The retrospective dietary study and hospital admission and follow-up laboratory and clinical investigation of 505 patients with suspected acute myocardial infarction (AMI), as reported in this issue by Singh et al , provides insight into epidemiologic observations that have suggested different explanations of geographic and ethnic differences in incidence of coronary arterial disease (CAD). Their findings support the established implication of high intake of cholesterol and total fat by those developing AMI and other CAD, and also support the premise that low magnesium (Mg) levels increase the risk of arrhythmias. Although Mg intakes of the cardiac patients were only moderately lower than that of noncardiac patients, the serum Mg levels that were marginally low in almost all of the patients were lowest in patients with rhythm disturbances.
Their observations also suggest that the etiology is multifactorial, implicating not only excess fat and low Mg, but also low potassium (K), fiber, and antioxidant intakes. Group A (335 patients) had enzymatic and electrocardiographic proof of AMI; Group B (64 patients), the patients with convincing chest pain but lower enzyme levels, and those with unstable angina (Group C: 42 patients), had had significantly greater fat, cholesterol, and carbohydrate intakes, and somewhat lesser Mg, K, and fiber intakes than did those (Group D: 42 patients) who had no characteristics of CAD. Notable is the higher pre-study intake of fiber from fruit and vegetables in the group free of CAD than in the cardiac patients. In a study recently published elsewhere , Singh et al reported cardiac improvement in post-AMI patients consuming fruits, legumes and other vegetables and nuts (foods rich in antioxidants, as well as in Mg and fiber).
In the paper published in this issue, Singh et al make brief reference to the relationship of increased catecholamine levels, found in AMI patients, and accept the premise that the reduction of serum Mg they observed in their arrhythmic patients might have been caused by a shift of circulating Mg to ischemic cells, caused by their increased metabolic requirements for Mg.
However, the high myocardial oxygen consumption—which has been attributed to catecholamine-induced lipolysis with increased free fatty acid (FFA) levels, through an energy wasting triglyceride—fatty acid cycle-has been blamed for the prevalence of post-infarction arrhythmias and sudden cardiac death [3,4]; this has been correlated with FFA binding of Mg . Furthermore, the risk of catecholamine-induced arrhythmias is greater when the Mg status is suboptimal. Mg deficiency increases secretion of catecholamines [6-9]. Additionally, the initial change in intracellular myocardial Mg after AMI and/or increased catecholamine secretion is likely to be decreased, rather than increased. Administration to rats of a single dose of catecholamine just sufficient to cause multifocal micronecrosis in the heart, rather than the large areas of necrosis that are produced by high dosage (a model of massive AMI) resulted in loss of myocardial Mg an hour after the injection—the earliest electrolyte derangement—which was followed by decreased K and increased calcium and sodium in the myocardial cells [10, 11]. On the other hand, elevation of myocardial Mg might result from mitochondrial damage caused by ischemia , with Mg present as non-functional crystalline deposits, in which the Mg is bound to inorganic phosphates , rather than from increased metabolic activity.
It is uncertain whether there is necessarily correlation of myocardial Mg levels with blood cell levels, which are influenced by genetic factors that also impact on vulnerability to cardiovascular disease. For example, type A subjects, who have lower erythrocyte Mg levels than do type B subjects, exhibit increased catecholamine secretion in response to stress, as well as greater prevalence of heart disease [14,15].
Freedman et al have shown that vitamin E protects against Mg deficiency cardiomyopathy (CMP)  and that catecholamine-induced CMP is intensified by Mg deficiency, which they propose is caused by reduction in the threshold antioxidant capacity, that is caused by Mg deficiency . Mg supplements, especially when vitamin E supplements were also given, were protective against catecholamine cardiotoxicity . The protection afforded by vitamin E against damage to the heart caused by catecholamines might be explained by the demonstration by Singal et al  that catecholamine auto-oxidation generates highly toxic free radicals that participate in the CMP process. In a study designed to test the hypothesis that a free radical-mediated mechanism is involved in both catecholamine- and Mg deficiency-induced cardiac damage, the research groups of Weglicki and Bloom  concluded that since Probucol, a drug with both antilipidemic and antioxidant effects, was effective against both types of cardiac damage, each of which entails free radical damage, it was the antioxidant activity that was protective.
The observation by Singh et al that the cardioprotective diets they studied were rich in antioxidants , and that the patients with acute manifestations of cardiac disease had consumed diets low in these substances, as well as in Mg , provides important supportive clinical evidence.
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15. Henrotte JG: Recent advances on genetic factors regulating blood and tissue magnesium concentrations; relationship with stress and immunity. In Durlach J, Itokawa Y (eds): "Magnesium in Health and Disease." London: Libbey, pp 285-289, 1989.
16. Freedman AM, Atrakshi AH, Cassidy MM, Weglicki WB: Magnesium deficiency-induced cardiomyopathy; protection by vitamin E. Biochem Biophys Res Commun 170:1102-1106, 1990.
17. Freedman AM, Cassidy MM, Weglicki WB: Magnesium-deficient myocardium demonstrates an increased susceptibility to an in vivo oxidative stress. Magnesium Res 4:185-189, 1991.
18. Singal PK, Kapur N, Dhillon KS, Beamish RE, Dhall NS: Role of free radicals in catecholamine-induced cardiomyopathy. Can J Physiol Pharmacol 60:1390-1397, 1982.
19. Atrakchi AH, Bloom S, Dickens BF, Mak IT, Weglicki WB: Hypomagnesemia and isoproterenol cardiomyopathies: protection by probucol. Cardiovasc Pathol 1:155-160, 1992.
Mildred S. Seelig, MD, MPH, Master ACN
Received November 1993.
Journal of the American College of Nutrition, Vol. 13, No.2, 116-117 (1994) Published by the American College of Nutrition
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