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Serum Magnesium and Potassium in Acute Myocardial Infarction: Relationship to Existing β-Blockade and Infarct Size

Knud Landmark, M.D., Ph.D.

Department of Internal Medicine, Ullevål University Hospital, Oslo Norway

Petter Urdal, M.D., Ph.D.

Department of Clinical Chemistry, Ullevål University Hospital, Oslo Norway

Knud Landmark, M.D., Ph. D.

Department of Internal Medicine Ullevål University Hospital N-0407 Oslo 4, Norway

Patients (n = 314) with acute myocardial infarction (AMI) were divided into three groups according to the time elapsed from onset of chest pain to when the first sample for determination of magnesium (s-Mg1) and potassium (s-K1) was drawn (A: hours 0-6; B: hours 6-10, and C: hours 10-24). Potassium and Mg were also measured in a second sample drawn three to twelve days (mean 6.3 days) later (s-Mg2, s-K2). Whereas s-Mg1 was lower than s-Mg2 in all three groups, s-K1 was reduced only in group A. Ten patients in group A receiving nonselective β-blockers had an attenuated drop in s-Mg1, whereas the drop in s-K1 was completely inhibited. The differences between s-Mg2 and s-Mg1 ({Delta} s-Mg) in all groups, and between s-K2 and s-K1 ({Delta} s-K) in group A, increased with increasing mean peak creatine kinase (CKmax) levels to approximately 1300-1800 U/L.

In conclusion, these observations suggest that the initial drop in s-Mg and s-K in the early phase of AMI is due to increased stimulation of β2-adrenergic receptors; these changes can be prevented partly or completely by the use of nonselective β-blockers.

Angiology, Vol. 44, No. 5, 347-352 (1993)
DOI: 10.1177/000331979304400502
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