In Australia, 1 in 4 deaths occur due to cardiovascular disease. In the majority of cases, we do not fully understand the molecular underpinnings of a healthy heart and what goes wrong in disease. While environmental factors and healthy living play a role, a significant proportion of disease is thought to have a genetic basis. However, as limited mutations are present in the coding genome, the focus has now been redirected towards non-coding elements. Alternative polyadenylation (APA) is a co-transcriptional processing mechanism that affects the 3’ untranslated regions (3’UTRs) of mRNA. Transcriptomic studies show that ~70% of human genes have multiple functional poly(A) sites, so the 3’UTR length depends on whether the proximal or distal poly(A) site is selected for polyadenylate tail addition. It is known that 3’UTRs contain regulatory information pertaining to mRNA stability, localisation, and translation as well as protein localisation and function. Despite the ability of APA to regulate events on the transcriptomic and proteomic levels, its role in the heart has not been investigated. Here we sought to identify normal APA signatures of cardiac genes, by analysing the single-nuclear RNA-seq data from the human heart cell atlas project with polyApiper. With this approach, we were able to identify for the first-time 7,864 genes that express alternative 3’UTR isoforms and 350-550 genes that undergo differential APA between atrial and ventricular cardiomyocytes. Next, based on the expression of multiple 3’UTR isoforms we have been able to prioritise genes to investigate the functional significance of their alternative 3’UTRs in vitro. For example, preliminary results indicate that the longer TBX5 3’UTR correlates with lower protein expression. These findings can further our understanding of how APA regulates gene expression and/or protein function in a healthy heart and how dysregulation contributes to disease.