Marginal copper intakes over a protracted period in genetically and nongenetically susceptible heart disease rats disturb electrocardiograms and enhance lipid deposition

The research question posed was does marginal copper (MC) intake over a protracted period lead to cardiac pathology in rodents either genetically susceptible or nonsusceptible to heart disease? We used the spontaneously hypertensive heart failure (SHHF) rat strain, a genetic model of hypertrophic cardiomyopathy, and the Long-Evans rat strain that does not develop heart disease genetically. Rats from both strains were fed either a control diet with adequate levels of copper (6.7 mg Cu/kg diet) or marginal in copper (2.8 mg Cu/kg diet) for 3, 6, or 10 months. At each time point, electrocardiographic measures were obtained from leads I and aVF, and hearts were processed for histological evaluation by transmission electron microscopy. There were no differences between strain or treatment in terms of mitochondrial or myofibrillar volume density. However, MC rats, regardless of strain and age, had increased lipid droplets in the myocardium. There were strain differences in electrocardiograms with SHHF rats, demonstrating abnormalities in traces, but they were not made any worse by MC intake. However, overall, the rats fed MC, regardless of strain, did demonstrate increased R-wave amplitude and duration in the QRS complex and some changes in P and T waves, which have been reported for severe copper deficiency. We conclude that MC intake over a protracted period is deleterious to cardiac health but that the genetic susceptibility of the heart to other forms of cardiac disease does not hasten or worsen the copper effect.