Magnesium in atherosclerotic cardiovascular disease and sudden death

Magnesium ions are important for maintaining the functional and structural integrity of the myocardium. Epidemiologic studies suggest that myocardial hypomagnecytia can predispose to sudden cardiac death and that hard water protective factor preventing heart attack could be magnesium. Recent studies show that infarcted portion of the myocardium has lowered magnesium content as compared to noninfarcted segment. Magnesium deficiency sensitises the myocardium to the toxic effect of various drugs, hypoxia etc. and magnesium administration is protective. The metabolic, biochemical and electrophysiologic effects of magnesium appear to be significant in treatment of myocardial ischaemia. Magnesium is a metal-coenzyme and activates adenosine-triphosphatase which may be inhibited by nonglucose fuels like lactate and free fatty acids. Magnesium deficiency may be responsible for the chronic electrical instability of the myocardium predisposing to sudden cardiac death. The acute precipitating stress dependent trigger which lie in the brain may also be related to magnesium. In addition to fast Na and Ca channels there could be a Mg-carrying transport system maintaining the electrical activity of the myocardium. There is sufficient evidence to suggest the use of magnesium salts against ischaemic heart disease and sudden cardiac death. Magnesium is cardioprotective and influences action potential duration, membrane potential and perhaps maintains the fast response. The therapeutic and prophylactic value of magnesium needs further assessment.