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EDITORIALS

Magnesium in Acute Myocardial Infarction (International Study of Infarct Survival 4)

Mildred S. Seelig, MD

The fourth International Study of Infarct Survival (ISIS-4), examining the effects of an angiotensin converting enzyme-inhibitor and a controlled-release oral mononitrate, includes intravenous magnesium as the sulfate administered as a 24-hour infusion alone or in combination with either or both drugs.1 The protocol calls for planned randomized studies of 40.000 patients with acute myocardial infarction in 400 clinical centers. Since efficacy of antiplatelet use of aspirin and fibrinolytic agents has been demonstrated,. use of 1 or both before entry in ISIS-4 is not precluded.

The evaluation of magnesium infusion in a multicenter study of treatment of acute myocardial infarction is welcome news to the investigators who conducted the controlled trials in the last decade2-13 that provided direct justification for such a wide scale study. The new intervention study is also good news to those who have reported the efficacy of magnesium in the management of cardiac arrhythmias in clinical trials that were not double-blinded. but sometimes correlated with the correction of magnesium deficiency.14-24 Among arrhythmias responsive to prophylactic as well as therapeutic administration of magnesium are those found in patients with hypertension and congestive heart failure who are receiving magnesium-wasting medication. and a variety of arrhythmias with and without hypomagnesemia.

Intravenous bolus injections or infusions of magnesium sulfate (over a 24-hour period) to control arrhythmias use the pharmacologic activity of magnesium that results from elevation of circulating (extracellular) magnesium levels for the duration of the infusion and for a relatively short time thereafter. It is noteworthy that in the most recent of the double-blind trials with intravenous magnesium infusions it has been customary to provide magnesium infusions for 36 hours to 5 days.3-7,9-12 The incidence of acute arrhythmias and mortality has been reduced by as much as 50% with such therapy.2,5,9,13

The gratifying results achieved by these controlled clinical trials of infusions of magnesium can be attributed to not only their direct increase of the threshold for electrical excitation of myocardial cells and their reduction of vascular resistance with the increase of cardiac output (mentioned by the ISIS protocol), but also their reduction of the release of catecholamines that is caused by stress (like that induced by infarction), which in turn leads to excess release of free fatty acids that can inactivate circulating magnesium.25,26 Magnesium's correction of hypokalemia.14-18,22,27 and its calcium-blocking28,29 and antivasospastic effects17 can all contribute to magnesium's immediate cardioprotection. Furthermore. it is possible that the antithrombotic effect of magnesium22,27,29,30 may militate against reinfarction and that the coronary vasodilatation of hypermagnesemia induced over the short-term may help limit the size of the infarction. Experimental magnesium deficiency of dogs subjected to coronary occlusion increased the size of the necrotic area: repair of the deficiency limited the size of the dogs' myocardial infarcts.30

Long-term follow-up (1 year) of patients receiving intravenous magnesium showed that the improved prognosis seemed due only to decreased arrhythmias during the acute postinfarction phase.8 Partial repair of underlying cellular deficits of this essential cation is probably achieved by a short-term pharmacologic approach. but the low renal threshold for magnesium causes elimination of most of the infused dose. Since magnesium is predominantly an intracellular cation that protects against damage to membranes such as that caused by ischemia,15,26,27 long-term (oral) magnesium supplementation may well enhance protection against later reinfarctions and arrhythmias. It is hoped that the findings of ISIS-4, relevant to magnesium, will bring renewed attention to the epidemiologic and experimental evidence that magnesium deficiency or loss contributes to structural arterial and myocardial lesions that increase vulnerability to ischemic heart disease. arrhythmias and sudden (unexpected) cardiac death.26,27,29

REFERENCES

1. Sleight P. Chairman Steering Comm. ISIS-4 Protocol.....Radcliffe Infirmary. Oxford.

2-30. Remaining references are missing


Am J Cardiology 68:1221-1222 (1991)

From New York Medical College. Valhalla. New York. Manuscript received May 30, 1991; revised manuscript received June 13. 1991. and accepted June 14.

Address for reprints: Mildred S. Seelig, MD. American College of Nutrition. 722 Robert E. Lee Drive. Wilmington. North Carolina 28412. DECEASED


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