Amiodarone-induced torsades de pointes: the possible facilitatory role of digoxin

Bajaj, Bindu; Baig, M.W.; Perrins, E J

doi:10.1016/0167-5273(91)90369-z

Cited by 16 publications

(7 citation statements)

References 4 publications

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“…This can however cause TdP in some patients, which is preceded by marked prolongation of the QT interval. In general, the induction of TdP by amiodarone is attributed to an idiosyncratic reaction to amiodarone itself, which is facilitated by electrolytic abnormalities [10,12,15].…”

Section: Discussionmentioning

confidence: 99%

Incidence of and Predicting Factors for Torsades de Pointes during Intravenous Administration of Amiodarone

Psirropoulos¹,

Lefkos²,

Boudonas³

et al. 2001

Heart Drug

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Objective: There is considerable knowledge of the incidence of torsades de pointes (TdP) during the administration of amiodarone The aim of our study was to determine the incidence of TdP during the loading phase of intravenous administration of amiodarone, intended to reverse paroxysmal atrial fibrillation (PAF) to sinus rhythm (SR), and to test the hypothesis that their prevalence is greater among women than men, as reported earlier. We also sought to determine factors predisposing to the occurrence of TpD, such as atrium size and hyperglycemia. Methods: We evaluated 189 patients (M = 107, F = 82, mean age = 56 ± 19 years), who were admitted for PAF, and for whom amiodarone was selected as the first-choice drug for PAF reversion. During the first 24 h of the loading phase (300 mg rapid i.v. administration within 20 min and 1,500 mg i.v. for 24 h) we recorded all ventricular arrhythmias. All patients were on anticoagulant treatment and all of them were evaluated for corrected QT (QTc), as well as additional risk factors (atrial size, serum glucose, hypopotassemia, hypomagnesemia, severe bradycardia). Patients with heart failure, hypertrophic obstructive cardiomyopathy, a history of coronary artery disease or ventricular tachycardia, as well as those treated with drugs prolonging the QT interval, were excluded from the study. Results: 108 patients (57.1%) experienced successful conversion of PAF into SR on amiodarone. Five patients (2.6%), all female, mean age 53.0 ± 1.2 years, developed TpD. All episodes occurred at the end of the loading phase (21–24 h) of amiodarone administration. None of them had hypopotassemia, hypomagnesemia, or bradycardia (HR <55 bpm). Two of the TpD patients had elevated glucose levels, and all of them had prolonged QTc immediately prior to the TpD. Conclusion: We confirm that women are at increased risk of developing TpD during the administration of amiodarone. TpD develop towards the end of the intravenous loading phase; the electrocardiographic changes should be closely monitored towards the end of the loading phase. The presence of diabetes mellitus or temporal hyperglycemia and prolonged QTc seems to be predicting factors for TpD during i.v. amiodarone administration.

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Section: Discussionmentioning

confidence: 99%

Incidence of and Predicting Factors for Torsades de Pointes during Intravenous Administration of Amiodarone

Psirropoulos¹,

Lefkos²,

Boudonas³

et al. 2001

Heart Drug

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“…As highlighted by this case, amiodarone is another drug that health care practioners must be especially wary of in the setting of LQT. Amiodarone is thought to prolong QT interval and generate ventricular arrhythmias by blocking the I kr delayed rectifier current and prolonging the duration of the ventricular action potential, thereby increasing refractoriness [17]. Even so, amiodarone is thought to have a low incidence of adverse cardiac events [18], and TdP is thought to occur with an incidence of less than 1%, likely because it also blocks the slow inward calcium current and does not increase QT dispersion [19].…”

Section: Discussionmentioning

confidence: 99%

Acquired QT Interval Prolongation & Methadone: The Risk of Pharmacological Interaction

Digby¹,

Fong²,

Methot³

et al. 2011

J Clinic Experiment Cardiol

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Methadone is known to be associated with acquired long QT (LQT) syndrome and the subsequent development of Torsades de Pointes (TdP). We describe a case of acquired LQT and TdP in a patient taking methadone maintenance therapy (MMT) in conjunction with medications known to prolong QT interval, and in the setting of hypokalemia and hypomagnesemia. We highlight the risk of QT interval prolongation when polypharmacy and electrolyte imbalances coexist, demonstrate the importance of early and effective therapy of LQT and suggest potential future alternatives to MMT that appear to have less QT prolonging properties in patients with multiple risks for LQT and TdP.

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“…The pro‐arrhythmic effect of digoxin has been known for over one hundred years, but it is only recently that the pro‐arrhythmic effects of other antiarrhythmics has been recognised 13,14 . Torsades de pointes seems to be associated particularly with drugs in Vaughan Williams classes la and III 15 .…”

Section: Discussionmentioning

confidence: 99%

The emergency department management of torsades de pointes

Carey

1994

Emergency Medicine

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Amiodarone-induced torsades de pointes: the possible facilitatory role of digoxin

Cited by 16 publications

References 4 publications

Incidence of and Predicting Factors for Torsades de Pointes during Intravenous Administration of Amiodarone

Incidence of and Predicting Factors for Torsades de Pointes during Intravenous Administration of Amiodarone

Acquired QT Interval Prolongation & Methadone: The Risk of Pharmacological Interaction

The emergency department management of torsades de pointes

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