Experimental and clinical studies have shown the antiarrhythmic activity of magnesium salts and the arrhythmogenic effect of hypomagnesemia. Both are observed mainly but not exclusively during treatment with digitalis. The Mg++ plays an essential role in transmembrane K+ exchange in that a deficit of magnesium leads to a loss of intracellular K+ which cannot be compensated simply by administering K+ supplements if the magnesium equilibrium is not restored. In vitro, changes in the atrial action potential induced experimentally by a fall in extracellular K+ or by digitalis overdose can be corrected by increasing the Mg++ concentration in the medium. Contrary to classical theory, Mg++ does not seem to act on Na+-K+-ATP-ase activity, the origin of potassium disturbances and, therefore, arrhythmias. On the other hand, given the known antagonism between Ca++ and Mg++ on the contractility of the muscular fibre, a similar antagonism might be active with regards to electrogenesis. The role of the inward calcium current in the induction of abnormal automaticity observed particularly in digitalis toxicity is well known. The antiarrhythmic effect of Mg++ would seem to be related mainly to its moderating effect on this calcium inflow which, conversely, would be favored by hypomagnesemia. We conclude that, in practice, prophylaxis of arrhythmias in patients on digitalis and diuretic therapy, should include prevention of magnesium loss.
Arch Mal Coeur Vaiss 1984 Apr;77 Spec No:49-52