Drugs that cause torsades de pointes and increase the risk of sudden cardiac death

Wolbrette, Deborah L.

doi:10.1007/s11886-004-0041-8

Cited by 30 publications

(22 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LQTS is characterized by prolongation of action potential duration (APD) and is a risk for SCD attributed to torsades de pointes arrhythmias (Oliveira et al 1999;Wolbrette 2004). APD reflects the balance of total currents through the membrane during repolarization, and is sensitive to the rapid delayed rectifier outward potassium channel (IKr), which is mainly encoded by the hERG gene.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory factors that contribute to upregulation of ERG and cardiac arrhythmias are suppressed by CPU86017, a class III antiarrhythmic agent

Dai

et al. 2008

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

The aim of this study was to verify whether exaggerated arrhythmogenesis is attributed to inflammatory factors actively involving an excess of reactive oxygen species (ROS), transforming growth factor (TGF)-b and endothelin (ET). We hypothesized that CPU86017, derived from berberine, which possesses multi-channel blocking activity, could suppress inflammatory factors, resulting in inhibition of over-expression of ether-a-go-go (ERG) and an augmented incidence of ventricular fibrillation (VF) in ischaemia/reperfusion (I/R). Rats with cardiomyopathy (CMP) induced by thyroxine (0.2 mg −1 kg −1 s.c. daily for 10 days) were treated with propranolol (10 mgkg −1 p.o.) or CPU86017(80 mgkg −1 p.o.) on days 6-10. On the 11th day, arrhythmogenesis of the CMP was evaluated by I/R.In the CMP control group, an increase in VF incidence was found with the I/R episode, accompanied by increased ROS, which manifested as an increased level of malondialdehyde and decreased activities of SOD, glutathione peroxidase and catalase in the myocardium. Levels of inducible nitric oxide synthase and TGF-b mRNA were increased in association with upregulation of preproET-1 and ETconverting enzyme. We found increased levels of ERG, which correlated well with arrhythmogenesis. Treatment with CPU86017 or propranolol reversed these changes. These experiments verified our hypothesis that the inflammatory factors ROS, iNOS, TGF-b and ET-1 are actively involved in upregulation of ERG and arrhythmogenesis. CPU86017 and propranolol reduced VF by suppressing these inflammatory factors in the myocardium.

show abstract

Section: Introductionmentioning

confidence: 99%

Inflammatory factors that contribute to upregulation of ERG and cardiac arrhythmias are suppressed by CPU86017, a class III antiarrhythmic agent

Dai

et al. 2008

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

show abstract

“…Cancer patients commonly face several symptoms which require pharmacologic interventions at once; therefore, it is important to evaluate the patient's medication profile to identify all drugs that may prolong the QT interval. Also, as many of the QT interval prolonging drugs are metabolized by the cytochrome P450 isoenzyme CYP3A4, interaction of these or inhibition of CYP3A4 increases the risk for a life-threatening Tdp [90]. A preexisting structural or vascular heart disease is another risk factor for a clinically relevant prolongation of the QT interval [61,86,[90][91][92].…”

Section: Considerations For Risk Assessmentmentioning

confidence: 99%

“…Also, as many of the QT interval prolonging drugs are metabolized by the cytochrome P450 isoenzyme CYP3A4, interaction of these or inhibition of CYP3A4 increases the risk for a life-threatening Tdp [90]. A preexisting structural or vascular heart disease is another risk factor for a clinically relevant prolongation of the QT interval [61,86,[90][91][92]. Certain chemotherapeutic agents, such as anthracyclines, alkylating agents, fluorouracil, bevacizumab or trastuzumab, and mediastinal radiation treatment can lead to structural heart damage.…”

Section: Considerations For Risk Assessmentmentioning

confidence: 99%

“…Therefore, a continuous monitoring of cardiac function may be necessary even for patients without any past cardiovascular history [14,23,31,40]. Electrolyte disorders, more specifically hypokalemia as well as hypomagnesemia and hypocalcemia, are very common in cancer patients due to malnutrition, polypharmacy, or infusion therapy and increase the risk of Tdp [67,90,93].…”

Section: Considerations For Risk Assessmentmentioning

confidence: 99%

See 1 more Smart Citation

Drug-induced QT interval prolongation in cancer patients

Becker

Yeung

2010

Oncol Rev

View full text Add to dashboard Cite

Cancer patients are at an increased risk for QT interval prolongation and subsequent potentially fatal Torsade de pointes tachycardia due to the multiple drugs used for treatment of malignancies and the associated symptoms and complications. Based on a systematic review of the literature, this article analyzes the risk for prolongation of the QT interval with antineoplastic agents and commonly used concomitant drugs. This includes anthracyclines, fluorouracil, alkylating agents, and new molecularly targeted therapeutics, such as vascular disruption agents. Medications used in the supportive care can also prolong QT intervals, such as methadone, 5-HT 3 -antagonists and antihistamines, some antibiotics, antifungals, and antivirals. We describe the presumed mechanism of QT interval prolongation, drug-specific considerations, as well as important clinical interactions. Multiple risk factors and drug-drug interactions increase this risk for dangerous arrhythmias. We propose a systematic approach to evaluate cancer patients for the risk of QT interval prolongation and how to prevent adverse effects.

show abstract

“…Ventricular dysrhythmias, including ventricular tachycardia (VT), torsade de pointes (TdP) and ventricular fibrillation (VF), have been reported in association with therapeutic use of or overdose by a number of drugs, most commonly antidepressant and antipsychotic agents [1][2][3][4][5]. Published clinical experience regarding ventricular arrhythmias and TdP in drug overdose is derived primarily from single case reports or small case series [6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Ventricular Dysrhythmias Associated with Poisoning and Drug Overdose: A 10-Year Review of Statewide Poison Control Center Data from California

Al-Abri

Woodburn

Olson

et al. 2015

Am J Cardiovasc Drugs

View full text Add to dashboard Cite

Key PointsThe most commonly involved therapeutic classes of drugs associated with ventricular fibrillation and/or tachycardia (VT/VF) were antidepressants (25 %) and stimulants (25 %).The drugs most commonly associated with torsade de pointes (TdP) were antidepressants (25 %) and methadone (25 %).Drug exposures with the greatest risk of death in association with VT/VF were antidepressant exposure [odds ratio (OR) 1.71] and antiarrhythmic exposure (OR 1.75), but neither association was statistically significant.

show abstract

Drugs that cause torsades de pointes and increase the risk of sudden cardiac death

Cited by 30 publications

References 42 publications

Inflammatory factors that contribute to upregulation of ERG and cardiac arrhythmias are suppressed by CPU86017, a class III antiarrhythmic agent

Inflammatory factors that contribute to upregulation of ERG and cardiac arrhythmias are suppressed by CPU86017, a class III antiarrhythmic agent

Drug-induced QT interval prolongation in cancer patients

Ventricular Dysrhythmias Associated with Poisoning and Drug Overdose: A 10-Year Review of Statewide Poison Control Center Data from California

Contact Info

Product

Resources

About