HYPOMAGNESEMIA - CHARACTERIZATION OF A MODEL OF SUDDEN CARDIAC DEATH

Objectives. We sought to compare the incidence of sudden death in rats treated with magnesium-deficient and control diets and to address the electrophysiologic characteristics associated with these end points. Background. Although magnesium deficiency is associated with an increa sed incidence of sudden cardiac death in patients, there has been no c lear cause and effect relation because of a number of covariables, inc luding diuretic use, hypokalemia, digitalis use and left ventricular d ysfunction. Methods. Hypomagnesemic rats and their paired control rats underwent in vivo electrophysiologic studies and measurements of the total calcium and magnesium content of their cardiac ventricles. Resul ts. Serum magnesium levels were 0.5 +/- 0.3 mEq/liter (mean +/- SD) in hypomagnesemic animals and 1.2 +/- 0.9 mEq/liter in control animals, A modest but significant prolongation of the repolarization time was s een at the apical epicardial site (83 +/- 8 ms in hypomagnesemic rats vs. 68 +/- 13 ms in control rats, p < 0.05), but not at the other site s studied. Bradyarrhythmias and tachyarrhythmias were observed in 82% of the hypomagnesemic rats during the in vivo electrophysiologic studi es, compared with 0% in the control group. During these studies, sudde n, unexpected asystolic deaths were observed in 4 of 11 hypomagnesemic rats and 0 of 8 control rats. Polymorphic nonsustained ventricular ta chycardia was provoked by rapid pacing in 5 of 11 hypomagnesemic rats and 0 of 8 control rats, Three of six hypomagnesemic rats exposed to a uditory stimuli developed seizures, followed immediately by sudden dea ths-two due to asystole and one due to ventricular fibrillation-althou gh no end points occurred in the control animals. Conclusions. In this model, magnesium deficiency results in sudden cardiac death, The pres ence of startle induction of sudden death preceded by seizures suggest s that sudden cardiac death results from a neurologic trigger.