Open AccessAbnormal qt intervals associated with negative t waves induced by antiarrhythmic drugs are rapidly reduced using magnesium sulfate as an antidote
Author(s) -
Gurfinkel Enrique,
Mautner Branco,
Pazos Angel Alvarez
Publication year - 1993
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960160108
Subject(s) - medicine , qt interval , amiodarone , cardiology , refractory period , magnesium , hypomagnesemia , antidote , repolarization , anesthesia , toxicity , electrophysiology , materials science , metallurgy , atrial fibrillation
This study was undertaken to determine whether prolonged QTc interval as a consequence of abnormal repolarization induced by coronary disease or antiarrhythmic drugs could be shortened by intravenous administration of magnesium sulfate. A total of 21 patients with basal prolonged QTc intervals (QTc > 500 ms) were divided in two groups: 7 with ischemic coronary disease and negative T waves (Group A), and 14 treated with antiarrhythmic drugs (Group B). Nine of the latter had negative T waves (Subgroup B‐1) and five had positive T waves (Subgroup B‐2) recorded in precordial leads. Nine patients were taking amiodarone and six quinidine. Magnesium sulfate was given intravenously in a bolus of 3.75 g (25% solution) over 3 min. Patients had normal electrolyte serum levels. The prolonged QTc and JTc intervals were shortened after magnesium sulfate in patients of Subgroup B‐1 from the basal values [QTc 20.7% and JTc 25.4%, (p = < 0.0001 and 0.02, respectively)]. None of the patients in Group A or Subgroup B‐2 experienced altered QTc or JTc intervals. While some antiarrhythmic drugs are capable of altering the refractoriness of ventricular cells, probably by causing changes in the intracellular metabolic pathways, in patients with coronary disease gaps in the membrane induced by ischemic injury let calcium enter the cells parallel with dispersion of ventricular repolarization. When secondary negative T waves are present, magnesium sulfate as an antidote probably acts as a blocking agent at the sarcoplasmic reticulum, thus reducing both QTc and JTc intervals.