Abstract Body: Introduction: Cardiac fibrosis is a major determinant of heart failure (HF) progression and a key barrier to myocardial recovery. Alternative polyadenylation (APA) regulates gene expression by remodeling 3′ untranslated regions (3′UTRs), yet its contribution to fibrotic remodeling and reversibility in human HF remains largely unexplored. Methods: We analyzed myocardial tissue from human donor hearts, patients with end-stage non-ischemic HF at the time of left ventricular assist device (LVAD) implantation, and LVAD-supported patients at the time of subsequent heart transplantation. Poly(A)-ClickSeq (PAC-seq) was used to profile transcriptome-wide APA events, and PolyA-miner was applied to identify significant 3′UTR remodeling. APA changes were integrated with differential gene expression and correlated with histological assessments of fibrosis and hypertrophy and clinical measures of cardiac function. Results: End-stage HF myocardium exhibited extensive 3′UTR shortening, predominantly affecting extracellular matrix and profibrotic genes, coinciding with severe interstitial fibrosis, cardiomyocyte hypertrophy, and markedly reduced ejection fraction. In contrast, myocardial samples obtained after LVAD support demonstrated partial reversal of fibrotic remodeling, with reduced collagen deposition and hypertrophy on histology. Importantly, a subset of fibrosis-associated transcripts that were 3′UTR-shortened in advanced HF displayed 3′UTR lengthening following mechanical unloading, accompanied by reduced expression of profibrotic genes. These APA changes paralleled structural and functional improvement of the myocardium. Conclusion: APA remodeling of fibrotic gene networks is a dynamic and reversible feature of human heart failure. Mechanical unloading with LVAD is associated with normalization of 3′UTR usage in key profibrotic transcripts, linking RNA processing to fibrosis regression and myocardial recovery. These findings identify APA as a mechanistic regulator and potential therapeutic target in cardiac fibrosis.