Ionized magnesium decreases significantly in a subset of patients following acute myocardial infarction, likely due to binding by stress-induced elevated free fatty acids, suggesting targeted rather than universal magnesium infusion therapy.
The most feared early complications after an acute myocardial infarction are ventricular arrhythmias. These may be initiated by changed concentrations of catecholamines and electrolytes. The present study shows a reduction of total serum magnesium after acute myocardial infarction which is normalized within a few days. Further, it could be shown that a more significant decrease of ionized Mg2+ (iMg2+) takes place at the day of acute myocardial infarction in the total group of myocardial infarction patients (n = 36). A closer investigation reveals that iMg2+ was considerably decreased in one third of the patients, whereas two thirds showed minor changes of iMg2+ in both directions. The pronounced decrease of iMg2+ in the first sub-group can be explained by the time course of free fatty acids in serum. On the day of the myocardial infarction free fatty acids in serum were increased. This is probably caused by beta-adrenergic-induced lipolysis due to catecholamines released by the stressful situation of an acute myocardial infarction. The increased free fatty acids in serum bind Mg2+, thus reducing iMg2+. As long as a beneficial effect of a general Mg infusion in all acute myocardial infarction patients is controversial, iMg2+ should be measured and Mg infusion therapy should be applied only in patients with low iMg2+.
Bertschat et al. (Sun,) studied this question.