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Magnesium and the Heart

Majid Ali, M.D.

A large body of data showing a relationship between low dietary intake of magnesium and the incidence of cardiac arrhythmias, sudden death, atherogenesis, ischemic coronary artery disease, hypertension, and stroke has been reviewed.106-108 Furthermore, low serum magnesium levels have been associated with coronary vasospasm, hypertension, and sudden death. In experimental studies, magnesium plays several regulatory roles in lipid metabolism, lipid uptake by macrophages, and intimal and smooth muscle responses to oxidative stress (oxidative coagulopathy) on blood elements.

There is an inverse relationship between serum and free erythrocyte magnesium and blood pressure. A similar relationship was observed in some, but not all, studies.107 Increased urinary catecholamines are often associated with increased urinary magnesium clearance, providing yet additional insight into the cardioprotective roles of magnesium.

Low magnesium content of drinking water has been epidemiologically recognized as a cardiovascular risk factor.108 On the other hand, magnesium supplementation was associated with lower incidence of hypomagnesemia, hypokalemia, and cardiovascular risk factors.109 Magnesium supplementation has also been thought to be associated with reduced myocardial oxygen demand. In other studies, the regulatory role of magnesium on myocardial membrane potential and the duration of such potential has been proposed.109

In Sweden, water hardness reflecting content of magnesium, calcium and other minerals was inversely related to ischemic coronary artery disease and stroke in seven mid-region counties where a large regional east-west gradient in cardiovascular mortality was observed during the years 1969-1983.110 I may point out here that serum and lymphocyte magnesium levels do not show any correlation with myocardial or skeletal muscle magnesium levels as determined with biopsy during cardiac surgery.111

I include below some text from Integrative Cardiology, the fourth volume of this series, to provide a framework of reference for understanding the clinical observations concerning the use of magnesium in cardiac disorders.

Three types of cell membrane channels play critical roles in nodal excitation and conducting phenomena: (1) fast sodium channels; (2) slow calcium-sodium channels; and (3) potassium channels.

The speed of electron and ion transfer during the creation and conductance of action potentials (propagating energy waves) is astounding. Opening of the fast sodium channels for a few 10,000ths of a second results in massive influx of positively charged sodium ions with a quick spike-like onset of action potential (up to +20 mV), which creates an observable contraction of the ventricular myocyte. This is followed by a plateau-like action potential (from +20 to about -10 mV) at the cell membrane produced by much slower opening of the slow calcium-sodium channels. The plateau-like action potential lasts for a few tenths of a second. The cycle is completed when potassium channels open at the end of that period, permitting a rapid movement of positively charged potassium ions out of the cell, thus restoring the original 'resting' level of the electrical state.

The A-V node links the atrial myocytes to the ventricular musculature through right and left bundles of Purkinje cell. The action potentials of the ventricular cells are faster both in development and dissipation than those of the sinus node. This is due to the lower negativity (-55 to -60 mV) of the sinus node than of the ventricular fibers (due to the natural membrane leakiness of some of the nodal cells as described above). On the inside aspect of the cell membrane, the 'gates' of the fast sodium channel remain closed when the value is -60 mV or greater.

As indicated earlier, magnesium not only is involved in the synthesis of ion channel proteins (as components of the overall protein synthetic pathways), it also specifically influences the function of calcium channels and, through them, of sodium, potassium, and other channels.

When Is Magnesium Superior to Calcium Channel Blockers?

One of my clearest memories from medical school is of giving intravenous magnesium sulfate to women critically ill with eclampsia in 1961. In 2003, the New England Journal of Medicine112 published an article conclusively demonstrating the superiority of magnesium sulfate over the calcium channel blocker nimopidine. It is gratifying to note that 42 years later, magnesium still remains the most effective therapy for this devastating disorder.

About four percent of pregnancies are complicated by preeclampsia charcaterized by rapid onset hypertension, proteinuria, water retention, weight gain, and edema. In one-fourth of those cases, preeclapsia proceeds to life-threatening full blown eclampsia charcaterized by diffuse vascular spasticity, malignant hypertension, hepatic failure, generalized toxicity, and clonic convulsions followed by coma. Delivery of the baby or and termination of pregnancy leads to rapid resultion of eclampsia.113-120

Related Links

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k Enzymes: Oxygen's Workhorses

k Vitamins - Oxygen's Special Agents

k Minerals - An Overview

k Magnesium - the Miracle Mineral

k  Magnesium and the Heart

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