Magnesium in coronary artery disease is reviewed with regard to its role in the pathogenesis of arteriosclerosis, coronary spasm, myocardial function, acute myocardial infarction and ventricular arrhythmias. Experimentally, magnesium depletion potentiates and supplementation retards the effect of atherogenic diets. Evidence from human studies is circumstantial. Reactivity of arterial smooth muscle is enhanced by low and suppressed by high magnesium media. Evidence that magnesium depletion may initiate coronary spasm is provided by dog and retrospective human studies. Although experimental magnesium deficiency disrupts myocardial mitochondria, there are no studies which show that magnesium deficiency will lead to cardiac failure or that replacement will improve cardiac function. It is known that an infarcted or ischaemic myocardium loses magnesium and this may be the basis for ventricular arrhythmias. Coronary occlusion in a previously magnesium-depleted heart will result in a larger area of necrosis and ischaemia. The fall in serum magnesium in acute myocardial infarction is probably due to the formation of soap in fat cells undergoing catecholamine lipolysis. Ventricular fibrillation in coronary artery disease will respond to parenteral magnesium, even in the presence of normal serum concentrations.