Different classes of anticancer treatments, including anthracyclines, other chemotherapies, small-molecule inhibitors, monoclonal antibodies, and immune checkpoint inhibitors, converge to initiate interconnected mechanisms that drive cardiotoxicity. Early oxidative stress and mitochondrial dysfunction disturb metabolic homeostasis and calcium handling, leading to redox-sensitive ion channel changes and electrophysiological abnormalities such as QT prolongation and arrhythmias. Persistent injury promotes endothelial dysfunction, with loss of nitric oxide signaling, vascular inflammation, and microvascular rarefaction. These processes enhance immune activation and cytokine release, ultimately resulting in cardiomyocyte loss, fibrotic remodeling, and progressive contractile failure. Each step in the cascade may be differentially engaged by specific therapy classes (entry arrows), yet together they form a shared pathogenic framework. The diagram also conveys a temporal gradient in which upstream events (steps i–iv) are potentially reversible, while chronic structural remodeling (step v) becomes increasingly irreversible.