Abstract

We examined whether or not the degree of intracellular magnesium (Mg) deficiency correlates with disease activity of variant angina (VA) and the effect of oral Mg supplementation. Eighteen patients with VA (17 men and a woman) were divided into 2 groups according to the frequency of occurrence of angina attacks (inactive and active group > 3 angina attacks per week). We measured Mg status by serum, urinary excretion, 24-hour Mg retention rate. Intracellular Mg content of mononuclear cell (MNC) and erythrocyte were also measured by atomic absorption spectrophotometry We also examined the effect of oral Mg supplementation (Mg oxide 0.6 g/day , more than 2 months) to refractory patients (n = 4) with Mg deficiency. There were no significant differences in serum Mg content between active and inactive groups. Urinary Mg excretion in a day in active group (136.4 ± 36.6 mg/dat) was significantly higher than in inactive group (59.1 ± 7.0; P < 0.05). Retention rate and intracellular Mg content of MNC and erythrocyte were 57.0 ± 7.3 vs 24.7 ± 3.2% (p < 0.01), 151.3 ± 14.4 vs 214.3 ± 8.0 fg/cell (p < 0.01) and 3.8 ± 0.5 vs 5.1 ± 0.4 fg/cell (p < 0.05). respectively. Retention rate and intracellular Mg content of MNC and erythrocyte correlated well with the frequency of angina attacks in these patients (r = 0.78, p < 0.01: r = 0.76, P < 0.01: r = -0.50, p < 0.05). With oral Mg supplementation, the response to calcium antagonist was improved, coupled with the increase of intracellular Mg content, from 151 ± 19.8 to 226.8 ± 17.0 fglcell in MNC and from 3.0 ± 0.6 to 5.0 ± 0.3 fg/cell in erythrocyte. It is concluded that the degree of intracellular Mg deficiency correlates well with disease activity of VA, suggesting that Mg deficiency plays an important role in accelerating disease activity. Oral Mg supplementation appears to be an effective and less expensive regimen for patients with VA.

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