Heart failure (HF) is traditionally classified by etiology or ejection fraction, but these categories do not fully explain the mechanisms driving disease progression. Increasing evidence suggests that both ischemic and non-ischemic HF are shaped by maladaptive interactions between immune activation and metabolic remodeling. In ischemic HF, acute cardiomyocyte death and reperfusion stress trigger a phase dependent inflammatory response requiring coordinated adaptation across immune, vascular, stromal, and myocardial cells. In non-ischemic HF, chronic cardiometabolic and hemodynamic stress impairs metabolic fitness in these compartments, promoting endothelial dysfunction, mitochondrial injury, fibrosis, and loss of myocardial reserve. Despite distinct triggers, both phenotypes converge on a shared immunometabolic substrate marked by inflammatory persistence, impaired metabolic flexibility, organelle stress, redox imbalance, and fibroinflammatory remodeling. This review highlights failed immunometabolic state transitions as a unifying mechanism in HF and examines roles for immune and metabolic memory, organelle stress networks, mitochondrial lipid crosstalk, and regulated lipid peroxidation.