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A Review of the Literature

Michael Shechter, MD; Elieser Kaplinsky, MD; Babeth Rabinowitz, MD

Arch Intern Med. 1992;152(11):2189-2196.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

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 deficient^3,4 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 . . . [Full Text PDF of this Article]

Author Affiliations
From the Heart Institute, Sheba Medical Center, Tel-Hashomer, Israel.

Footnotes
Accepted for publication March 20 1992.

Reprint requests to Heart Institute, Sheba Medical Center, 52621 Tel-Hashomer, Israel (Dr Shechter).

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