Magnesium for the Treatment and Prevention of Atrial Tachyarrhythmias

Alexandria A. Piotrowski, PharmD; James S. Kalus, PharmD


Pharmacotherapy. 2004;24(7) 

In This Article

Abstract and Introduction


Atrial tachyarrhythmias, including atrial fibrillation and flutter, occur frequently. Magnesium has been studied in the early conversion and prevention of atrial tachyarrhythmias, as well as in prevention of atrial tachyarrhythmias after coronary artery bypass graft surgery. Early conversion of atrial tachyarrhythmias and control of heart rate may be greater with magnesium than with common antiarrhythmic agents. Magnesium appears to be less useful for preventing recurrent atrial tachyarrhythmias; however, discrepancies in study methodologies make interpretation of results difficult. The use of magnesium for prevention of postoperative atrial arrhythmias has produced conflicting results, likely due to differences in study design. From the limited data available, magnesium appears to have some inherent antiarrhythmic properties. Certain patient populations may derive benefit from magnesium for the treatment of atrial tachyarrhythmias. However, further study is necessary to define the role of magnesium clearly for the treatment or prevention of atrial tachyarrhythmias.


Atrial fibrillation and flutter are the most prevalent atrial tachyarrhythmias, afflicting nearly 2 million people in the United States and accounting for 400,000 hospitalizations annually.[1] Atrial fibrillation and flutter occur most commonly in men and are especially prevalent among those aged 65-80 years.[1] Approximately one third and one half of patients with atrial fibrillation and flutter have heart failure or hypertension, respectively.[1]

One proposed mechanism for atrial fibrillation and flutter is that multiple reentrant circuits develop within the atria, causing rapid depolarization of the surrounding atrial tissue.[2] Formation of the substrate for reentry possibly is related to atrial stretch, which occurs in patients with such disease states as heart failure or hypertension. An increased concentration of the neurohormone angiotensin II is associated with both hypertension and heart failure. This increase in angiotensin II is known to increase the L-type calcium current and the transient outward potassium current in the myocardium.[3] These electrolyte current alterations may explain angiotensin II-induced atrial fibrosis in canine models of heart failure.[4] The development of atrial fibrosis could provide a substrate for the initiation of atrial fibrillation and flutter and facilitate the perpetuation of the arrhythmia as well.

Magnesium regulates cellular enzymatic and metabolic processes throughout the body. In myocardial cells, magnesium antagonizes calcium[5] and potassium channels.[6] In addition, electrophysiologic studies have demonstrated slowed cardiac conduction and increased cardiac refractoriness with administration of magnesium.[7,8] These actions suggest that magnesium may inhibit substrate formation and the development of reentrant circuits within the atria that are responsible for the development and propagation of atrial tachyarrhythmias, such as atrial fibrillation and flutter.

Magnesium has an accepted role in the management of ventricular arrhythmias, including torsade de pointes[9]; however, the role of magnesium in the treatment and prevention of atrial tachyarrhythmias is less well defined.