Differential Effects of Intravenous Magnesium on Atrioventricular Node Conduction in Supraventricular Tachycardia

Evidence from noninvasive studies suggests magnesium has a differential effect on atrioventricular nodal (AVN) pathways. To further explore the electrophysiologic effects of intravenous magnesium sulfate (MgSO4) on supraventricular tachycardia, with particular reference to AVN conduction pathways, we studied 23 patients with supraventricular tachycardia at the time of electrophysiologic study. Tachycardia cycle length; AH, HV, and VA intervals; anterograde and retrograde Wenckebach thresholds; slow and fast pathway effective refractory periods (ERPs); accessory pathway ERP; right atrial and ventricular ERPs; blood pressure; and serum magnesium were evaluated before and after administration of MgSO4 during sustained tachycardia. AVN reentry was induced in 14 patients and atrioventricular reentry was induced in 9; 1 of the latter had dual AVN physiology with tachycardia using the slow pathway. Serum magnesium level increased from 0.88 ± 0.11 to 1.79 ± 0.14 mmol/L (p <0.0001). Magnesium increased tachycardia cycle length to a greater extent in those with dual AVN physiology than those without: 340 ± 54 to 370 ± 57 ms versus 347 ± 29 to 350 ± 30 ms (p = 0.01). This was associated with greater increase in AH interval in those with dual AVN physiology than in those without: 241 ± 59 to 270 ± 60 ms versus 144 ± 16 to 140 ± 20 ms (p = 0.003). Presence of dual AVN physiology was more frequently associated with reversion to sinus rhythm: 5 of 15 versus 0 of 8 (p = 0.06). MgSO4 did not alter other measured parameters. In conclusion, magnesium increases tachycardia cycle length and AH interval in patients with dual AVN physiology through a dominant effect on the slow AVN pathway.