Magnesium is an important intracellular cation and cofactor for many human enzymes. Intravenous magnesium therapy has been shown to be useful in reducing mortality in thombolysis-ineligible patients with acute myocardial infarction. Magnesium also has been shown to suppress platelet activation. Schechter and associates evaluated the effectiveness of oral magnesium treatment on potential mediators of acute thrombus formation in patients with coronary artery disease (CAD).

Patients with stable, documented CAD were eligible for the double-blind, crossover, placebo-controlled study if they did not have concomitant unstable angina, congestive heart failure or other serious medical problems. Those who met the inclusion criteria were randomized to receive magnesium oxide tablets in a dosage of 800 to 1,200 mg per day or placebo for three months, followed by a four-week washout period, and then the alternate treatment for an additional three months. All other regular medications were continued throughout the study. All patients underwent a physical examination, blood tests for measurement of platelet-dependent thrombosis (PDT), platelet aggregation and other laboratory tests before and after each phase of the study.

A total of 36 patients completed the study. After three months of oral magnesium treatment, median PDT decreased by 35 percent. This change was not related to the presence of other risk factors such as hypertension, diabetes or smoking. Magnesium treatment appeared to have no effect on platelet aggregation, serum lipid levels, fibrinogen or apolipoprotein A-I and B. In addition, no serious adverse effects associated with the study medication were apparent.

The authors conclude that oral magnesium therapy reduced acute PDT, possibly because of its antiplatelet adhesion effects. The antithrombotic effect of magnesium treatment occurred despite 100 percent use of aspirin therapy. The clinical relevance of this observation needs further confirmation with a larger cohort of patients before any specific recommendation can be made.

editor's note: Hypomagnesemia has been shown to selectively impair the release of nitric oxide from the coronary endothelium. Because nitric oxide is a vasodilator and inhibitor of platelet aggregation and adhesion, hypomagnesemia may stimulate vasoconstriction and possibly even coronary thrombosis. This suggests that low magnesium levels may even contribute to the development of coronary atherosclerosis. Recently, intravenous infusions of magnesium have been used in an attempt to decrease infarct size in the immediate post-myocardial infarction period. Magnesium seems to have an important beneficial coronary vascular effect. More study is needed to determine how to actually harness magnesium's positive effects and whether its benefit will be generalizable.—r.s.