Mutagenic heterocyclic amines are produced during the ordinary cooking of meats and fish. When metabolically activated, heterocyclic amines will form covalent adducts with DNA, which, if not repaired, may affect the flow of genetic information in a cell. It has been proposed previously that heterocyclic amine mutagens contribute to the incidence of dietary-related cancers because they cause somatic cell mutations and induce tumors in rodents and nonhuman primates. Recent work has shown that some cooked food mutagens preferentially produce DNA damage in heart cells, DNA adduct levels are directly related to dose and duration of mutagen exposure, the dietary damage persists for long intervals in cardiac tissue, and mitochondrial DNA is more vulnerable than nuclear DNA to these mutagens. Because cardiac myocytes are terminally differentiated cells that have lost their ability to divide, the capacity to repair DNA damage is a critical factor in the proper function of cardiomyocytes, and cardiac myocytes seem to have limited DNA repair capabilities. DNA damage formed by dietary components, such as heterocyclic amines, might accumulate with time because of inefficient repair and thereby affect heart cell function or viability. The possibility that dietary habits play a role in idiopathic cardiomyopathies and congestive heart disease should be explored in greater depth.