Heart failure (HF) remains one of the leading health problems globally. It is often characterized by unresolved inflammation, adverse cardiac remodeling, and tissue damage. Efferocytosis, the process by which phagocytes clear apoptotic cells, is a key process that helps to resolve inflammation and maintain tissue homeostasis. In the healthy heart, efferocytosis ensures the proper removal of apoptotic cardiac cells (e.g., cardiac fibroblasts and cardiomyocytes) and promotes inflammation resolution and secretion of anti-inflammation cytokines. However, emerging evidence suggests that this process is often impaired in patients with heart failure, and as a result leads to chronic inflammation, secondary necrosis, and tissue scarring. This review explores the cellular and molecular processes guiding efferocytosis and how its dysregulation potentially contributes to advanced heart failure. It also explores how factors like macrophage and endothelial cell phenotypes, lipid mediators, and nuclear transcription factors influence the efficiency of efferocytosis in the myocardium. By synthesizing current findings, we propose that restoring efficient efferocytosis in the failing heart may present a promising therapeutic approach to resolving inflammation and improving the outcomes of patients with heart failure.