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Ventricular tachycardia on chronic fingolimod treatment for multiple sclerosis
  1. Tamara Castillo-Trivino1,2,3,
  2. Itziar Lopetegui1,
  3. Jose Antonio Alarcón-Duque4,
  4. Adolfo López de Munain2,5,6,
  5. Javier Olascoaga1,2
  1. 1Multiple Sclerosis Unit, Department of Neurology, Donostia University Hospital, San Sebastian, Spain
  2. 2Department of Neuroscience Area, Biodonostia Research Institute, San Sebastian, Spain
  3. 3Department of Neurology, Zumarraga Hospital, Zumarraga, Spain
  4. 4Department of Cardiology, Donostia University Hospital, San Sebastian, Spain
  5. 5Department of Neurosciences, University of Basque Country, San Sebastian, Spain
  6. 6CIBERNED, Carlos III Health Institute, Madrid, Spain
  1. Correspondence to Dr Tamara Castillo-Trivino, Multiple Sclerosis Unit, Department of Neurology, Donostia University Hospital/Biodonostia Research Institute, Paseo Dr Beguiristain s/n, San Sebastian 20014, Spain; tamaracastillo.tri{at}gmail.com

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Introduction

Fingolimod, the first approved oral treatment for relapsing multiple sclerosis (MS), reduces clinical and radiological activity and slows down disability progression. Cardiovascular monitoring is necessary at treatment initiation due to the infrequent but potentially life-threatening risk of bradycardia, bradyarrythmia, sinus bradycardia and atrioventricular block. After first dose administration, there are no specific recommendations regarding cardiological monitoring. Ventricular tachycardia (VT) has never been described on treatment with fingolimod but, very rarely, patients are referred for Holter-ECG. VT can be the trigger of ventricular fibrillation, subsequent asystolia and sudden death.

We describe a case of a young patient with non-specific complaint of dizziness and asthenia who had a documented episode of VT on Holter-monitoring within the first month of fingolimod initiation.

Case report

We present a case of an underweight 37-year-old woman with MS since the age of 23 years, with no history of cardiac disease, cardiovascular risk factors nor family cardiac disease. Between 1997 and 2006, she presented with a total of nine relapses, but repeatedly refused injectable MS therapy due to needle phobia. From 2006 to mid-2007, she received mitoxantrone and did not experience any relapse or radiological activity during that time (total dose 108.72 mg/m2, height 1.67 m, weight 48 kg). At that time, mitoxantrone was discontinued; EDSS was 6.0. From 2008 to 2011, she had three relapses and experienced increased EDSS to 6.5. Her cardiac function was evaluated periodically with cardiac echocardiography as standard monitoring during and after mitoxantrone treatment. The last echocardiogram obtained in June …

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Footnotes

  • Contributors TC-T was involved in the study concept, acquisition of data, interpretation of data and writing of the manuscript. IL involved in the acquisition of data and critical revision of the manuscript. JAA-D and JO were involved in the interpretation of data and critical revision of the manuscript for important intellectual content. ALdM was involved in the study concept, interpretation of data and critical revision of the manuscript for important intellectual content.

  • Competing interests TC-T has received travel expenses for attending meetings from Biogen-Idec, Merck and Novartis. JO has received honoraria as a consultant on the scientific advisory board of Biogen-Idec, Genzyme and Novartis, and also for his participation in meetings, as an organiser, speaker or moderator, as well as for his participation in clinical trials or research projects promoted by Allmirall, Bayer, Biogen—Idec, Merck, Novartis and Teva pharmaceuticals.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement All relevant data were included in this study.

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