Magnesium is the second most abundant intracellular cation in the human body, next to potassium, and is involved in more than 300 different enzymatic reactions, including glucose use; the synthesis of fat, protein, and nucleic acids; the metabolism of adenosine triphosphate; muscle contraction; and some membrane transport systems.1,2
Over recent years, evidence has accumulated that patients with acute myocardial infarction (AMI) are magnesium deficient3,4 and develop an increased hypomagnesemia during the acute phase of the infarct.5-8 Hypomagnesemia might be due to migration from extracellular to intracellular space,9 which is caused by catecholamine-induced lipolysis forming in soluble magnesium soaps, as demonstrated in animal experiments.6,10,11 Furthermore, experiments in animals and humans have shown that the acute as well as the chronic reduction in extracellular magnesium levels are harmful to the myocardium in the setting of acute ischemia.12-14 While the metabolism of magnesium in AMI and the incidence
Shechter M, Kaplinsky E, Rabinowitz B. The Rationale of Magnesium Supplementation in Acute Myocardial Infarction: A Review of the Literature. Arch Intern Med. 1992;152(11):2189–2196. doi:10.1001/archinte.1992.00400230015003
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