Tissue repair is characterized by 3 phases: inflammation, repair, and resolution. Inflammation can be initiated both locally or systemically and functions to eliminate the source of injury and remove damaged tissue. In the heart, it is characterized by local cell death, loss of CCR2− resident macrophages, and replacement by recruited CCR2+ monocyte-derived macrophages. Repair is initiated after engulfment and clearance of apoptotic cardiomyocytes, stimulating the release of cytokines, including IL-10 and TGF-β, which activate fibroblasts to replace and remodel the tissue. Resolution is achieved following elimination of the injurious source and clearance of dead cells and debris. It is characterized by apoptosis and egress of the reparative machinery and restoration of homeostasis. In both HFrEF and HFpEF, the failure to resolve inflammation is correlated with pump dysfunction and ultimately, end-stage HF.