CINACALCET-INDUCED TORSADES DE POINTES IN A HAEMODIALYSIS PATIENT

8 Feb 2025 12 a.m. 12 a.m.
WCN25-AB-290, Poster Board= SAT-037

Introduction:

We herein report a case of a 64-year-old male patient with a complex medical history that has the following: chronic kidney disease stage 5 on intermittent haemodialysis, hypertension, type 2 diabetes mellitus, diastolic heart failure, gout, pancytopenia and atrial fibrillation. He developed central chest pain radiating to the back 15 minutes into a haemodialysis session; in which he rapidly became unresponsive. His telemetry data revealed a ventricular tachycardia (“VT”) rhythm; necessitating immediate cardiopulmonary resuscitation (“CPR”), administration of calcium gluconate, and three defibrillation shocks to achieve the return of spontaneous circulation (“ROSC”). Right after, the patient experienced Torsades de Pointes, requiring another CPR and defibrillation to achieve another ROSC.

Methods:

While his serum electrolyte imbalance was suspected to be the cause of his Torsades de Pointes rhythm, laboratory results confirmed normal levels of calcium, magnesium, sodium, potassium, bicarbonate and phosphate. His bedside echocardiogram revealed normal systolic function with a mildly calcified aortic valve; continuous monitoring of his telemetry data showed a return to sinus rhythm. Notably, his corrected QT Bazett interval (“QTc”) ranged from 530 to 560 msec (i.e normal range for males is less than 430 msec); raising concerns about drug-induced QT prolongation. Given his medication profile of multiple antihypertensives, erythropoietin, calcitriol and cinacalcet; cinacalcet was identified as a potential culprit, leading to its discontinuation. Subsequently, his QTc interval normalized to 360 to 400 msec upon reevaluation four months later.

Results:

This case emphasises the potential for cinacalcet, a calcimimetic agent commonly used to manage secondary hyperparathyroidism in haemodialysis patients, in inducing life-threatening arrhythmias even in the absence of hypocalcaemia. Though hypocalcaemia did not develop in this patient’s case, calcium-independent mechanisms contributing to QT prolongation still need to be researched.

Conclusions:

This is the first documented case of cinacalcet-induced Torsades de Pointes in Australasia. Such case highlights the potential risks associated with cinacalcet and the need for vigilance among clinicians when prescribing this medication, particularly in haemodialysis patients who are predisposed to prolonged QT intervals and increased QT dispersion. Early recognition and management of this adverse effect is critical to prevent fatal outcomes.

I have no potential conflict of interest to disclose.

I did not use generative AI and AI-assisted technologies in the writing process.