Magnesium deficiency detected by intravenous loading test in variant angina pectoris

doi:10.1016/0002-9149(90)91375-G

The American Journal of Cardiology

Volume 65, Issue 11, 15 March 1990, Pages 709-712

https://doi.org/10.1016/0002-9149(90)91375-G Get rights and content

Abstract

To study whether magnesium (Mg) deficiency is present in patients with variant angina, 24-hour Mg retention of low dose Mg (0.2 mEq/kg lean body weight) administered intravenously over 4 hours in 20 patients with variant angina was examined. No patient had received calcium antagonists before or during the study. All had attacks of chest pain associated with ST elevation on electrocardiograms. Twenty-one subjects without ischemic heart disease were studied as control subjects. Ten patients with variant angina were restudied 10 to 529 days (mean 235 ± 30) after the treatment with calcium antagonists (diltiazem 120 to 240 or nifedipine 40 to 80 mg/day), which resulted in complete suppression of anginal attacks. The mean serum Mg concentrations in the patients with variant angina and the control subjects were 2.1 ± 0.05 and 2.1 ± 0.03 mg/dl, respectively (difference not significant). However, 24-hour Mg retention in the patients with variant angina was 60 ± 5%, while that in the control subjects was 36 ± 3% (p < 0.001), suggesting that Mg deficiency is present in at least some patients with variant angina. The mean serum Mg concentrations before and after calcium antagonist treatment in 10 patients with variant angina were 2.1 ± 0.09 and 2.1 ± 0.07 mg/dl, respectively (difference not significant). However, 24-hour Mg retention decreased significantly (p < 0.01) from 60 ± 6 to 34 ± 7% after the treatment. There is Mg deficiency in many patients with variant angina and it is corrected after treatment with calcium antagonists.

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Citation Excerpt :
The magnesium tolerance test is another way to accurately assess magnesium status. With this test, the percentage of magnesium retained after parenteral administration of magnesium is determined: it is increased in magnesium deficiency and is inversely correlated with the concentration of magnesium in bone.12 However, this test depends on normal renal function and is of minimal value in patients with renal magnesium loss (Table 3).
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Citation Excerpt :
These reports suggest a close association between Mg deficiency and the onset and/or outcome of multiple pathophysiological states, including ischemic heart disease and the metabolic syndrome. A decrease in the Mg content of cardiac myocytes has been observed in angina pectoris (Goto et al., 1990), myocardial infarction (Shi et al., 1995), and sudden cardiac death (Eisenberg, 1992). Conversely, it has been reported that high Mg content has a protective effect on the myocardium in ischemic heart disease (Woods et al., 1992; Chakraborti et al., 2002) and during cardiac surgery (Shakerinia et al., 1996).
Magnesium (Mg) deficiency has been reported to be associated with the development of the metabolic syndrome, cardiovascular diseases, and sudden death. We examined the influence of chronic Mg deficiency on cardiac tolerance to hypoxia/reoxygenation injury.
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In Mg-deficient mice, the Mg concentration in whole blood was markedly decreased; however, that in the heart remained unchanged. When the hearts of control mice were exposed to hypoxia/reoxygenation, removal of extracellular Mg from a normal Krebs solution containing 1.2 mM Mg resulted in a significant decrease in the recovery of the tension-rate product (TRP) upon reoxygenation. In Mg-deficient mice, the recovery of TRP in the heart was reduced significantly in the absence of extracellular Mg compared to that in controls. The addition of Mg to the perfusate did not improve TRP recovery. During hypoxia/reoxygenation, cardiac damage evaluated by myocardial aspartate amino trasferase (AST) release was greater in hearts of Mg-deficient mice than in that of control mice.
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Metals
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^☆: This study was supported in part by a grantin-aid for scientific research (B62480218) from the Ministry of Education and a research grant (61C-4) from the Ministry of Health and Welfare, Japan.

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Magnesium deficiency detected by intravenous loading test in variant angina pectoris☆

Abstract

Am Heart J

Am J Cardiol

Am J Cardiol

Am J Cardiol

JACC

Am Heart J

JACC

Am J Clin Nutr

Metabolism

Coronary arterial spasm in Prinzmetal's angina. Documentation by coronary arteriography

N Engl J Med

Coronary arterial spasm in ischemic heart disease and its pathogenesis: a review

Circ Res

Arteriographic evidence of coronary arterial spasm in acute myocardial infarction

Circulation

Coronary vasospasm as a possible cause of myocardial infarction. A conclusion derived from the study of “preinfarction” angina

N Engl J Med

Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nerve system in the pathogenesis of coronary artery spasm

Circulation

AHA Committee Report

Circulation