The aim of this study was to evaluate the toxic effects of methamphetamine on the histological structure of the heart muscle in adult male white rats, to assess the potential protective effects of vitamin E against the toxic effects of methamphetamine, and to evaluate the anti-oxidative effects of vitamin E. Three hundred and two white adult Sprague–Dawley rats were randomly allocated to four major groups, 8 rats per group. Each main group was then split into two subgroups according to length of treatment (15 or 30 days). The control group received daily doses for 15 days while the first group of experimental animals were given daily doses of methamphetamine (0.1 mg/kg, 1 mL/day) and the third group daily doses of vitamin E (0.1 mL/day) for 30 days. The animals were hyperactive and moved around more in the cages, were very agitated and eating and drinking less after being treated with methamphetamine. Heart samples were taken at the end of each experimental period and subjected to histopathology. Observed were coronary blood vessels, an infiltration of inflammatory cells, hemorrhage, and some muscle fiber atrophy, also with loss of the nuclei, and increase in the intramuscular connective tissue, the degree of the latter changing with the duration of the exposure. Some histological changes also were observed in the vitamin E group, which may be due to dose or time of administration. Group treated with methamphetamine and vitamin E had a lesser reduction in the severity of some histological lesions than the methamphetamine only group, but the pathological changes were not completely prevented. The study found that methamphetamine creates progressive tissue toxicity in the heart muscle, with the severity of the toxicity increasing as the amount of time the body was exposed to the drug, indicating a cumulative effect of the drug on cardiac tissue. The outcomes further suggest a partial protection of vitamin E against cardiac toxicity induced by chronic methamphetamine exposure, but not enough to prevent all histological changes, thus necessitating further research to determine the optimal dose and mechanism of protection during chronic methamphetamine exposure.