Justification for intravenous magnesium therapy in acute myocardial infarction

Recent studies have shown that patients with acute myocardial infarction (AMI) are magnesium-deficient and develop an additional transient decrease in serum magnesium concentrations (S-Mg c) during the acute phase of the infarct. Animal experiments, as well as studies on humans, have indicated that the acute decrease in S-Mg c as well as a more chronic magnesium (Mg) deficiency state are harmful to the myocardium in the setting of acute ischaemia. This knowledge has led during the last couple of years to the performance of four double-blind placebo controlled studies in which the effect of i.v. magnesium therapy on mortality and incidence of arrhythmias in patients with AMI has been evaluated. Magnesium treatment more than halved the acute mortality and incidence of arrhythmias requiring treatment in three of the four intervention studies. The mechanisms behind the beneficial effect of magnesium therapy are probably multifactorial; a direct depressive effect on the cardiac conducting system; a peripheral dilatory effect on the arteries, reducing the afterload on the myocardium; a reduced infarct size; an ion-stabilizing effect, maintaining stable intra and extracellular concentrations of potassium, sodium and calcium; an improved energy generation in the myocardium; and an inhibitory effect on platelet aggregation. No side-effects were observed in any of the clinical intervention studies. Against this background, the author suggests that i.v. magnesium treatment should be adopted as part of routine practice for patients with acute myocardial infarction.