Elisabeth Ryzen

Magnesium deficiency in a medical ICU population

The serum magnesium level was measured in 94 consecutive patients admitted to the medical ICU of Los Angeles County/University of Southern California Medical Center over a 2-month period. Sixty-five percent of patients with serum creatinine concentrations of 1.1 mg/dl or less were hypomagnesemic. Of these, one third had hypocalcemia that was corrected with magnesium supplementation. Physicians should be alert to the high incidence of magnesium deficiency in critically ill patients.

Low blood mononuclear cell magnesium in intensive cardiac care unit patients

Magnesium deficiency may play a role in the pathogenesis of atherosclerosis, cardiac arrhythmias, and coronary spasm. Because less than 1% of magnesium (Mg) is extracellular, the serum magnesium (sMg) does not always accurately reflect intracellular Mg stores. To determine the frequency of Mg deficiency in patients with cardiovascular disease, we measured blood mononuclear cell Mg content (mMg) and sMg concentrations in 104 unselected patients admitted to our intensive cardiac care unit (CCU). Twenty-seven normal healthy controls and 33 hypomagnesemic patients with chronic alcoholism and/or malabsorption syndrome served as reference groups. The sMg concentration in the CCU patients was 2.05 +/- 0.03 mg/dl (mean +/- SEM), and did not differ from normal controls (mean 2.01 +/- 0.03 mg/dl). Only 8 of 104 CCU patients were hypomagnesemic (7.7%). mMg in the CCU patients, however, was significantly lower than in the normal controls (1.15 +/- 0.02 micrograms/mg protein and 1.34 +/- 0.02 micrograms/mg protein respectively, p less than 0.001). Fifty-three percent (55 of 104) of CCU patients had mMg contents less than 1.119 micrograms/mg protein, i.e., below that of the lowest normal control. mMg was significantly lower in those patients with congestive heart failure (mMg = 1.08 +/- 0.03 micrograms/mg protein) when compared to those patients without congestive heart failure (1.23 +/- 0.02 micrograms/mg protein, p less than 0.001). We conclude that the incidence of intracellular Mg deficiency in patients with cardiovascular disease is much higher than the sMg would lead one to suspect, and may contribute to clinical cardiovascular morbidity.

Electrophysiologic effects of intravenous magnesium in patients with normal conduction systems and no clinical evidence of significant cardiac disease

Parenteral magnesium has been used for several decades in the empiric treatment of various arrhythmias, but the data on its electrophysiologic effects in man are limited. We evaluated the electrophysiologic effects of magnesium sulfate (MgSO4) administration in eight normomagnesemic patients with normal mononuclear cell magnesium content, who had no clinically significant heart disease and had normal baseline electrophysiologic properties. After administration of intravenous MgSO4, serum magnesium rose significantly from 1.9 +/- 0.1 to 4.4 +/- 1.7 mg/dl (p less than 0.02). During a maintenance magnesium infusion, we observed significant prolongation of the ECG PR interval (145 +/- 18 to 155 +/- 26 msec, p less than 0.05), AH interval (77 +/- 27 to 83 +/- 26 msec, p less than 0.002), antegrade atrioventricular (AV) nodal effective refractory period (278 +/- 67 to 293 +/- 67 msec, p less than 0.05), and sinoatrial conduction time (60 +/- 34 to 76 +/- 32 msec, p less than 0.02). No significant effect was observed on sinus cycle length, sinus node recovery time, intra-atrial or intraventricular conduction times, QRS duration (during both sinus rhythm and ventricular pacing), QT interval, HV interval, paced cycle length resulting in AV nodal Wenckebach block, AV nodal functional refractory period, retrograde ventriculoatrial (VA) effective refractory period, or atrial and ventricular refractory periods. These findings, in conjunction with the demonstrated ability of magnesium to block slow channels for sodium movement, may provide an explanation of the mechanism by which magnesium exerts its effect in the treatment of atrial and junctional arrhythmias.

Prospective evaluation of parenteral magnesium sulfate in the treatment of patients with reentrant AV supraventricular tachycardia

This study prospectively assessed the electrophysiologic effects of parenteral magnesium sulfate administration on paroxysmal atrioventricular (AV) reentrant supraventricular tachycardia and the efficacy of magnesium to terminate these arrhythmias. Eleven normomagnesemic patients, seven with orthodromic reentrant supraventricular tachycardia that used an accessory AV pathway, and four with typical AV nodal reentry were examined. All patients had a history of sustained supraventricular tachycardia requiring pharmacologic therapy or electrical cardioversion for termination of tachycardia. After baseline electrophysiologic study, including documentation of sustained supraventricular tachycardia that was reproducibly induced, parenteral magnesium sulfate (a bolus of 0.3 mEq/kg of elemental magnesium infused over a 10-minute period followed by a maintenance infusion of 0.2 mEq/kg/hr) was administered during sustained supraventricular tachycardia. The serum magnesium concentration increased from (mean +/- standard deviation) 1.9 +/- 0.2 mg/dl to 4.0 +/- 0.6 mg/dl (p = 0.0001). Except for flushing and mild diaphoresis during infusion of the magnesium sulfate bolus, and dry heaves in one patient, there were no untoward effects or significant changes in systolic blood pressure. During administration of magnesium, the tachycardia cycle length increased from 319 +/- 39 msec to 348 +/- 43 msec (p = 0.0001). Slowing of the tachycardia occurred predominantly in the antegrade limb of the circuit at the level of the AV node with the AH interval increasing from 171 +/- 66 msec to 197 +/- 68 msec (p = 0.0001), whereas there was no significant change in the HV interval (43 +/- 3 msec to 43 +/- 4 msec, p = NS) or the VA interval (106 +/- 43 msec to 110 +/- 47 msec, p = NS) during tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypercalcemia and abnormal 1,25-dihydroxyvitamin D concentrations in leprosy

Two patients with lepromatous leprosy and hypercalcemia are presented. Serum immunoreactive parathyroid hormone and urinary cyclic adenosine monophosphate concentrations were suppressed. Serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] concentrations were elevated in one patient and normal in the other. Urinary hydroxyproline excretion was slightly high in both patients. Hypercalcemia resolved excretion was slightly high in both patients. Hypercalcemia resolved with prednisone therapy. Abnormal 1,25-(OH)2D production and/or metabolism may play a role in the pathogenesis of hypercalcemia in some patients with leprosy.