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Magnesium Deficiency in Patients With Ischemic Heart Disease With and Without Acute Myocardial Infarction Uncovered by an Intravenous Loading Test
Henrik Sandvad Rasmussen, MD;
Peter McNair, PhD;
Lasse Gøransson, MD;
Steen Balsløv, MD;
Ole Graff Larsen;
Peter Aurup, MD
Arch Intern Med. 1988;148(2):329-332.
Abstract
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• An Intravenous magnesium-loading test with 30 mmol/L of magnesium was used to evaluate the magnesium status in 38 patients with ischemic heart disease (IHD) admitted to the coronary care unit with suspected acute myocardial infarction (AMI), in ten healthy volunteers (control group), and in nine patients with chronic IHD in a stable phase of their disease (chronic IHD group). Sixteen of the patients admitted with acute disease proved to have AMI (AMI group) and 22 did not (non-AMI group). Patients with IHD both with and without AMI retained significantly more magnesium (9.3 and 10.7 mmol/L [22.6 and 26 mg/dL], respectively) than did the control group (1.4 mmol/L [3.4 mg/dL]). This 34% magnesium retention points to a state of magnesium deficiency in patients with IHD. However, since the patients with and without AMI did not differ, the observations do not indicate that AMI is associated with a more severe magnesium deficiency than that found in other IHD patients without AMI. When the patients with IHD were subgrouped according to long-term diuretic treatment, the patients (n=19) receiving long-term diuretic treatment had a 39% retention of magnesium (11.6 mmol/L [28.2 mg/dL]) compared with a 29% retention (8.7 mmol/L [21.1 mg/dL]) observed in 19 patients who were not receiving long-term diuretic treatment. This observation was not influenced by the presence or absence of AMI. An even higher level of magnesium retention (17.1 mmol/L [41.6 mg/dL] equals 57% retention) was found when investigating patients with chronic ischemic heart disease in a stable phase of their disease. This indicates that patients with IHD may be severely magnesium deficient; that long-term diuretic treatment contributes to this deficiency, but that diuretic treatment per se Is not the only cause of this condition.
(Arch Intern Med 1988;148:329-332)
Author Affiliations
From the Departments of Internal Medicine, Divisions of Cardiology and Gastroenterology, and Department of Clinical Chemistry, Hvidovre (Denmark) Hospital, and the Medical Department, Bispebjerg Hospital, Copenhagen.
Footnotes
Accepted for publication Aug 31, 1987.
Reprint requests to Department of Clinical Chemistry, 339 Hvidovre Hospital, DK-2650 Hvidovre, Denmark (Dr Rasmussen).
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