Effect of intravenous magnesium sulfate on supraventricular tachycardia

Wesley, Robert C.; Haines, David E.; Lerman, Bruce B.; DiMarco, John P.; Crampton, Richard S.

doi:10.1016/0002-9149(89)90092-1

Cited by 72 publications

(15 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In studies evaluating the effects of magnesium in supraventricular tachycardia, magnesium has mostly been given intravenously, resulting in a higher serum level of magnesium than in our study [7][8][9]10,11,[16][17][18]23] . In patients with normal renal function it seems to be difficult to achieve corresponding serum levels of magnesium with oral administration.…”

Section: Limitationsmentioning

confidence: 73%

“…In earlier reports examining the efficacy of magnesium for conversion of supraventricular tachycardia, magnesium had been given intravenously [10,11,23] . Since these studies were not placebo-controlled and were performed in patients with atrioventricular re-entry tachycardia [23] , or mixed supraventricular tachycardia [10,11] , it is still undecided as to whether magnesium had an effect on conversion in atrial fibrillation.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The effect of oral magnesium, alone or as an adjuvant to sotalol, after cardioversion in patients with persistent atrial fibrillation

Frick

Darpö²,

Östergren³

et al. 2000

European Heart Journal

View full text Add to dashboard Cite

show abstract

Section: Limitationsmentioning

confidence: 73%

Section: Discussionmentioning

confidence: 99%

The effect of oral magnesium, alone or as an adjuvant to sotalol, after cardioversion in patients with persistent atrial fibrillation

Frick

Darpö²,

Östergren³

et al. 2000

European Heart Journal

View full text Add to dashboard Cite

show abstract

“…Mg also has antiarrhythmic effects; it prolongs the PR interval and the sinuatrial conduction time, increases the AV nodal refractory period, and reduces automaticity [15]. Therefore, it is not surprising that magnesium is successful in the termination of supraventricular tachycardia [16], atrial fibrillation [17], intractable ventricular arrhythmia [18], multifocal atrial tachycardia [19] and torsades de pointes [20,21].…”

Section: Discussionmentioning

confidence: 99%

Magnesium Fortification of Drinking Water Suppresses Atherogenesis in Male LDL-Receptor-Deficient Mice

et al. 1999

View full text Add to dashboard Cite

Magnesium, an important cofactor of more than 300 enzymes, has previously been found to modulate blood lipid levels, atherogenesis and atherosclerosis in rabbits, when added to their diet. The aim of this study was to examine whether magnesium fortification of drinking water, without a change in diet content, can affect atherogenesis. The study included six groups of LDL-receptor-deficient mice. The mice received either distilled water or water containing 50 g of magnesium sulfate per liter. In the first (12 weeks) and second (6 weeks) stages of the experiment, the mice received low- and high-cholesterol diets, respectively. At the end of each stage, blood was drawn for the determination of plasma magnesium, calcium and lipid levels. In addition, the extent of atherosclerosis was determined at the aortic sinus. In both males and females, magnesium fortification was associated with higher levels of plasma magnesium (50 and 37% increase, respectively), without any differences in plasma calcium content. The extent of atherosclerosis at the aortic sinus in the male mice that received high levels of magnesium was a third of that of the male mice that received distilled water. However, these differences were not found in the female groups. Surprisingly, the female mice that received water fortified with magnesium had higher levels of cholesterol after stage 2, whereas no differences regarding plasma lipid levels were found among the male mice. These results confirm that magnesium fortification of drinking water is capable of inhibiting atherogenesis in male LDL-receptor-deficient mice. The mechanisms of action are yet to be discovered, and are probably not related to diminished lipid excretion, but possibly to the prevention of calcium influx into vascular smooth muscle cells, elevated antioxidative capacity, or other yet undetermined mechanisms.

show abstract

“…A consistent adverse and sometimes severe effect ofa Mg2+-bolus injection is a typical feeling of flush and heat and in rare cases vomiting, bradycardia and hypotension [29], which limits very rapid injections of Mg 2+. Comparing Mg > and Verapamil (bolus injection plus infusion) in the treatment of paroxysmal atrial fibrillation and tachycardia, the success rate seems to be simular showing conversion rates of 60 or 50% at 24 hours.…”

Section: Summary: Clinical and Electrophysioiogica| Effects Of Magnesiummentioning

confidence: 99%

Klinisch-elektrophysiologische Effekte von Magnesium, insbesondere bei supraventrikulären Tachykardien

Vester

1997

Herz

View full text Add to dashboard Cite

Clinical electrophysiological effects of magnesium (Mg2+) are known for more than 60 years. Mg2+ is a cation to be found ubiquitously in the human body and is involved in more than 300 different enzymatic reactions. However, so far this ion has not been established as a standard therapeutic tool for the treatment of supraventricular tachyarrhythmia. This may be explained by the inconsistent efficacy of Mg2+, partly in relationship to a given plasma Mg(2+)-concentration, partly caused by the uncertainty regarding the dosage and injection rate or the unawareness of the clinical effects of the cation. Mg2+ influences myocardial metabolism by its effects on contractility and electrical activity. Both effects are closely linked. About 12% of cardiac Mg2+ is found in the mitochondria and 2 to 3% in the myofibrils. A large portion is incorporated in adenosin mono-, di- and triphosphate. Mg2+ affects intracellular calcium by inhibiting the influx of calcium into the myocyte through sarcolemmal channels, by modulation of cyclic AMP and by competing with calcium for binding to a single high affinity site on actin. Mg2+ has been linked to a naturally occurring calcium channel blocker. Furthermore Mg2+ blocks the outward current through some potassium channels resulting in an inward rectification of these channels. This suggests that internal magnesium functions as a potassium channel-blocking agent. Early afterdepolarizations are oscillations in the membrane potential and lead to triggered activity and therefore are the electrophysiological substrate of "torsade de pointes" type of ventricular flutter. Mg2+ is able to inhibit both early afterdepolarizations and tachyarrhythmias. Additionally Mg2+ interferes with the sodium-potassium-ATPase system by stabilizing the transmembrane gradient of both cations. Mg2+ deficiency alters this balance and leads to increased neuromuscular excitability. Digitalis is able to block the sodium-potassium-ATPase system, which can be cancelled by Mg2+. Thus the first clinical reports of the therapeutic use of Mg2+ refer to digitalis-induced atrial arrhythmia and ventricular ectopy which could be converted to sinus-rhythm or suppressed by the intravenous application of Mg2+ in 1935. Some years later, the first successful termination of paroxysmal supraventricular and ventricular tachycardia following application of 1.5 to 3 g of Mg2+ was published. But only in the late eighties, systematic studies of the electrophysiological effects of Mg2+ were performed and clinical use was first tested in random fashion in the nineties. Summarizing studies in older patients with different heart diseases and young healthy volunteers the most pronounced and clinically important effect seems to be related to the modulation of the AV node function. The prolongation of the PR interval by 7 to 12% without changing significantly heart rate, QRS duration and QT duration, can be considered a consistent and reproducible effect of Mg2+. In electrophysiological studies a prolongation of the AH interval by 8 to 18%, of t...

show abstract

Effect of intravenous magnesium sulfate on supraventricular tachycardia

Cited by 72 publications

References 8 publications

The effect of oral magnesium, alone or as an adjuvant to sotalol, after cardioversion in patients with persistent atrial fibrillation

The effect of oral magnesium, alone or as an adjuvant to sotalol, after cardioversion in patients with persistent atrial fibrillation

Magnesium Fortification of Drinking Water Suppresses Atherogenesis in Male LDL-Receptor-Deficient Mice

Klinisch-elektrophysiologische Effekte von Magnesium, insbesondere bei supraventrikulären Tachykardien

Contact Info

Product

Resources

About