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… 
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30 Citations

Torsade-de-pointes in a patient under flecainide treatment, an unusual case of proarrhythmicity.

Flecainide Induced Ventricular Tachycardia (Torsades de Pointes)

A 68‐year‐old woman presenting with flecainide induced syncope due to torsades de pointes (TP) ventricular tachycardia is described, where before TP onset, the QTc interval reached 680 ms without changes in QRS duration.

Flecainide‐Associated Bradycardia‐Dependent Torsade de Pointes: Another Potential Mechanism of Proarrhythmia

A patient who experienced recurrent syncope due to bradycardia‐dependent TdP with QT prolongation can be considered as one of mechanisms of flecainide‐induced proarrhythmia.

Fast and furious: flecainide toxicity presenting as monomorphic ventricular tachycardia

A 63-year-old woman on flecainide, furosemide, and triamterene–hydrochlorothiazide presented with weakness and diarrhoea and had profound hyponatraemia, hypokalaemia and a pre-renal acute kidney injury (AKI), and was treated with aggressive electrolyte repletion and amiodarone.

The Case of Flecainide Toxicity: What to Look for and How to Treat.

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.

The Case of Flecainide Toxicity: What to Look for and How to Treat

What Is the Minimal Pacing Rate that Prevents Torsades de Pointes? Insights from Patients with Permanent Pacemakers

It remains to be seen if rate smoothing algorithms can prevent TP when the baseline rate is programmed ≤ 70 beats/min, as well as if programmable pause‐promoting features or oversensing can prevent it at programmed lower rates.

Flecainide cardiotoxicity precipitated by electrolyte imbalance. Caution with thiazide diuretics

This case demonstrates the importance of strict electrolyte control in patients who are on flecainide and would discourage concomitant use of flecainside and bendroflumethiazide, and reports that support the use of hypertonic sodium salts to reverse fleCainide toxicity via antagonism at the receptor.

Flecainide Toxicity Secondary to Accidental Overdose: A Pediatric Case Report of Two Brothers

Two brothers aged 2 and 4 who presented two years apart with unstable wide-complex tachyarrhythmia suspicious for severe flecainide toxicity are reviewed, and two cases where it was avoided due to aggressive multimodal management with sodium bicarbonate, electrolyte repletion, and 20% intravenous lipid emulsion are presented.

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.

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To the Editor: From September 1993, the month in which the marketing of cisapride began, to April 1996, the Food and Drug Administration's MedWatch reporting program received reports of 34 patients in whom torsade de pointes developed and 23 in whom prolonged QT intervals developed while using this drug.

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It is concluded that the electrophysiological characteristics of cisapride may explain the recently reported propensity to prolong the QT interval and to induce torsades de pointes in susceptible patients, although a structurally related benzamide, mosapride, did not appear to have electrophYSiological features of relevance for induction of torsade de pointe in common with cisAPride.

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