Is hypomagnesemia arrhythmogenic?

Abstract

Summary: An understanding of the role of magnesium in cardiac conduction is complicated by the multiplicity of intracellular events coordinated by the magnesium ion. Several reports have cited magnesium deficiency as the cause of a variety of ventricular and supraventricular arrhythmias. On further inspection, the circumstances of each report strongly suggest the coexistence of significant potassium depletion; isolated hypomagnesemia as a cause of arrhythmia is not reported. This discussion brings together new data from basic science with that of clinical research to refute the suggestion that isolated hypomagnesemia is arrhythmogenic. However, there is sufficient evidence to indicate that hypomagnesemia will significantly exacerbate the proarrhythmic effect of hypokalemia, particularly if occumng in the presence of digoxin toxicity. Potassium and magnesium depletion are commonly concomitant, and simultaneous repletion of both ions in the presence of hypokalemia-induced arrhythrma would be both logical and effective. The beneficial effects of intravenous magnesium in the acute control of ventricular tachyarrhythmia are concluded to occur as a result of a separate antiarrhythmic action, quite independent of underlying magnesium balance.

Hypomagnesemic down-regulation of L-type Ca2+ channel in cardiomyocyte as an arrhythmogenic substrate in rats

“…Controversy exists as to whether hypomagnesemia increases intracellular Ca 2+ content in the heart [2,6]. Some studies have reported that a long-term depletion of Mg produced an increase in the Ca 2+ content in the heart [21,22], whereas others have indicated that Mg depletion did not change Ca 2+ concentrations in cardiomyocytes [23,24].…”

“…However, a cause and effect relation was not clearly defined in humans and experiments. It is well documented both in clinical and experimental reports that Mg depletion can induce changes in the electrocardiogram (ECG) including prolonged QR intervals, widened QRS complex, and prolonged PR intervals [1,6]. These changes in ECG parameters in hypomagnesemia would be causally related to, in part, the loss of a naturally occurring Ca 2+ antagonist in serum in the condition.…”

“…The similarities in changes of ECG parameters between longterm depletion of Mg and hypermagnesemia at the initial phase have long let all electrocardiologist confused [6]. In this regard, our observation that the Ca V 1.2-L-type Ca 2+ channel was down-regulated by Mg depletion has led to the understanding of intracellular Mg as a long-term regulator of Ca 2+ signaling and excitability, which allowed us to identify hitherto unrecognized functions of Mg 2+ signals in the heart.…”

“…The various disease states are associated with hypomagnesemia, which include chronic alcoholism, primary aldosteronism, and hyperthyroidism [1]. Hypomagnesemia is also associated with a variety of arrhythmias, both in the atrium and the ventricle [6]. Several recent studies also demonstrated an association of low serum Mg level and increased risk of atrial fibrillation and sudden cardiac death [13,14].…”

“…In the heart, it is certainly recognized that hypomagnesemia is associated with a variety of arrhythmias in clinical and experimental studies [1,6]. Despite the well-known Ca 2+ antagonistic effect of acute application of Mg in various excitable cells [2][3][4]6], by contrast, it is unknown about whether Mg depletion results in tachyarrhythmias, bradyarrhythmias and other electrophysiologic effects or whether these electrophysiologic effects are related to loss of Ca 2+ antagonistic effect of endogenous Mg [1,6]. Conventional understanding of arrhythmogenecity in hypomagnesemia is based on the notion that Mg 2+ is a natural intrinsic blocker of the Ca 2+ channel [2][3][4].…”