Why the study?
Does a copper-deficient diet worsen cardiac responses in rats genetically susceptible to hypertensive, hypertrophic cardiomyopathy?
Does a copper-deficient diet worsen cardiac responses in rats genetically susceptible to hypertensive, hypertrophic cardiomyopathy?
A copper-deficient diet induces electrical and structural cardiac changes in rats but does not appear to hasten or worsen the onset of genetically predisposed hypertensive, hypertrophic cardiomyopathy.
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Copper deficiency may induce cardiac changes in susceptible rat models; leaves open relevance to human hypertrophic cardiomyopathy and need for clinical studies.
OBJECTIVE: Rats with a genetic tendency to develop hypertensive, hypertrophic cardiomyopathy were fed copper-deficient diets and their cardiac responses were investigated. METHODS: Five male weanling rats of the Long-Evans and SHHF/Mcc-fa(cp) strains were randomly selected to receive diets containing either adequate quantities of copper (94.5 micromol Cu/kg diet) or reduced quantities of copper (<15.8 micromol Cu/kg diet) for 6 weeks, (n=5 within each group). Echocardiograms and electrocardiograms were recorded and analyzed at the end of the 6-week interval. RESULTS: Electrocardiograms from copper deficient groups showed longer Q-T intervals and increased QRS amplitudes than controls. Both the copper deficient and control SHHF groups demonstrated significant QRS complex prolongation compared to Long-Evans rats. Echocardiography analysis showed significant increases in left ventricular area, free wall dimension, and myocardial cross-sectional areas in rats fed a copper deficient diet. The frequency of systolic cardiac murmurs increased in copper deficient rats and were related to the presence of valvular regurgitation as determined from echocardiography. DISCUSSION: However, the data do not suggest that a copper-deficient diet fed to a strain of rats genetically susceptible to heart disease later in life, hastens or worsens the onset of cardiac disease. The genetic predisposition and copper-deficient states exert independent effects upon the heart.
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Shiry et al. (1999) studied this question.
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