Heart failure is the gradual inefficacy of the heart to pump blood around the body and contributes at least 10% of the mortality rate in the UK. Hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are the two main pathophysiological states, the former often progressing into the latter as the condition increases in severity. Although clinically distinct conditions, changes in myocardium gene expression are similar and it is believed there are common underlying biochemical mechanisms. The revolution in high throughput sequencing technology has enabled unbiased de novo whole transcriptome profiling. It is now known that at least 70% of the genome is transcribed to RNA, with just around 2% of this made up by the known protein-coding genes. The majority of the mammalian genome is transcribed into long non-coding RNAs (lncRNAs), defined as polyribonucleotides of ≥200 nucleotides. Mechanically stretching neonatal mouse cardiac myocytes with equibiaxial stretch apparatus mimics pathological hypertrophy in the heart and well established alterations in gene expression in cardiac hypertrophy were confirmed by RT-qPCR. My project aims to discover whether the myocardial transcriptome array of lncRNAs changes in our mouse model of HCM. Paired end RNA-seq from a 300-400bp library of stretched and non-stretched neonatal mouse cardiomyocyte total RNA was carried to generate 30-40 million 76-mer sequence reads per sample. Stretching resulted in an upregulation of two lncRNAs, MIAT and MALAT-1. RT-qPCR anlaysis also detected upregulation of MALAT-1 and MIAT in the transverse aortic constriction (TAC) mouse model of pressure-overload induced heart failure, validating our findings in the stretched myocyte model. MIAT and MALAT-1 have previously been associated with increased risk of myocardial infarction and metastatic cancers respectively, but never before with cardiomyopathy. Mice undergoing surgery were anesthetized with an initial concentration of 3% isoflurane carried by medical oxygen, delivered via a nose cone. Mice were followed weekly with echocardiography. Compensated hypertrophy and cardiac dilatation were confirmed by weeks four and eight respectively. Two additional novel unannotated transcripts were identified that showed differential expression in stretched cardiomyocytes. These are regions of the genome that are currently unannotated and potentially transcribe novel lncRNA and differential expression was validated by RT-qPCR. LncRNA are increasingly recognised as playing a major role in genomic regulation. We therefore hypothesise that changes in expression of target genes which contribute to the deterioration of the failing heart could be due to the actions of these lncRNAs. Subsequent in vitro and in vivo experiments will seek to understand the role of these lncRNAs in cardiac biology and how they could contribute to the progression of this complex disease.