Arrhythmias is any cardiac rhythm different from the so-called sinusal rhythm, i.e. generated from the sinus node, a group of cells situated in the right atrium characterized by pacemaker function for their capacity to depolarize spontaneously. Numerous studies have been carried out in an attempt to define the role of both intracellular and extracellular magnesium in the physiopathology and treatment of arrhythmias.
Variations in both intracellular and extracellular magnesium can influence directly the activity of numerous ionic membrane channels, particularly calcium and potassium channels, as described in recent reviews.77,78
It is very difficult to establish the role of a lack of magnesium in vivo and at the same time the possible arrhythmogenic risk. This depends on various factors. In the first place, it is very difficult to know whether a patient is lacking in magnesium when we consider its prevalent location inside cells. The Framingham Heart Study fails to show any correlation between hypomagnesae-mia and the incidence of ventricular premature complexes with a rate of more than 10 per hour.79 However, they did show an increased risk of frequent or complex ventricular premature complexes in the case of serious reductions in magnesaemia. Although both supraventricular and ventricular arrhythmias have been associated with hypomagnesaemia,80 the interpretation of this relationship is made less clear by the limited correlation between the intracellular concentration of magnesium in myocites (i.e. myocardial contractile cells) and in plasma.81
'Torsade de pointes' or polymorphic ventricular tachycardia is the form of arrhythmia for which treatment with magnesium seems most appropriate. The American Heart Association's 1992 Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiac Care included the infusion of magnesium sulphate in the treatment of torsade de pointes. In the past, the treatment aimed at reducing the (QT) interval (i.e. a portion of the electrocardiogram, in particular, an interval which comprises the electrical activity corresponding to both ventricular contraction and diastole or ventricular depolarization and repolarization) through sympathicomimetics or cardiac pacing. In 1984 the use of magnesium sulphate as a treatment for torsade de pointes was described for the first time.82 The treatment consisted in the infusion of an 8 mmol IV bolus of magnesium sulphate and was followed by the resolution of the arrhythmia without relapse in all three patients treated. Since then there have been many reports of the efficacy of magnesium in the treatment of this kind of arrhythmia,83 with the exception of one report in which neither the infusion of magnesium alone, nor cardiac pacing was sufficient to restore stability to the sinusal rhythm but the two associated methods were successful.84 Magnesium therapy is not useful in the long-term management of long QT syndrome, a disorder of cardiac repolarization that may precipitate torsade de pointes. For other forms of arrhythmias such as atrial fibrillation, ventricular tachycardia, re-entrant supraventricular tachycardia there are only anecdotical reports. Thus, the role of magnesium appears to be secondary and limited to those patients for whom other drugs are contraindi-cated or have been shown to be ineffective (for review see Ref. 78).
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