Drug-Induced Arrhythmia

Heist, E. Kevin; Ruskin, Jeremy N.

doi:10.1161/circulationaha.109.894725

Cited by 98 publications

(77 citation statements)

References 94 publications

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“…Spinner et al [5] The QT interval prolongation related to loperamide has been attributed to inhibition of the human ether-a-go-go-related gene (hERG) responsible for the rapid delayed rectifier potassium current (Ikr); a known mechanism of many QT interval prolonging drugs as well as congenital long QT syndrome type 2 (LQTS2) [3,[9][10][11]. This current mediates cardiac myocyte repolarization and terminates the action potential; hERG inhibition leads to delayed repolarization, predisposes to early after-depolarizations (EADs), heterogeneous myocardial repolarization, and TdP [10].…”

Section: Discussionmentioning

confidence: 99%

“…This current mediates cardiac myocyte repolarization and terminates the action potential; hERG inhibition leads to delayed repolarization, predisposes to early after-depolarizations (EADs), heterogeneous myocardial repolarization, and TdP [10]. Drug-mediated slowing of cardiac depolarization (QRS complex prolongation) has also been associated with ventricular arrhythmias particularly with the use of Class IC antiarrhythmic drugs in patients with infarcted or ischemic myocardium [11]. Further, Class IC antiarrhythmic agents are known to cause bradyarrhythmias such as junctional or ventricular escape.…”

Section: Discussionmentioning

confidence: 99%

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Conduction Disturbances and Ventricular Arrhythmias Associated with High- Dose Loperamide

Leung

Altshuler²,

Goldenberg³

et al. 2016

J Clinic Toxicol

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Although loperamide has been widely used for the treatment of diarrhea, there is growing popularity over its abuse potential in alleviating opioid-withdrawal symptoms and achieving euphoria. Toxic levels of loperamide have been associated with life-threatening ventricular tachyarrhythmias and cardiac arrest. We report a case of high-dose loperamide ingestion in a patient presenting initially with unstable bradycardia followed by episodes of polymorphic ventricular tachycardia, and an unmasked Brugada ECG pattern. This is the first such report of the Brugada pattern being unmasked on ECG with loperamide ingestion. The patient stabilized with supportive care without the need for inotropic support. We discuss potential mechanisms of toxicity leading to conduction abnormalities and provide a literature review of all published cases of loperamide toxicity to describe proposed treatment options. Recognition of the abuse potential and hazards of this over-the-counter anti-diarrheal therapy will alert the clinician of associated toxidromes and management strategies.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Conduction Disturbances and Ventricular Arrhythmias Associated with High- Dose Loperamide

Leung

Altshuler²,

Goldenberg³

et al. 2016

J Clinic Toxicol

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“…3 Excessive QT prolongation can lead to the development of early after-depolarisations that can then trigger severe polymorphic ventricular tachycardia or Torsades de Pointes (TdP). If TdP is rapid or prolonged, it can lead to ventricular fibrillation or arrhythmia.…”

Section: Discussionmentioning

confidence: 99%

“…Research has demonstrated that an SCN5A promoter polymorphism common in Asians modulates the duration of the PR and QRS intervals, thereby altering the action potential. 3 Cabergoline is absorbed from the gastrointestinal tract within 0.5 to 4 h 2 and has an average elimination half-life of 65 h that may provide continuous dopaminergic stimulation when administered once daily. 8 Although the patient had delayed onset of symptoms, the long elimination half-life of cabergoline may contribute to its prolonged duration of action and persistence of symptoms even after drug withdrawal, as observed in our patient.…”

Section: Discussionmentioning

confidence: 99%

Cabergoline Induced Supraventricular Tachycardia with QT Prolongation

Menon¹,

Gaddipati²,

Venkatesh³

et al. 2017

IJOPP

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Background:Cabergoline is commonly known to cause valvular disorders. Cases of supraventricular tachycardia with QT prolongation are seen, albeit, extremely rare. Aim: We report a case of supraventricular tachycardia with QT prolongation presumed secondary to cabergoline use. Clinical Details: A 30-year-old post-partal female complained of palpitation and syncope after two days of cabergoline usage. Her past medical history was insignificant. Electrocardiogram showed QT prolongation of 489 ms. Based on her presentation, we presume that the patient's condition was the result of cabergoline. Outcomes: Causality assessment was suggestive of a probable relationship between the patient's symptoms and her use of cabergoline. Symptoms improved significantly after the offending drug was withdrawn with an objective reduction in QTc. Conclusion: Electrocardiogram should be monitored in individuals receiving more than one QT prolonging medication or with symptoms of arrhythmia or are at high risk of QT prolongation/Torsades de Pointes.

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“…Genetic mutations (Shah et al, 2005), post-translational modification (Hund and Mohler, 2014), and drug binding (Heist and Ruskin, 2010) perturb these movements to alter channel function, causing or preventing deadly cardiac arrhythmias. Despite much progress in understanding how channels sense voltage and selectively allow ions to cross into and out of the cell, the conformational changes that determine AP dynamics are not welldefined.…”

Section: Introduction To Voltage-clamp Fluorometrymentioning

confidence: 99%

Molecular motions that shape the cardiac action potential: Insights from voltage clamp fluorometry

Zhu

Varga

Silva

2016

Progress in Biophysics and Molecular Biology

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Very recently, voltage-clamp fluorometry (VCF) protocols have been developed to observe the membrane proteins responsible for carrying the ventricular ionic currents that form the action potential (AP), including those carried by the cardiac Na þ channel, Na V 1.5, the L-type Ca 2þ channel, Ca V 1.2, the Na þ /K þ ATPase, and the rapid and slow components of the delayed rectifier, K V 11.1 and K V 7.1. This development is significant, because VCF enables simultaneous observation of ionic current kinetics with conformational changes occurring within specific channel domains. The ability gained from VCF, to connect nanoscale molecular movement to ion channel function has revealed how the voltage-sensing domains (VSDs) control ion flux through channel pores, mechanisms of post-translational regulation and the molecular pathology of inherited mutations. In the future, we expect that this data will be of great use for the creation of multi-scale computational AP models that explicitly represent ion channel conformations, connecting molecular, cell and tissue electrophysiology. Here, we review the VCF protocol, recent results, and discuss potential future developments, including potential use of these experimental findings to create novel computational models.

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Drug-Induced Arrhythmia

Cited by 98 publications

References 94 publications

Conduction Disturbances and Ventricular Arrhythmias Associated with High- Dose Loperamide

Conduction Disturbances and Ventricular Arrhythmias Associated with High- Dose Loperamide

Cabergoline Induced Supraventricular Tachycardia with QT Prolongation

Molecular motions that shape the cardiac action potential: Insights from voltage clamp fluorometry

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