Targeted cancer therapies can induce cardiovascular toxicities through distinct molecular mechanisms, leading to characteristic clinical presentations and requiring specific management strategies. (A) Small-molecule inhibitors cause cardiotoxicity via hERG channel inhibition, mitochondrial dysfunction with increased glycolysis, endoplasmic reticulum stress, and endothelial damage, manifesting as hypertension, arrhythmias, and contractile dysfunction. Management includes cardiovascular risk assessment, lifestyle modifications, and pharmacologic therapies, such as antihypertensive agents, statins, and SGLT2 inhibitors. (B) Monoclonal antibodies targeting receptors like VEGF and HER2 impair nitric oxide production, induce vascular remodeling, and alter cardiomyocyte survival signaling, causing hypertension, arterial thrombosis, and reductions in left ventricular ejection fraction (LVEF). Management strategies involve early detection using cardiac biomarkers (e.g., troponin I, myosin light chain-1) and pharmacologic therapy with statins, beta blockers, ACE inhibitors, and calcium channel blockers. (C) Immune modulators, including immune checkpoint inhibitors and adoptive cell therapies, increase autoimmunity in the heart through CD8⁺ T cell infiltration, cytokine release (e.g., IFN-γ, IL-6), and autoantibody production, leading to myocarditis, accelerated atherosclerosis, arrhythmias, and heart failure. Management focuses on corticosteroids, immunomodulatory agents (e.g., abatacept, tocilizumab), and supportive care with intravenous fluids, vasopressors, dexamethasone, and anticoagulation in cases of cytokine release syndrome (CRS). This integrated approach highlights the importance of understanding distinct pathogenic mechanisms to guide timely monitoring, prevention, and treatment of cardiovascular changes while maintaining oncologic efficacy.