scholarly journals PARP inhibitor-induced torsades de pointes in long QT syndrome: a case report

2019 ◽  
Vol 4 (1) ◽  
pp. 1-5
Author(s):  
Louise Segan ◽  
Ashley Beekman ◽  
Shane Parfrey ◽  
Mark Perrin
Keyword(s):  
Qt Interval ◽  
Parp Inhibitor ◽  
Torsades De Pointes ◽  
Parp Inhibitors ◽  
Qt Prolongation ◽  
Long Qt ◽  
Brca Mutations ◽  
Case Summary ◽  
Dose Dependent Increase ◽  
Dose Dependent

Abstract Background Poly ADP-ribose polymerase (PARP) inhibitors target pathogenic BRCA mutations in chemotherapy-resistant malignancies. PARP inhibitors cause modest dose-dependent QT prolongation in the setting of a normal baseline QT interval. Case summary We describe a case of PARP inhibitor-induced torsades de pointes (TdP) in an 86-year-old gentleman prescribed rucaparib due to chemotherapy-resistant, metastatic prostate cancer with pre-existing long QT, with an apparent dose-dependent increase in QT interval. The patient presented with syncope and recurrent TdP requiring direct cardioversion reversion (200 J biphasic) and an isoprenaline infusion (2 μg/min). There were no other QT prolonging agents and no electrolyte or metabolic disturbance to account for this arrhythmia. Improvement in QT interval was observed within 72 h of rucaparib cessation. Discussion PARP inhibitors cause a modest, dose-dependent increase in QT interval in patients with a normal baseline. The safety of PARP inhibitors in patients with pre-existing long QT has not been evaluated. This is the first reported case of rucaparib-associated TdP in a patient with pre-existing long QT, highlighting the amplified effect of this agent in individuals with pre-existing QT prolongation and the risk of fatal arrhythmias.

scholarly journals Drug-Induced QT Prolongation as a Result of an Escitalopram Overdose in a Patient with Previously Undiagnosed Congenital Long QT Syndrome

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Paul Singh ◽  
J. Martin Maldonado-Duran
Keyword(s):  
Qt Interval ◽  
Torsades De Pointes ◽  
Qt Prolongation ◽  
Long Qt ◽  
Drug Induced ◽  
Prolonged Qt Interval ◽  
Prolonged Qt ◽  
Qt Syndrome ◽  
Congenital Lqts ◽  
Congenital Long Qt Syndrome

We present a case of drug-induced QT prolongation caused by an escitalopram overdose in a patient with previously undiagnosed congenital LQTS. A 15-year-old Caucasian female presented following a suicide attempt via an escitalopram overdose. The patient was found to have a prolonged QT interval with episodes of torsades de pointes. The patient was admitted to the telemetry unit and treated. Despite the resolution of the torsades de pointes, she continued to demonstrate a persistently prolonged QT interval. She was seen by the cardiology service and diagnosed with congenital long QT syndrome. This case illustrates the potential for an escitalopram overdose to cause an acute QT prolongation in a patient with congenital LQTS and suggests the importance of a screening electrocardiogram prior to the initiation of SSRIs, especially in patients at high risk for QT prolongation.

QT prolongation and torsades de pointes in a patient with heart block and a pacemaker

2015 ◽  
Vol 26 (1) ◽  
pp. 161-163 ◽  
Author(s):  
Brett S. Bernstein ◽  
Eric S. Silver ◽  
Leonardo Liberman
Keyword(s):  
Qt Interval ◽  
Heart Block ◽  
Complete Heart Block ◽  
Torsades De Pointes ◽  
Qt Prolongation ◽  
Long Qt ◽  
Junctional Tachycardia

AbstractProlongation of the QT interval and development of torsades de pointes are known in patients with complete heart block and profound bradycardia. We report the case of a patient with complete heart block and torsades, with long QT seen during a period of junctional tachycardia at a rate faster than the minimum pacemaker rate.

scholarly journals Safety and effectiveness of drug therapy for the acutely agitated patient (Part I)

2013 ◽  
pp. 127-136
Author(s):  
Gianluca Airoldi
Keyword(s):  
Heart Rate ◽  
Qt Interval ◽  
Physical Restraint ◽  
Safety Data ◽  
Surrogate Marker ◽  
Diagnostic Procedures ◽  
Torsades De Pointes ◽  
Long Qt ◽  
Drug Induced ◽  
Qt Interval Prolongation

Acute agitation occurs in a variety of medical and psychiatric conditions, and the management of agitated, abusive, or violent patients is a common problem in the emergency department. Rapid control of potentially dangerous behaviors by physical restraint and pharmacologic tranquillization is crucial to ensure the safety of the patient and health-care personnel and to allow diagnostic procedures and treatment of the underlying condition. The purpose of this article (the first in a 2-part series) is to review the extensive safety data published on the antipsychotic medications currently available for managing situations of this type, including older neuroleptics like haloperidol, chlorpromazine, and pimozide as well as a number of the newer atypical antipsychotics (olanzapine, risperidone, ziprasidone). Particular attention is focused on the ability of these drugs to lengthen the QT interval in surface electrocardiograms. This adverse effect is of major concern, especially in light of the reported relation between QT interval and the risk of sudden death. In patients with the congenital long-QT syndrome, a long QT interval is associated with a fatal paroxysmal ventricular arrhythmia knownas torsades de pointes. Therefore, careful evaluation of the QT-prolonging properties and arrhythmogenic potential of antipsychotic drugs is urgently needed. Clinical assessment of drug-induced QT-interval prolongation is strictly dependent on the quality of electrocardiographic data and the appropriateness of electrocardiographic analyses. Unfortunately, measurement imprecision and natural variability preclude a simple use of the actually measured QT interval as a surrogate marker of drug-induced proarrhythmia. Because the QT interval changes with heart rate, a rate-corrected QT interval (QTc) is commonly used when evaluating a drug’s effect. In clinical settings, themost widely used formulas for rate-correction are those of Bazett (QTc=QT/RR^0.5) and Fridericia (QTc=QT/RR^0.33), both of which standardize themeasuredQTinterval to an RRinterval of 1 s (heart rate of 60 bpm).However, QT variability can also be influenced by other factors that are more difficult to measure, including body fat, meals, psycho-physical distress, and circadian and seasonal fluctuations.

scholarly journals Prolonged QTc: "Mind the Gap"

2014 ◽  
Vol 2 (1) ◽  
pp. 44-45
Author(s):  
Ahmad Mursel Anam ◽  
Raihan Rabbani ◽  
Farzana Shumy ◽  
M Mufizul Islam Polash ◽  
M Motiul Islam ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Long Qt Syndrome ◽  
Qt Interval ◽  
Torsades De Pointes ◽  
Junior Doctors ◽  
Long Qt ◽  
Acquired Long Qt Syndrome ◽  
Prolonged Qt Interval ◽  
Prolonged Qt ◽  
Qt Syndrome

We report a case of drug induced torsades de pointes, following acquired long QT syndrome. The patient got admitted for shock with acute abdomen. The initial prolonged QT-interval was missed, and a torsadogenic drug was introduced post-operatively. Patient developed torsades de pointes followed by cardiac arrest. She was managed well and discharged without complications. The clinical manifestations of long QT syndromes, syncope or cardiac arrest, result from torsades de pointes. As syncope or cardiac arrest have more common differential diagnoses, even the symptomatic long QT syndrome are commonly missed or misdiagnosed. In acquired long QT syndrome with no prior suggestive feature, it is not impossible to miss the prolonged QT-interval on the ECG tracing. We share our experience so that the clinicians, especially the junior doctors, will be more alert on checking the QT-interval even in asymptomatic patients. DOI: http://dx.doi.org/10.3329/bccj.v2i1.19970 Bangladesh Crit Care J March 2014; 2 (1): 44-45

scholarly journals Managing drug-induced QT prolongation in clinical practice

2020 ◽  
pp. postgradmedj-2020-138661
Author(s):  
Rani Khatib ◽  
Fatima R N Sabir ◽  
Caroline Omari ◽  
Chris Pepper ◽  
Muzahir Hassan Tayebjee
Keyword(s):  
Qt Interval ◽  
Simple Algorithm ◽  
Torsades De Pointes ◽  
Daily Practice ◽  
Qt Prolongation ◽  
Key Factors ◽  
Drug Induced ◽  
Electrolyte Disturbances ◽  
Related Risk ◽  
Life Threatening

Many drug therapies are associated with prolongation of the QT interval. This may increase the risk of Torsades de Pointes (TdP), a potentially life-threatening cardiac arrhythmia. As the QT interval varies with a change in heart rate, various formulae can adjust for this, producing a ‘corrected QT’ (QTc) value. Normal QTc intervals are typically <450 ms for men and <460 ms for women. For every 10 ms increase, there is a ~5% increase in the risk of arrhythmic events. When prescribing drugs associated with QT prolongation, three key factors should be considered: patient-related risk factors (eg, female sex, age >65 years, uncorrected electrolyte disturbances); the potential risk and degree of QT prolongation associated with the proposed drug; and co-prescribed medicines that could increase the risk of QT prolongation. To support clinicians, who are likely to prescribe such medicines in their daily practice, we developed a simple algorithm to help guide clinical management in patients who are at risk of QT prolongation/TdP, those exposed to QT-prolonging medication or have QT prolongation.

Immunosuppressant associated torsades de pointes after acute heart rejection in an 8-year-old boy

2020 ◽  
Vol 30 (8) ◽  
pp. 1194-1195 ◽  
Author(s):  
Liu Hsin-Ming ◽  
Tseng Wei-Chieh ◽  
Chiu Shuenn-Nan
Keyword(s):  
Acute Rejection ◽  
Heart Transplantation ◽  
Genetic Variants ◽  
Ventricular Tachyarrhythmia ◽  
Torsades De Pointes ◽  
Orthotopic Heart Transplantation ◽  
Long Qt ◽  
Anchoring Protein ◽  
Life Threatening ◽  
Dose Dependent

AbstractTorsades de pointes is a kind of life-threatening ventricular tachyarrhythmia. We report a case of torsades de pointes in an 8-year-old boy with acute rejection after orthotopic heart transplantation. The causes of torsades de pointes could be either congenital or acquired. In this case, various causes including acute rejection-related repolarisation heterogeneity, dose-dependent acquired long QT resulting from treatment with immunosuppressants, and AKAP9 (A-kinase anchoring protein 9) genetic variants are the possible mechanisms.

scholarly journals QT Prolongation and Associated Ventricular Tachycardia due to Cardiac Iron Load in a Patient with Thalassemia Major

2019 ◽  
Vol 2019 ◽  
pp. 1-3
Author(s):  
Derya Demirtas ◽  
Abdullah Orhan Demirtas ◽  
Hilmi Erdem Sumbul ◽  
Ayse Selcan Koc
Keyword(s):  
Ventricular Tachycardia ◽  
Qt Interval ◽  
Thalassemia Major ◽  
Qt Prolongation ◽  
High Dose ◽  
Resonance Imaging ◽  
Long Qt ◽  
Blocker Therapy ◽  
Iron Load ◽  
Magnetic Resonance Imaging Mri

We report the case of a 23-year-old male with thalassemia major who developed long QT and continuous ventricular tachycardia (VT). Electrocardiography, echocardiography, and cardiac magnetic resonance imaging (MRI) were used for diagnosis and risk stratification. VT causes and treatments are presented and discussed. Ventricular arrhythmia can be treated by normalizing QT interval with high-dose beta-blocker therapy. However, MRI-compatible internal cardiac defibrillator implantation was performed due to the high risk in this patient.

scholarly journals Acquired Long QT Interval: A Case Series of Multifactorial QT Prolongation

2011 ◽  
Vol 34 (9) ◽  
pp. 577-582 ◽  
Author(s):  
Geneviève C. Digby ◽  
Andrés Ricardo Pérez Riera ◽  
Raimundo Barbosa Barros ◽  
Christopher S. Simpson ◽  
Damian P. Redfearn ◽  
...  
Keyword(s):  
Qt Interval ◽  
Case Series ◽  
Qt Prolongation ◽  
Long Qt ◽  
Long Qt Interval

scholarly journals QT-prolongation and noncompaction

2019 ◽  
pp. 01-03
Author(s):  
Josef Finsterer ◽  
Claudia Stöllberger
Keyword(s):  
Ventricular Fibrillation ◽  
Long Qt Syndrome ◽  
Qt Interval ◽  
Genetic Defect ◽  
Neuromuscular Disorder ◽  
Left Ventricular ◽  
Qt Prolongation ◽  
Long Qt ◽  
Qt Syndrome

In a recent article, Szulik et al. reported about a 22 years old female with ventricular fibrillation, QT-prolongation, and left ventricular hypertrabeculation/noncompaction (LVHT) who died from hypoxic cerebral damage 5 days after admission [1]. We have the following comments and concerns. Patients with LVHT have a disposition for any type of cardiac arrhythmia [2,3]. This is why ventricular fibrillation not only could be due to hereditary long-QT syndrome but also due to LVHT. Ventricular fibrillation was either due to LVHT or a consequence of QT-prolongation. QT-prolongation is not unusual in LVHT and has been reported in several cases (table 1) [3-7]. LVHT has been also reported in association with long-QT-syndrome due to mutations in the KCNQ1 gene [8], in the KCNH2 gene [9], or due to an unidentified genetic defect (table 1) [10]. In a study of 105 patients with LVHT, the QT-interval increased during a mean follow up of 3.6y in 15 patients and normalized in 21 patients [11]. The increase was associated with the extension of LVHT and the presence of a neuromuscular disorder (NMD) [11].

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