Clinical intervention studies on magnesium in myocardial infarction

Patients with acute myocardial infarction (AMI) display a significant decrease in serum magnesium concentrations (S-Mg,c) during the initial 48 h after infarction. This decrease is not due to an increased renal magnesium loss, neither is it a dilution phenomenon. Consequently, a migration of Mg from the extracellular to intracellular space might take place, which probably is due to a catecholamine-induced increased lipolysis, forming insoluble intracellular Mg soaps. As the Mg ion is crucial in maintaining the electrical stability of the myocardium, we found it rational to avoid this postinfarctional hypomagnesemia by administration of Mg. In a double-blind, placebo-controlled trial, 130 patients with AMI were randomly allocated to receive a total of 62 mmol magnesium chloride or placebo intravenously during the initial 48 h in hospital. Mg treatment was associated with a reduction in the acute mortality from 19% in the placebo group to 7% in the Mg group (p = 0.045). This reduction was primarily due to a reduction in the number of deaths due to cardiogenic shock. The incidence of arrhythmias needing treatment was more than halved (from 47% in the placebo group to 21% in the Mg group; p = 0.003), primarily due to a reduction in the incidence of supraventricular tachyarrhythmias. Finally, Mg treatment significantly influenced the AMI diagnosis, as only 56/136 Mg-treated patients (41%) versus 74/137 placebo-treated patients (54%) developed an infarction (p less than 0.05). The mechanisms behind this beneficial effect of the Mg infusions are extensively discussed in this paper. Our results have now been confirmed by three other different groups with similar protocols. On the basis of this, we conclude that immediately instituted intravenous Mg treatment should be adopted as part of the routine treatment for patients presenting with AMI.