Key result
Acute myocardial infarction was associated with a significant decrease in erythrocyte magnesium concentration on day 1 compared to controls (4.86 vs 5.26 mg/dl, P<0.05), which gradually normalized by day 28.
Why the study?
Does intracellular magnesium deficiency correlate with the severity of acute myocardial infarction in patients with transmural acute myocardial infarction?
Observational (n=69)
No
Does intracellular magnesium deficiency correlate with the severity of acute myocardial infarction in patients with transmural acute myocardial infarction?
Absolute Event Rate: 4.86% vs 5.26%
p-value: p=<0.05
Intracellular magnesium deficiency occurs during the acute phase of myocardial infarction and correlates with infarct size and the occurrence of serious arrhythmias.
Observational data in 49 AMI patients; leaves open whether intracellular magnesium deficiency contributes to pathogenesis or severity.
It has been hypothesized that intracellular magnesium deficiency is a pathogenetic factor in acute myocardial infarction. This study examined the time course of changes in the erythrocyte magnesium concentration and the correlation between the erythrocyte magnesium concentration and the severity of acute myocardial infarction in 49 consecutive patients with transmural acute myocardial infarction. The data were compared with results from 20 control patients without ischemic heart disease. The erythrocyte magnesium concentration (mg/dl) decreased significantly during the acute phase of the infarction (4.86 +/- 0.09 on day 1, 4.89 +/- 0.10 on day 2 and 4.86 +/- 0.10 on day 3 versus 5.26 +/- 0.19 for controls, all P < 0.05) and then normalized gradually to 5.25 +/- 0.10 on day 28. The serum magnesium concentration (mg/dl) also decreased significantly during the acute phase of the infarction (1.93 +/- 0.04 on day 1 and 2.11 +/- 0.03 on day 2 versus 2.26 +/- 0.08 for controls, all P < 0.05), before recovering to 2.28 +/- 0.06 on day 28. There were significant correlations between the erythrocyte magnesium concentration on day 1 and maximal values of serum cardiac enzymes (r = -0.30 for creatine kinase, r = -0.34 for glutamic oxaloacetic transaminase and r = -0.57 for lactate dehydrogenase, all P < 0.05). Moreover, the erythrocyte magnesium concentration was significantly lower in patients with (4.32 +/- 0.08 mg/dl, n = 13) than in those without (5.06 +/- 0.09 mg/dl, n = 36, P < 0.0001) serious arrhythmias. These data indicate that intracellular magnesium deficiency is involved in the acute phase of myocardial infarction.
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Tsutsui et al. (1993) conducted an observational in Acute Myocardial Infarction (n=69). Acute myocardial infarction vs. Patients without ischemic heart disease was evaluated on Erythrocyte magnesium concentration on day 1 (mg/dl) (p=<0.05). Acute myocardial infarction was associated with a significant decrease in erythrocyte magnesium concentration on day 1 compared to controls (4.86 vs 5.26 mg/dl, P<0.05), which gradually normalized by day 28.
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