Studies of magnesium in heart transplantation: further insights into magnesium and cardiac physiology.

Magnesium deficit in man is very difficult to detect and even more difficult to study. However, a chance observation led to the investigation of cardiac transplant recipients as an in vivo model of drug-induced magnesium depletion. Clinical circumstances were such that the question of the correlation of serum and tissue magnesium levels might be addressed. Using the same model, investigation of myocardial calcium levels was undertaken. Significant myocardial magnesium depletion accompanied persistent hypomagnesaemia in over 50 per cent of cardiac transplant recipients. Repletion of myocardial magnesium occurred some weeks later than normalization of serum levels; these time lags may explain the lack of correlation of serum and tissue magnesium levels in these circumstances. Myocardial calcium levels were generally higher than expected from control studies, and were particularly high in magnesium-depleted subjects. These findings are keeping with those predicted from animal studies. Electrophysiological studies in the transplanted denervated heart are free of many of the confounding features of such studies in the native heart. Preliminary work involving pacing protocols designed to induce abnormalities of phase 4 of the action potential suggests that myocardial magnesium deficit does not produce a clinical arrhythmogenic substrate in the denervated heart. However, shortening of the effective ventricular refractory period in hypomagnesaemic patients was observed, and it was noted that concurrent hypokalaemia in this circumstance would be particularly disadvantageous. The data collected in the course of these studies is discussed, and mechanisms for the observed benefit of magnesium as a possible anti-ischaemic agent in the period following acute myocardial infarction are proposed.