Congestive heart failure is characterized by contractile dysfunction and frequent complex ventricular ectopy. Despite advances in
therapy, mortality from
heart failure is substantial, estimated
at 10-80 percent per year, and
sudden death is common.
Magnesium is the second most common intracellular
cation, strongly influences cardiac cell membrane function, and is an important catalyst of many enzymatic reactions in the myocyte. Epidemiological studies have implicated
magnesium deficit in the genesis of
sudden death. Patients with
congestive heart failure are predisposed to
magnesium deficit for many reasons, including neurohormonal activation, poor gastrointestinal absorption, and
drug therapy. Hypomagnesaemia is common in these patients and has been linked to an increased frequency of complex ventricular ectopy. Several early, uncontrolled studies have suggested a beneficial effect of
magnesium administration on ventricular arrhythmias in patients with
congestive heart failure. Two recent randomized, double blind, placebo-controlled trials have shown that both intravenous and
oral administration of
magnesium chloride results in a significant reduction in the frequency and complexity of ventricular arrhythmias in patients with
congestive heart failure.
Magnesium administration is well tolerated and serious adverse effects are rare. The potential mechanisms of the antiarrhythmic action of
magnesium and limitations of the available data are discussed. The evidence reviewed suggests that serum
magnesium concentrations should be monitored and corrected in patients with
congestive heart failure. Ventricular arrhythmias may respond to acute intravenous
magnesium administration, which should be considered as
early therapy. Further study is needed to define
magnesium dose and the effect of concomitant
potassium administration. A prospective clinical trial is warranted to determine the chronic effects of
magnesium administration in patients with
heart failure.