Abstract

IntroductionThe QT interval prolongation is an adverse effect associated with moxifloxacin. This adverse effect can lead to potentially life-threatening arrhythmias such as Torsades de pointes. We describe a case of severe QT interval prolongation associated with moxifloxacin which may cause the development of Torsades de pointes. There have been no reported case of severe corrected QT interval prolongation caused by moxifloxacin in the patient of normal heart rate.Case presentationIn an 85-year-old Japanese woman, oral moxifloxacin 400 mg daily was initiated for the forearm cellulitis. On the sixth day of oral moxifloxacin administration, monitor electrocardiogram showed prolongation of the corrected QT interval to 523 ms at a rate of 40 beats/min. Electrocardiogram before moxifloxacin therapy showed the corrected QT interval to 460 ms at a rate of 72 beats/min. On the sixth day after moxifloxacin discontinuance, monitor electrocardiogram showed the corrected QT interval to 432 ms at a rate of 70 beats/min.ConclusionThis case suggests that electrocardiogram monitoring during moxifloxacin therapy may be necessary in the patients even if they do not have high risk factors for QT interval prolongation.

Highlights

  • The QT interval prolongation is an adverse effect associated with moxifloxacin

  • This case suggests that electrocardiogram monitoring during moxifloxacin therapy may be necessary in the patients even if they do not have high risk factors for QT interval prolongation

  • We describe a case of severe QT interval prolongation associated with moxifloxacin which may cause the development of Torsades de pointes (TdP)

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Summary

Introduction

We describe a case of severe QT interval prolongation associated with moxifloxacin which may cause the development of TdP. According to Bazett's formula, the QTc interval was 460 ms Medications she was using just before admission included slowrelease nifedipine 10 mg twice daily and famotidine 10 mg twice daily. On the sixth day of moxifloxacin administration, her pulse rate indicated 40 beats/min that was bradycardia, so monitor ECG was performed and it showed prolongation of the QT interval to 640 ms. When the severe QTc interval prolongation was developed, the serum electrolytes, renal function and hepatic function were normal. On the sixth day after moxifloxacin discontinuance, monitor ECG showed the QT interval to 400 ms with a sinus rhythm at a rate of 70 beats/min. According to Bazett's formula, the QTc interval was 432 ms that was improved to normal range (Figure 2)

Discussion
Conclusion
Owens RC Jr
US Food and Drug Administration
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