The mechanisms of magnesium action and the possible benefits of its use in treating acute myocardial infarction are reviewed. Magnesium is an essential cofactor in more than 300 enzymatic reactions, including those responsible for the production, storage, and use of energy. It influences impulse generation and action potential propagation of the cardiac and pacemaker cells and affects muscular contraction within the myocardium and arterial smooth muscle. Magnesium has been used successfully for the treatment of arrhythmias and has been shown to produce hemodynamic changes including suppression of vasospasm and reduction of vascular resistance. In clinical trials to assess the usefulness of intravenous magnesium in the treatment of acute myocardial infarction, several beneficial effects were found, including a smaller mean infarction size, a reduction in the occurrence of supraventricular tachycardia, fewer occurrences of serious ventricular arrhythmias, and a lower incidence of early mortality. A bolus dose of magnesium followed by a prolonged infusion to maintain elevated serum magnesium levels appears necessary to obtain the beneficial effects. Studies indicate that magnesium may reduce the incidence of early mortality after acute myocardial infarction. The mechanism of action is still unclear, but it may be a direct cardioprotective effect.