Journal of Applied Physiology AJP: Heart and Circulatory Physiology
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J Appl Physiol 93: 746-751, 2002. First published March 1, 2002; doi:10.1152/japplphysiol.01144.2001
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Vol. 93, Issue 2, 746-751, August 2002

Earliest cardiac toxicity induced by iron overload selectively inhibits electrical conduction

Kenneth A. Schwartz1, Zy Li1, Dianne E. Schwartz1, Thomas G. Cooper2, and W. Emmett Braselton3

1 Departments of Medicine, 2 Radiology, and 3 Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824

Female guinea pigs were injected intraperitoneally with 0.083 g/kg iron dextran (Fe-D) to achieve progressively increasing levels of iron load; controls received dextran. Delayed and blocked cardiac conductivity at the Purkinje fiber-papillary muscle junction was initially observed with Fe-D loads of 0.33 g/kg. Serial magnetic resonance relaxation time measurements obtained from livers of live animals showed a decrease (8.1 ± 0.86 vs. 14.8 ± 1.03 ms in controls, P < 0.001) that was first observed in animals loaded with 0.25 g/kg Fe-D. Iron concentrations in hearts and livers were significantly increased (P < 0.001). Left ventricular pressure measurements on 1.5 g/kg Fe-D animals failed to demonstrate a defect in contractility, but 27% (9/33) (P < 0.050) of the animals died without warning signs. We conclude that 1) initial decreases in liver magnetic resonance-relaxation time occur in the same range of iron excess as the threshold of iron load that induces delay or blockade of cardiac conduction and 2) a high incidence of sudden death, presumably from cardiac arrhythmias, was observed with large doses of iron that did not decrease left ventricular contractility.

arrhythmia; cardiomyopathy; sudden death; electrophysiology


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