Cardiovascular disease (CVD) is the global leading cause of death. Contributing to the poor outcomes associated with CVD is the non-proliferative phenotype of mature mammalian cardiomyocytes, which prevents cardiac tissue from regenerating in response to injury. Regenerative medicines in the heart have thus far had limited success, compounded by a paucity of knowledge about early cardiac development; to achieve regeneration, it is important to understand the way these cells are generated initially. Chromatin consists of DNA and associated proteins, and its organisation in cell nuclei plays a known role in many developmental processes, but little research has been conducted on condensed heterochromatin. Previous research in the Pennings lab identified gross changes in the distribution of H3K9me3-marked heterochromatin in mouse cardiomyocytes between embryonic days E10.5 and E13.5. This study describes changes in the epigenetic profile of (peri)centromeric heterochromatin composition during the time window of interest in mouse cardiac tissue compared to other tissues. Two mechanisms known to regulate constitutive heterochromatin are also investigated: the nuclear lamina, which anchors chromatin to the nuclear periphery, and mitochondrial metabolism, which generates the co-factors for the epigenetic regulatory enzymes. A combination of wet lab and bioinformatics techniques were used to characterise events in cardiac chromatin occurring during the time window of interest, from E10.5 to E13.5 and in adult. Chromatin Immunoprecipitation (ChIP) qPCR and analysis of ChIP-seq data were used to explore changes in levels of active (H3K36me3 and H3K4me3) and repressive (H3K9me3 and H3K27me3) epigenetic marks on constitutive heterochromatin. Activity of individual complexes in the mitochondrial electron transport chain were investigated through spectrophotometric assays. RNA-seq analysis and western blot identified changes in mRNA and protein expression of these complexes, respectively. Western blot also revealed levels of proteins comprising the nuclear lamina, complemented by RNA-seq data analysis and initial bioinformatic analysis investigating constitutive chromatin-nuclear lamina interactions between E9.5 and E12.5 in heart. These experiments suggested there may be a dynamic epigenetic landscape in constitutive heterochromatin during cardiac development. Notably, a strong downward trend in H3K9me3 on centromeres and modest reduction on pericentromeres at E12.5 in heart, which was not observed in other tissues. Further, an upward trend in active epigenetic marks, H3K36me3 and H3Kme3, occurred on major satellites between E10.5, E12.5 and E15.5 in heart, but not liver. At E11.5, a peak of lamin A protein was observed in heart, whilst liver remained stable. Further, a reduction in lamin B1-centromeric chromatin interactions occurred at E12.5 vs. E9.5 in heart. Meanwhile, the activity of the complexes in the mitochondrial electron transport chain and protein levels of these complexes did not change between E10.5 and E13.5, although increases were observed between E13.5 and adult across experiments. Overall, these findings suggest there may be a cardiac-specific epigenetic state changes of constitutive heterochromatin during early development. A hypothetical model is proposed in which the increase in active epigenetic marks on major satellites may point to a rise of transcription of the pericentromeric repeats, whereas the dynamics of H3K9me3 may also relate to changes in the nuclear lamina. An increase of lamin A protein at E11.5 may be associated with a mechanosensitive response, in which H3K9me3-marked heterochromatin potentially plays a role. The data presented here offer promising clues as to possible mechanisms in early cardiac development that may be important for tissue regeneration.