Author + information
- Received May 24, 2016
- Revision received June 27, 2016
- Accepted July 14, 2016
- Published online December 1, 2016.
- aCardiology Department, St. John of God Hospital, Budapest, Hungary
- bDepartment of Haematology and Stem Cell Transplantation, St. László Hospital, Budapest, Hungary
- ↵∗Reprint requests and correspondence:
Dr. János Tomcsányi, St. John of God Hospital, Cardiology, 1023 Budapest, Árpád fejedelem u.7, Hungary.
A 74-year-old female patient had a history of left bundle branch block and atrial fibrillation. Therapy using the tyrosine kinase inhibitor ibrutinib was initiated to treat the recurrence of chronic lymphocytic leukemia characterized by trisomy 12 and a progressive course with therapy-resistant autoimmune hemolysis necessitating splenectomy in 2014. Hematologic remission was maintained with 140 to 280 mg daily of ibrutinib.
The first syncopal episode was seen at rest, 14 months after the beginning of ibrutinib therapy. The results of the noninvasive cardiological investigations were inconclusive. One month later, an event recorder (implantable loop recorder) was implanted following a second episode of syncope. Another month later, the patient presented with dizziness and pre-syncope. The implantable loop recorder showed a polymorphic ventricular tachycardia lasting 70 s (Figures 1A and 1B). A coronary angiogram revealed no coronary stenosis. The next episode of syncope occurred 5 weeks later while the patient was lying in bed; an episode of polymorphic ventricular tachycardia degenerated into ventricular fibrillation, which was terminated by the implantable cardioverter-defibrillator (Figures 1C and 1D), also causing a transient conversion to sinus rhythm for a short period (Figure 1E). Some tyrosine kinase inhibitors in large doses delay the repolarization and prolong the QT interval in large doses by blocking the hERG subunit of Ikr, although this has not been proven for ibrutinib.
This case demonstrates a recurrent polymorphic ventricular tachycardia under ibrutinib therapy without evidence of a different cause. The exact pathomechanism of this polymorphic ventricular tachycardia is not known as the QT-interval was not prolonged (Figure 1E), and Figure 1A shows the tachycardia was short-short-coupled, not typical for torsade.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received May 24, 2016.
- Revision received June 27, 2016.
- Accepted July 14, 2016.
- American College of Cardiology Foundation