LETTERS TO THE EDITOR
Mercury and idiopathic dilated cardiomyopathy
Fritz Lorscheider, PhDa and
Murray Vimy, DMDb
a Faculty of Medicine, 3330 Hospital Drive N.W., University of Calgary, Canada T2N 4N1
b Department of Medicine, Faculty of Medicine, University of Calgary, Canada
We read with interest the recent report on trace metals and idiopathic dilated cardiomyopathy by Frustaci et al. (1). As far as we know, this is the first report to show that markedly increased concentrations of mercury (Hg) in cardiac tissue are associated with a specific cardiac pathology.
A recent review cites a number of studies that clearly establish that the largest source of nonoccupational Hg exposure for the general population is their dental amalgam fillings (2). At least 70% of all Hg ions excreted in human urine originate solely from amalgam fillings (3). Therefore, we wonder if it would be possible for Frustaci et al. to obtain dental histories for their patients.
The suggestion offered by Frustaci et al., that Hg++ acts as a Ca++ antagonist at the actin–myosin junction, thereby inhibiting sarcomere contraction and ultimately myocyte function, is certainly a possibility. Another possibility they might wish to consider is that Hg causes disruption of the microtubule structure, a major cytoskeletal component of most cells. We have demonstrated this phenomenon in brain neurons where Hg inhibits guanosine triphosphate nucleotide binding to beta-tubulin, thereby blocking an essential step in the polymerization of tubulin molecules for microtubule formation (4). Perhaps the same phenomenon also occurs in myocardial cells.
We encourage Frustaci et al. to pursue the matter of dental histories for their patients, which may account for the inordinately high levels of Hg (22,000 times greater than that in control subjects) seen in the heart tissue of patients with idiopathic dilated cardiomyopathy.
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References
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1. Frustaci A, Magnavita N, Chimenti C, et al. Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction. J Am Coll Cardiol. 1999;33:1578–1583[Abstract/Free Full Text]
2. Lorscheider FL, Vimy MJ, Summers AO. Mercury exposure from ‘silver’ tooth fillings: emerging evidence questions a traditional dental paradigm. FASEB J. 1995;9:504–508[Abstract]
3. Aposhian HV, Bruce DC, Alter W, Dart RC, Hurlbut KM, Aposhian MM. Urinary mercury after administration of 2,3-dimercaptopropane-1-sulfonic acid: correlation with dental amalgam score. FASEB J. 1992;6:2472–2476[Abstract]
4. Pendergrass JC, Haley BE, Vimy MJ, Winfield SA, Lorscheider FL. Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer diseased brain. Neurotoxicology. 1997;18:315–324[Medline]
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