Sotalol unmasks susceptibility to drug-induced long QT syndrome and torsades de pointes

Letsas, Κonstantinos P.; Efremidis, Michael; Sideris, Antonios

doi:10.1016/j.ijcard.2007.01.061

Cited by 6 publications

(4 citation statements)

References 7 publications

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“…Yalta et al [81] reported a case with a severely prolonged QT interval and TdP after an initial intake of low dose sotalol (80 mg), indicating a probable inherent individual oversensitivity to sotalol. Letsas et al [82], regarding this last report, suggested that pharmacologic challenge with sotalol may successfully identify patients with normal QTc intervals and reduced repolarization reserve that are at increased risk to develop drug-induced long QT syndrome and TdP.…”

Section: Class III Antiarrhythmic Drugsmentioning

confidence: 96%

Cardiovascular Drugs Inducing QT Prolongation: Facts and Evidence

Taira¹,

Opezzo²,

Mayer³

et al. 2010

CDS

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Acquired QT syndrome is mainly caused by the administration of drugs that prolong ventricular repolarization. On the other hand, the risk of drug-induced torsades de pointes is increased by numerous predisposing factors, such as genetic predisposition, female sex, hypokalemia and cardiac dysfunction. This adverse reaction is induced by different chemical compounds used for the treatment of a variety of pathologies, including arrhythmias. As it is known, antiarrhythmic agents and other cardiovascular drugs can prolong the QT interval, causing this adverse reaction. Of the 20 most commonly reported drugs, 10 were cardiovascular agents and these appeared in 348 of the reports (46%). Class Ia antiarrhythmic agents have frequently been linked to inducing arrhythmia, including torsades de pointes. Sotalol and amiodarone, class III antiarrhythmics, are known to prolong the QT interval by blocking I(Kr). Due to the severity of events caused by the therapeutic use of these drugs, in this work of revision the cardiovascular drugs that present this property and the factors and evidence will be mentioned.

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Section: Class III Antiarrhythmic Drugsmentioning

confidence: 96%

Cardiovascular Drugs Inducing QT Prolongation: Facts and Evidence

Taira¹,

Opezzo²,

Mayer³

et al. 2010

CDS

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“…All known antifungal triazoles may cause QTP directly by blocking IKR channels, and by inhibiting cytochrome P450-dependent metabolism of other drugs that can cause QTP (15). Antifungal drugs are often co-administered with other drugs, and polypharmacy is a risk factor for drug interactions (35). Therefore, patients who are receiving multiple P450 isoform inhibitors or arrhythmia inducers should be monitored closely; the more concomitant medications used, the greater is the possibility of pharmacokinetic and pharmacodynamic interactions (36).…”

Section: Discussionmentioning

confidence: 99%

Association of Torsade de Pointes and QT Prolongation With Antifungal Triazoles: Analysis Using a Pharmacovigilance Database

OHYAMA,

AKIYAMA,

IIDA

et al. 2023

In Vivo

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Background/Aim: Torsade de pointes (TdP)/QT prolongation (QTP) is one of the most life-threatening adverse effects of antifungal triazoles. The aim of the present study was to evaluate the association of antifungal triazoles with TdP/QTP by age group and the profile of the time of TdP/QTP onset by analyzing the spontaneous adverse event database for Japan. Patients and Methods: Data registered in the Japanese Adverse Drug Event Report database (JADER) from April 2004 to March 2022 were analyzed. The association between the administration of antifungal triazoles and TdP/QTP according to age was evaluated using an adjusted reporting odds ratio (aROR). In addition, the time-to-onset of TdP/QTP after antifungal triazole treatment was analyzed using the Weibull distribution according to the route of administration. Results: Antifungal triazole treatment was associated with TdP/QTP (aROR=1.77, 95% confidence interval=1.52-2.07). In the subgroup analyses by age group, antifungal triazole treatments in patients ≤29 years old and ≥50 (except ≥90) years old were associated with TdP/QTP. The medians (quartiles) of time-to-onset for intravenous and oral antifungal triazole treatment were 8 (6-12) and 23 (8-86) days, respectively. In addition, the shape parameter in the Weibull distribution analysis of oral triazole treatment revealed that the hazard exhibited an early failure profile. Conclusion: TdP/QTP is associated with antifungal triazoles even in young patients, and patients should be monitored for the development of TdP/QTP, especially early after the initiation of treatment.

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“…Could a drug challenge with a QT prolonging drug58 59 unmask a malignant phenotype in asymptomatic patients carrying a QT prolonging associated mutation?…”

Section: Discussionmentioning

confidence: 99%

Post-acute management of the acquired long QT syndrome

Barra

Agarwal

Begley

et al. 2014

Postgraduate Medical Journal

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The mechanisms underlying drug induced QT prolongation and the immediate treatment of torsade de pointes have been extensively studied but the post-acute management of the Acquired Long QT Syndrome (ALQTS) remains to be addressed. We aimed to review the state of the art data regarding risk stratification, arrhythmic prevention and treatment of patients with ALQTS. A comprehensive review of the scientific data collectable from MEDLINE, EMBASE and COCHRANE (from inception to April 2013) was performed, and descriptive and qualitative information was extracted from the most relevant manuscripts. QT prolonging drugs are widely used in hospital clinical practice, and several studies have shown a high prevalence of QT interval prolongation in patients admitted to hospital and a high rate of prescription of QT interval prolonging drugs to patients presenting with QT interval prolongation. Therefore, the acute and post-acute management of ALQTS is of the utmost importance. Avoidance of offending triggers, electrocardiographic screening, pacing at a relatively fast lower rate limit and using pause prevention programming (preferably with concomitant β blocker treatment), implantable defibrillators in the highest risk patients, genetic testing and counselling in selected cases, and family screening are among the potentially applicable strategies. The latter is justifiable by the fact that some studies unveiled a surprisingly similar positive mutation rate in drug induced LQTS compared with congenital LQTS, supporting the hypothesis that the former can be regarded as a latent form of the latter. Drug challenge with D,L-sotalol in suspected LQTS and treatment with a carvedilol analogue, verapamil or an Ikr activating drug are still in need of further investigation. The post-acute management of patients with ALQTS has received scarce attention in the past, probably due to the fact that it is considered a reversible phenomenon in most cases. Considering the relatively high risk of arrhythmic recurrence in the highest risk ALQTS patients, effective preventive and treatment strategies are warranted, and further research is needed.

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Sotalol unmasks susceptibility to drug-induced long QT syndrome and torsades de pointes

Cited by 6 publications

References 7 publications

Cardiovascular Drugs Inducing QT Prolongation: Facts and Evidence

Cardiovascular Drugs Inducing QT Prolongation: Facts and Evidence

Association of Torsade de Pointes and QT Prolongation With Antifungal Triazoles: Analysis Using a Pharmacovigilance Database

Post-acute management of the acquired long QT syndrome

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