Background: This study aimed to examine whether the copper-deficient rat might be a model for cardiac ventricular rupture in humans.

Materials and Methods: Male weanling rats were fed diets that were adequate (5.7 mg/kg diet) or deficient (0.3 mg/kg diet) in copper for 49 days, and 24% of the copper- deficient rats died of cardiac rupture. The autopsy samples of heart and liver were obtained from rats who died of cardiac rupture or controls who died of noncardiac causes.

Results: Trace element measurements indicated that organ copper concentration was reduced by copper-deficiency in rats, the manganese concentration in organs of copper- deficient rats was higher than that of the controls. Iron concentration was lower in the rats with the ruptured hearts and not different in the ruptured copper-deficient hearts compared to the controls and liver iron concentration was higher than controls in copper deficiency and was not different from controls in rats with cardiac rupture. Macromineral measurements indicated that: magnesium concentration was lower in ruptured hearts of copper-deficient rats than it was in their respective controls phosphorus was elevated in both sets of ruptured hearts, as was sodium and calcium concentration in ruptured hearts of copper-deficient rats was higher than in controls.

Conclusion: The trace element changes, especially for copper, are not associated with cardiac rupture in rats, but similar macromineral changes associated with rupture in copper-deficient rats probably reflect the common endpoint of both conditions, tissue necrosis.