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J Appl Physiol (March 1, 2002). doi:10.1152/japplphysiol.01144.2001
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Articles in PresS, published online ahead of print March 1, 2002
J Appl Physiol, 10.1152/jap.01144.2001
Submitted on November 16, 2001
Accepted on February 27, 2002

The earliest cardiac toxicity induced by iron overload selectively inhibits electrical conduction

Kenneth A. Schwartz1*, ZY Li1, Dianne E. Schwartz1, Thomas G. Cooper1, and W. Emmett Braselton1

1 Department of Medicine, Michigan State University, East Lansing, MI, USA

* To whom correspondence should be addressed. E-mail: schwart7{at}pilot.msu.edu.

Female guinea pigs were injected intraperitoneally with 0.083 gm/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 (PF-PM) junction was initially observed with Fe-D loads of 0.33 gm/kg. Serial MR-T2 measurements obtained from livers of live animals showed a decrease (8.1±.86 msec vs 14.8±1.03 msec in controls, p<.001) that was first observed in the animals loaded with 0.25 gm/kg Fe-D. Iron concentrations in hearts and livers were significantly increased (p<.001). Left ventricular pressure measurements on 1.5 gm/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 concluded that: 1. initial decreases in liver MR-T2 relaxation times occur in the same range of iron excess as the threshold of iron load that induces delay or blockade of cardiac conduction; 2. A high incidence of sudden death, presumably from cardiac arrhyrhmias, was observed with large doses of iron that did not decrease left ventricular contracticility.




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