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Letter to the Editor
ARTICLE IN PRESS
doi:
10.25259/IJN_542_2025

Ventricular Tachycardia as a Rare Manifestation of Tacrolimus-Induced QT Prolongation

Department of Nephrology, AIIMS, Jodhpur, Jodhpur, Rajasthan, India

Corresponding author: Rajesh Jhorawat, Department of Nephrology, AIIMS Jodhpur, Jodhpur, Rajasthan, India. E-mail: jhorawat2000@gmail.com

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This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

How to cite this article: Thomas E, Agarwal A, Jhorawat R, Chaturvedy M. Ventricular Tachycardia as a Rare Manifestation of Tacrolimus-Induced QT Prolongation. Indian J Nephrol. doi: 10.25259/IJN_542_2025

Dear Editor,

Tacrolimus-induced QTc prolongation is rare but potentially life-threatening, primarily reported with intravenous administration.1,2 An 18-year-old male with ESKD was admitted for live-related renal transplantation. He had well-controlled hypertension on β-blockers, with preoperative evaluation revealing mild left ventricular hypertrophy and a normal QTc interval of 388 ms. Tacrolimus was initiated 3 days prior to surgery. During central line placement under general anaesthesia, the patient developed hemodynamically unstable VT requiring cardioversion. His QTc was >500 ms, despite normal electrolytes, cardiac enzymes, and thyroid function. Surgery was deferred, and immunosuppressants were withheld; the QTc normalized within 24 hours. Holter monitoring revealed a single non-sustained VT, and cardiac MRI was unremarkable. General anaesthesia was initially suspected as the cause.

However, upon rescheduling surgery, QTc prolongation (>500 ms) recurred after four doses of tacrolimus, confirming drug-induced QT prolongation [Figure 1]. Tacrolimus was replaced with cyclosporine, and the patient underwent renal transplantation. Due to increased cyclosporine metabolism, diltiazem was briefly initiated to optimize drug levels but was stopped along with the β-blocker by postoperative day 3 due to bradycardia. By postoperative day 7, the patient remained stable, with a normal QTc and serum creatinine of 0.9 mg/dL.

Trend of QTc interval following tacrolimus initiation. Red arrow indicates the introduction of tacrolimus. QTc peaked on 14th January, normalized after discontinuation, and prolonged again upon reintroduction, supporting drug-related causality.
Figure 1:
Trend of QTc interval following tacrolimus initiation. Red arrow indicates the introduction of tacrolimus. QTc peaked on 14th January, normalized after discontinuation, and prolonged again upon reintroduction, supporting drug-related causality.

Our case is unique in demonstrating recurrent QTc prolongation upon reintroduction of tacrolimus, thereby confirming the causal relationship. Switching to cyclosporine was safe and effective in this scenario. This case underscores the importance of vigilant QTc monitoring in transplant recipients, particularly during the perioperative period.

Conflicts of interest

There are no conflicts of interest.

References

  1. , , , . QT prolongation and Torsades de Pointes after administration of FK506. Transplantation. 1992;53:929-30.
    [CrossRef] [PubMed] [Google Scholar]
  2. , , , , , . QT prolongation and near fatal cardiac arrhythmia after intravenous tacrolimus administration: A case report. Transplantation. 1998;66:535-7.
    [CrossRef] [PubMed] [Google Scholar]

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