Anthracyclines contain an aromatic ring structure that intercalates in between DNA base pairs. The mechanism of cardiotoxicity appears to be inhibition of the function of topoisomerase II. This enzyme is critical in allowing DNA to undergo efficient repair. Most important, these agents generate free radicals that can damage cell membranes partly by lipid peroxidation. Amsacrine and mitoxantrone produce lower quantities of free radicals and cause less cardiotoxicity and cardiomyopathy compared with the doxorubicin, daunorubicin, idarubicin, and epirubicin. Cardiac tissues possess a low ability to detoxify these free radicals because of the presence of only small amounts of catalase that converts hydrogen peroxide to water.
In addition, anthracyclines chelate iron. These anthra-cycline–ironcomplexes produce cardiac-damaging hydroxyl radicals. Research is required in this area to find molecules that may modify these toxic effects. One agent, dexrazox-ane, undergoes hydrolysis to a carboxylamine that is capable of removing iron from the anthracycline–iron complex. It is partly effective in protecting the myocardium from damage.
Listed below are electrocardiographic manifestations of anthracycline cardiac damage.

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