title: Hypomagnesemia: characterization of a model of sudden cardiac death.
abstract: OBJECTIVE
  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 increased incidence of sudden cardiac death in patients, there has been no clear cause and effect relation because of a number of covariables, including diuretic use, hypokalemia, digitalis use and left ventricular dysfunction.
  
  
  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
  
  
  RESULTS
  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 seen 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 sites studied. Bradyarrhythmias and tachyarrhythmias were observed in 82% of the hypomagnesemic rats during the in vivo electrophysiologic studies, compared with 0% in the control group. During these studies, sudden, unexpected asystolic deaths were observed in 4 of 11 hypomagnesemic rats and 0 of 8 control rats. Polymorphic nonsustained ventricular tachycardia was provoked by rapid pacing in 5 to 11 hypomagnesemic rats and 0 of 8 control rats. Three of six hypomagnesemic rats exposed to auditory stimuli developed seizures, followed immediately by sudden deaths-two due to asystole and one due to ventricular fibrillation-although no end points occurred in the control animals.
  
  
  CONCLUSIONS
  In this model, magnesium deficiency results in sudden cardiac death. The presence of startle induction of sudden death preceded by seizures suggests that sudden cardiac death results from a neurologic trigger.
authors.affiliation: Cardiovascular Research Group, University of Calgary, Alberta, Canada.
authors.forename: C
authors.initials: C
authors.lastname: Fiset
authors.forename: M E
authors.initials: ME
authors.lastname: Kargacin
authors.forename: C S
authors.initials: CS
authors.lastname: Kondo
authors.forename: W M
authors.initials: WM
authors.lastname: Lester
authors.forename: H J
authors.initials: HJ
authors.lastname: Duff
mesh_terms: D000818:Animals; D002118:Calcium / Q000032:analysis; D002304:Cardiac Pacing, Artificial; D016757:Death, Sudden, Cardiac / Q000209:etiology*; D004195:Disease Models, Animal; D004562:Electrocardiography; D008274:Magnesium / Q000032:analysis; D008275:Magnesium Deficiency / Q000150:complications* / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000737:chemistry; D051381:Rats; D017207:Rats, Sprague-Dawley; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000503:physiopathology
chemical_list: D008274:Magnesium; D002118:Calcium