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Clinical Applications and Untoward Reactions of Chelation in Cardiac Arrhythmias

ALFRED SOFFER, M.D.; TAFT TORIBARA, Ph.D.; DOMINIC MOORE-JONES, M.D.; DONALD WEBER, M.D.
Arch Intern Med. 1960;106(6):824-834. doi:10.1001/archinte.1960.03820060076008.
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It is not surprising that metal binding may become a valuable technique in the management of cardiac arrhythmias. The ease with which serum calcium is bound by the chelating agents such as edathamil disodium (EDTA) and the prominent though poorly understood place that the calcium ion has in myocardial function made the application of chelation in cardiac malfunction inevitable. Dramatic responses to such induced hypocalcemia have been explained by a direct action of edathamil upon the heart1 or by reduction of serum calcium ions.2 Experimental evidence suggests that decrease in extracellular calcium may enhance an influx of potassium into myocardial cells by altering permeability of the cell membrane.3 Since calcium may potentiate the action and toxicity of digitalis, immobilization of calcium ions by chelation appealed to clinicians as an antidote for hearts poisoned by overdigitalization.4 It has been suggested that calcium binding could be used to ascertain the degree of

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