantially different editing efficiencies across the cell types tested. We also compared adenine base editor (ABE) and PE for gene correction of a common LMNA mutation. Our work highlights the potential of PE for the treatment of genetic heart diseases.