Drug-Induced QT Prolongation and Torsades de Pointes: An All-Exclusive Relationship or Time for an Amicable Separation?

Drug Safety ◽  
2017 ◽  
Vol 41 (1) ◽  
pp. 11-17 ◽  
Author(s):  
Luc M. Hondeghem
2021 ◽  
Vol 131 ◽  
pp. 104281
Author(s):  
Alaa Alahmadi ◽  
Alan Davies ◽  
Jennifer Royle ◽  
Leanna Goodwin ◽  
Katharine Cresswell ◽  
...  

2020 ◽  
pp. postgradmedj-2020-138661
Author(s):  
Rani Khatib ◽  
Fatima R N Sabir ◽  
Caroline Omari ◽  
Chris Pepper ◽  
Muzahir Hassan Tayebjee

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.


2020 ◽  
Vol 9 (13) ◽  
Author(s):  
Magdalene M. Assimon ◽  
Lily Wang ◽  
Patrick H. Pun ◽  
Wolfgang C. Winkelmayer ◽  
Jennifer E. Flythe

Background The rate of sudden cardiac death in the hemodialysis population exceeds that of the general population by >20‐fold. Hemodialysis patients may be particularly susceptible to sudden cardiac death provoked by drug‐induced QT prolongation because of their substantial cardiovascular disease burden, exposure to electrolyte shifts during dialysis, and extensive polypharmacy. However, population‐specific data regarding the frequency and patterns of QT prolonging medication use are limited. Methods and Results We conducted a descriptive drug utilization study using 3 administrative databases, the United States Renal Data System, MarketScan, and Medicare claims. We characterized the extent and patterns of QT prolonging medication use by adult hemodialysis patients and individuals without end‐stage kidney disease annually from 2012 to 2016. We also identified instances of high‐risk QT prolonging medication use among hemodialysis patients. In total, 338 515 hemodialysis patients and 40.7 million individuals without end‐stage kidney disease were studied. Annual utilization rates of QT prolonging medications with known torsades de pointes risk in hemodialysis patients were ~1.4 to ~2.5 times higher than utilization rates in individuals without end‐stage kidney disease. Hemodialysis patients with demographic and clinical risk factors for drug‐induced QT prolongation were exposed to medications with known torsades de pointes risk more often than patients without risk factors. Conclusions Hemodialysis patients use QT prolonging medications with known torsades de pointes risk more extensively than individuals without end‐stage kidney disease. Given the widespread use and instances of high‐risk prescribing, future studies evaluating the cardiac safety of these drugs in the hemodialysis population are needed.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
J-Philippe Couderc ◽  
Sefan Kaab ◽  
Martin Hinterseer ◽  
Scott McNitt ◽  
Anthony Fossa ◽  
...  

Background: Assessing propensity to torsades de pointes (TdP) when exposed to QT-prolonging drug is challenging because baseline QT-prolongation has limited predictive value for identifying risk of TdP. The aim of this study was to determine whether computer-based repolarization morphology parameters could identify individuals who developed drug-induced TdP. Method: Five-minute standard digital 12-lead ECGs were acquired at baseline and after a controlled sotalol challenge (2 mg/kg BW, i.v.) in 34 cardiac patients of whom 17 had a history of TdP (+TdPs) in the context of a QT prolonging drug and 17 had no history of TdP (-TdPs).Computerized ECG parameters including QT, TpTe (T peak to T end interval) and a morphological measure of the duration of the early part of the repolarization interval (ERD) were implemented. All parameters were corrected for the effect of heart rate (HR). Results: There were 9 females among the + TdP patients and 12 females in the -TdP group (p = 0.8). The drugs triggering TdPs were: antidepressant, antibiotics, antiarrhythmic and anti-migraine. They included sotalol, amiodarone, bisacodyl, erythromycin, imipramime, cipramil and sumatriptan. The table below shows the comparison of baseline values and the on-sotalol changes of the repolarization parameters after HR correction. The analysis revealed a longer QT interval duration at baseline in patient +TdPs. This prolongation was only present in the early part of the T-wave (ERD, p = 0.02). On sotalol, the patients with a history of TdPs have longer QT prolongation associated with a significant increased late part of the repolarization (TpTe, p = 0.01). Conclusion : Our results revealed that specific repolarization features are present at baseline and on sotalol challenge in patients with and without history of TdPs. These parameters could complement the role of the QT prolongation as a proarrhythmic surrogate marker. Baseline values and sotalol-induced changes in ECG parameters


QJM ◽  
2007 ◽  
Vol 100 (10) ◽  
pp. 609-615 ◽  
Author(s):  
A. Chan ◽  
G.K. Isbister ◽  
C.M.J. Kirkpatrick ◽  
S.B. Dufful

Heart ◽  
2003 ◽  
Vol 89 (11) ◽  
pp. 1363-1372 ◽  
Author(s):  
Y. G. Yap

2020 ◽  
Vol 31 (10) ◽  
pp. 2696-2701
Author(s):  
Philipp Krisai ◽  
Konstantinos Vlachos ◽  
F. Daniel Ramirez ◽  
Yosuke Nakatani ◽  
Takashi Nakashima ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Paul Singh ◽  
J. Martin Maldonado-Duran

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.


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