Introduction: Cells can produce both microRNAs (miRNAs) and their mRNA 3’ untranslated region (3’UTR) targets as multiple processing variants. We aim to comprehensively document these processing variants in the heart and determine whether they are altered during cardiac hypertrophy. Methods: Transverse Aortic Constriction (TAC) was performed to induce cardiac hypertrophy in C57BL/6 mice. RNAs were extracted from sham-treated, pre-hypertrophic (2 days post-TAC), and hypertrophic (7 days post-TAC) hearts, then subjected to next generation sequencing of small RNAs and mRNA 3’ends. Results: There is a widespread occurrence of miRNA processing variations in the cardiomyocyte, which remained largely unchanged during hypertrophy. Our mRNA 3’end-sequencing data identified novel 3’UTRs for 91 hypertrophy-related genes, which could have profound impacts on the miRNA targeting of those genes. Notably, there was a significant global shift towards shorter 3’UTR variants during hypertrophy. Statistical analysis shortlisted 406 mRNAs with a pronounced change in the proportion of 3’UTR variants, 7 of which have been validated through qPCR. Polysome fractionation revealed that 3’UTR lengths affected translational efficiency of mRNAs.  Conclusion: We present in-depth information on miRNA and mRNA processing variants in cardiomyocytes. Importantly, the global shift towards shorter mRNA 3’UTRs, together with our demonstration of associated changes in translational efficiency represents a new paradigm of increased protein synthesis during hypertrophy. As a next step, we are currently using our datasets to build a systems-level understanding of miRNA-mediated regulation during normal and hypertrophic states of the heart, which will aid in the development of miRNA-based therapy for cardiac disease.