Torsades de Pointes Ventricular Tachycardia Induced by Mosapride and Flecainide in the Presence of Hypokalemia

@article{Ohki2001TorsadesDP,
  title={Torsades de Pointes Ventricular Tachycardia Induced by Mosapride and Flecainide in the Presence of Hypokalemia},
  author={Ruri Ohki and Masafumi Takahashi and Osamu Mizuno and Hideyuki Fujikawa and Takeshi Mitsuhashi and Taka-aki Katsuki and Uichi Ikeda and Kazuyuki Shimada},
  journal={Pacing and Clinical Electrophysiology},
  year={2001},
  volume={24}
}
OHKI, R., et al.: Torsades de Pointes Ventricular Tachycardia Induced by Mosapride and Flecainide in the Presence of Hypokalemia. We report a 68‐year‐old man who developed torsades de pointes ventricular tachycardia induced by combined use of mosapride and flecainide. He had a permanent pacemaker (DDD mode) implanted because of sick sinus syndrome (bradytachy syndrome) 6 years earlier. The patient had started taking mosapride for upper abdominal discomfort 2 weeks earlier. On admission, ECG… 

Flecainide Induced Ventricular Tachycardia (Torsades de Pointes)

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This case demonstrates the necessity of keeping flecainide toxicity on the physician's differential for patients who are taking the drug, as well as what electrocardiogram findings suggest it as the etiology.

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Flecainide cardiotoxicity precipitated by electrolyte imbalance. Caution with thiazide diuretics

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Flecainide-Induced Proarrhythmia Is Attributed to Abnormal Changes in Repolarization and Refractoriness in Perfused Guinea-Pig Heart

  • O. Osadchii
  • Biology, Medicine
    Journal of cardiovascular pharmacology
  • 2012
In nonischemic guinea-pig heart, flecainide-induced proarrhythmia may be partly attributed to abnormal spatial gradients in repolarization and refractoriness and impaired transepicardial activation-to-repolarization coupling.

QT Interval Prolongation as a Biomarker for Torsades de Pointes and Sudden Death in Drug Development

  • G. Sides
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    Disease markers
  • 2002
The basis for the use of the QT interval as a biomarker will be examined and drugs that increase heart rate show an apparent increase in QT intervals that confounds assessment of a true drug effect on cardiac ventricular repolarization.

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