Table 1. Summary of the main suggested mechanisms of cardiotoxicity by group of drugs.

Anthracyclines	DNA double-strand break (topoisomerase IIB)
	Oxidative stress (reactive oxygen species)
	Cell membrane hyperpermeability (lipid peroxidation)
	Ultrastructural changes
	Cytoplasmic vacuolization
	Apoptosis
Trastuzumab	Interruption of HER-2/ERBB2 receptor signaling – Neuregulin 1
	Inhibits cell repair
	Cell dysfunction
Cisplatin Cyclophosphamide	Direct endothelial injury
	Platelet activation and aggregation
	Coronary thrombosis
5-Fluorouracil	Acts on the molecular signaling pathway that regulates smooth muscle tone
	Vasospasm – vasoconstriction
Vascular endothelial growth factor (VEGF) inhibitors	Inhibit nitric oxide synthase activity
	Increase endothelin production
	Inhibit rho-kinase activation
	Vasospasm
Protease inhibitors	Interference with the degradation of dysfunctional proteins
	Functional changes in the myocyte
Immune checkpoint inhibitors	Increased T-cell activity
	Autoimmune activity in the heart muscle