Magnesium and the Heart

by Herbert C. Mansmann, Jr. M.D.

It has been known since the 1950s that alcohol is magnesuretic, causes loss of magnesium in the urine and it was suggested that alcoholics needed 7-10 mg/kg/day of Mg, rather than the recommended 6 mg/kg/day. It has since been demonstrated that they need more also because of a decreased oral Mg dietary intake. (Seelig, 1980).

Cardiac arrhythmia was discussed in one of the earliest books on Mg. (Wacker WC, 1980). On page 96, he mentions a patient with atrial and ventricular premature contractions and supraventricular tachycardia successfully treated with IV Mg sulfate in 1973.

Iseri reported in 1984, that magnesium was Natures calcium channel blocker. In 1990 he reported that; “Magnesium treatment is a viable therapeutic option when other antiarrhythmic agents fail to suppress ventricular tachycardia, ventricular fibrillation, multifocal atrial tachycardia, atrial fibrillation and supraventricular tachycardia (Iseri, 1990).

We have been interested in Torsades de pointes and have comprehensively reported on the effect of Mg treatment on the prolonged QT interval and Torsades, (Mansmann 1994) after antihistamine treatments. Of note is the fact that, IV MgSO4 stops the Torsades very rapidly, but the QT interval prolongation requires 3-7 days to revert to normal, suggesting the need for time to correct the intracellular components.

There has been an article by my son on the Magnesium Research Laboratory web site. That is now about 3-4 years old and since them we have had a lot of experience with MgD induced cardiac arrhythmias. Patients are usually symptomatic at serum levels of 1.2 mg/dl or less.

SYMPTOMS – Symptoms caused by cardiac arrhythmias can mimic those due to other medical disorders. Common symptoms associated with the arrhythmia itself include palpitations, dizziness, lightheadedness, syncope, chest discomfort, neck discomfort, dyspnea, weakness, and anxiety. Secondary consequences of arrhythmias, often due to underlying heart disease, are an additional source of symptoms (eg, congestive heart failure, ischemia, and thromboembolia.)

Cardiac arrhythmias can also have unusual symptomatic presentations such as tinnitus, visual changes, increased urinary frequency, abdominal discomfort, and peripheral edema. Arrhythmias may cause a change in sympathetic and vagal tone, hormonal changes, elevation of venous pressure, and reduced cardiac output, all of which can lead to an even longer list of other symptoms.

Symptom type and severity are related to the etiology and rate of the arrhythmia, to the nature and severity of underlying heart disease, and to the patient. The symptom severity often dictates the urgency for therapy or even the need to evaluate and treat. The presence of structural heart disease is also a key issue that frequently determines the urgency of intervention, evaluation, therapy, and the prognostic importance of the arrhythmia.

The value of obtaining an unhurried, careful, complete history cannot be overemphasized as it may help diagnose the type of arrhythmia and concomitant disease without the need to perform expensive or potentially risky tests.

In 2002, this subject has been expressed in another important way. “Dysrhythmia is the most common cardiovascular manifestation of hypomagnesemia. A number of studies demonstrate an increased incidence of supraventricular dysrhythmias (atrial fibrillation, [atrial flutter] multifocal atrial tachycardia, paroxysmal supraventricular tachycardia) and ventricular dysrhythmias (PVCs, ventricular tachycardia, torsades de pointes, ventricular fibrillation in patients who have MgD”. (Marz, 2002) To this list I have added atrial flutter. All of this is very important for every one with known MgD to appreciate, which reenforces the need to always remain in positive Mg balance, once the diagnosis of MgD has been established. Because its recurrence is an important serious risk factor, which can be rapidly corrected with high dose of the Mg salt called, Mg gluconate, (Magonate, Fleming & Co.) since the Mg from this salt of Mg is absorbed from the stomach, almost as effective as an intravenous injection. (2 to 4 g of 50% Mg sulfate [16.6 to 33.3 mEq] is a reasonable initial dose. This should be diluted in saline or dextrose and given over 30 to 60 minutes).

MY ATRIAL FLUTTER

I received electroconversion the first time, 15 years ago and “digital conversion” (rectal examination stimulation) the second time. Since then I have been able to convert in 1-3 hours with oral Mg. The dose I have personally used several times is 10 Magonate tablets (270 mg of el.Mg) every half hour for several doses, 2-4. I have been in the hospital two times with atrial flutter.

lone atrial fibrillation (LAF)

Over the past two years I am aware of about 25 persons successfully treated with Mg gluconate (Magonate, Fleming and Co) and Dr. Chambers is the first failure I have seen. Therefore, we are very interested in learning of others patients with atrial tachycardia, unresponsive to Mg, with or without LAF.

Ventricular Arrhythmias

Mg sulfate (100 mg/kg) before electrical cardioversion resulted in half of the group of 40 having diminished repolarization abnormalities and VA than in the control group. (Szyszka A 1997)

During treatment with Mg citrate (15 mmol) for 3 weeks, in a double blind controlled study in those with an acute myocardial infarction, there was statistically less VR, in spite of the fact that there was no change in sMg, RBCMg and 24hr urine. (Feyertag, J 1997)

References

1. Feyertag J, Laimer H, Herglotz P, Douglas T, Ekmekcioglu C, Bottcher E, Marktl W. Effect of low dose oral magnesium supplementation on different magnesium parameters and on ventricular arrhythmias. In Smetana R. Ed. Advances in Magnesium Research: 1. Magnesium in Cardiology.1997, John Libbey&Co., London:71-77.

2. Iseri LT, French JH. Magnesium: Nature’s physiologic calcium blocker. Am Heart J, 1984;108:188-199.

3. Iseri LT, Role of magnesium in cardiac tachyarrhythmias. Am J Cardiol 1990;65(23):47K-50K.

4. Mansmann, Jr., H.C.: Consider Magnesium Homeostasis. III. Cytochrome P-450 Enzymes and Drug Toxicity. Ped Asthma Allergy Immunol, 8:7-28;1994.

5. Marx: Rosen’s Emergency Medicine: Concepts and Clinical Practice, 5th ed., Copyright © 2002 Mosby, Inc

6. Seelig, SSm Magnesium Deficiency in the Pathogenesis of Disease: Early roots of cardiovascular, skeletal, and renal abnormalities. 1980 Plenum Publishing Corp. New york.

7. Stühlinger HG. Magnesium in Cardiovascular Disease. Journal of Clinical and Basic Cardiology 2002; 5 (1): 55-59.

8. Szyszka, A, et el Magnesium sulfate diminishes abnormalities of repolarization and ventricular arrhythmias after electrical cardioversion. In Smetana, R. Ed. Advances in Magnesium Research: 1. Magnesium in Cardiology. 1997, John Liddey&Co. London:83-85.

9. Wacker, WC. Magnesium and Man. 1980, Harvard Univ. Press, Cambridge Mass.

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