Hypomagnesemia is common in hospitalized patients, especiaLLy in the eLderLy with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with the risk of hypertension, type 2 diabetes mellitus, increased mortality from all cause and CAD. Higher magnesium intake, however, has been associated with a Lower risk of developing metabolic syndrome, a problem which exists in 25% of American adults. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves human endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially provides magnesium with physiologic and natural effects similar to adenosine-diphosphate inhibitors, such as clopidogrel. Data on magnesium supplementation in patients with acute myocardial infarction (AMI) are conflicting. ALthough a number of relatively small randomized cLinicaL trials have demonstrated a remarkable reduction in mortality when magnesium is administered to relativeLy high risk AMI patients, two recently published large-scale randomized cLinical trials (the Fourth International Study of Infarct Survival and Magnesium in Coronaries) failed to show any superiority of intravenous magnesium over placebo. Furthermore, the theoretical potential benefits of magnesium supplementation as a cardioprotective agent in CAD patients, its relatively low cost, easy administration, and relatively insignificant adverse effects, gives magnesium a place in treating CAD patients, especially those at high-risk and in life-threatening ventricular arrhythmias, such as Torsades de Points and intractable ventricular tachycardia.