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.
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Article info
Publication history
Accepted:
May 31,
2007
Received in revised form:
May 21,
2007
Received:
April 9,
2007
Identification
Copyright
© 2007 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
