Drug-Induced Prolongation of the QT Interval

Korantzopoulos, Panagiotis; Siogas, Konstantinos

doi:10.1056/nejm200406173502517

Cited by 15 publications

(1 citation statement)

References 12 publications

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“…However, SQTS diagnosis should be based on several findings, including a short QTc interval (≤360 ms in males; ≤370 ms in females) [145,146,147], syncope, episodes of VF or PVT, family history of short QT interval, syncope or VF, occurrence of AF, and no obvious heart disease or extracardiac conditions that abbreviate QT interval [85]. Additionally, there are several other ECG findings that may facilitate the correct diagnosis of SQTS such as the presence of tall, peaked, symmetrical, and narrow-based T waves, prominent U waves [148], depression of the PQ segment [149], or a QRS complex directly followed by a T wave [150].…”

Section: Short Qt Syndromementioning

confidence: 99%

Cardiac Channelopathies and Sudden Death: Recent Clinical and Genetic Advances

Fernández-Falgueras

Sarquella-Brugada

Brugada

et al. 2017

Biology

106

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Sudden cardiac death poses a unique challenge to clinicians because it may be the only symptom of an inherited heart condition. Indeed, inherited heart diseases can cause sudden cardiac death in older and younger individuals. Two groups of familial diseases are responsible for sudden cardiac death: cardiomyopathies (mainly hypertrophic cardiomyopathy, dilated cardiomyopathy, and arrhythmogenic cardiomyopathy) and channelopathies (mainly long QT syndrome, Brugada syndrome, short QT syndrome, and catecholaminergic polymorphic ventricular tachycardia). This review focuses on cardiac channelopathies, which are characterized by lethal arrhythmias in the structurally normal heart, incomplete penetrance, and variable expressivity. Arrhythmias in these diseases result from pathogenic variants in genes encoding cardiac ion channels or associated proteins. Due to a lack of gross structural changes in the heart, channelopathies are often considered as potential causes of death in otherwise unexplained forensic autopsies. The asymptomatic nature of channelopathies is cause for concern in family members who may be carrying genetic risk factors, making the identification of these genetic factors of significant clinical importance.

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Section: Short Qt Syndromementioning

confidence: 99%

Cardiac Channelopathies and Sudden Death: Recent Clinical and Genetic Advances

Fernández-Falgueras

Sarquella-Brugada

Brugada

et al. 2017

Biology

106

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Validation of visualized transgenic zebrafish as a high throughput model to assay bradycardia related cardio toxicity risk candidates

Wen

Liu

Chen³

et al. 2012

J of Applied Toxicology

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Drug-induced QT prolongation usually leads to torsade de pointes (TdP), thus for drugs in the early phase of development this risk should be evaluated. In the present study, we demonstrated a visualized transgenic zebrafish as an in vivo high-throughput model to assay the risk of drug-induced QT prolongation. Zebrafish larvae 48 h post-fertilization expressing green fluorescent protein in myocardium were incubated with compounds reported to induce QT prolongation or block the human ether-a-go-go-related gene (hERG) K⁺ current. The compounds sotalol, indapaminde, erythromycin, ofoxacin, levofloxacin, sparfloxacin and roxithromycin were additionally administrated by microinjection into the larvae yolk sac. The ventricle heart rate was recorded using the automatic monitoring system after incubation or microinjection. As a result, 14 out of 16 compounds inducing dog QT prolongation caused bradycardia in zebrafish. A similar result was observed with 21 out of 26 compounds which block hERG current. Among the 30 compounds which induced human QT prolongation, 25 caused bradycardia in this model. Thus, the risk of compounds causing bradycardia in this transgenic zebrafish correlated with that causing QT prolongation and hERG K⁺ current blockage in established models. The tendency that high logP values lead to high risk of QT prolongation in this model was indicated, and non-sensitivity of this model to antibacterial agents was revealed. These data suggest application of this transgenic zebrafish as a high-throughput model to screen QT prolongation-related cardio toxicity of the drug candidates.

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Current awareness: Pharmacoepidemiology and drug safety

2004

Pharmacoepidemiology and Drug

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In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of pharmacoepidemiology and drug safety. Each bibliography is divided into 19 sections: 1 Books, Reviews & Symposia; 2 General; 3 Anti‐infective Agents; 4 Cardiovascular System Agents; 5 CNS Depressive Agents; 6 Non‐steroidal Anti‐inflammatory Agents; 7 CNS Agents; 8 Anti‐neoplastic Agents; 9 Haematological Agents; 10 Neuroregulator‐Blocking Agents; 11 Dermatological Agents; 12 Immunosuppressive Agents; 13 Autonomic Agents; 14 Respiratory System Agents; 15 Neuromuscular Agents; 16 Reproductive System Agents; 17 Gastrointestinal System Agents; 18 Anti‐inflammatory Agents ‐ Steroidal; 19 Teratogens/fetal exposure; 20 Others. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted.

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Drug-Induced Prolongation of the QT Interval

Cited by 15 publications

References 12 publications

Cardiac Channelopathies and Sudden Death: Recent Clinical and Genetic Advances

Cardiac Channelopathies and Sudden Death: Recent Clinical and Genetic Advances

Validation of visualized transgenic zebrafish as a high throughput model to assay bradycardia related cardio toxicity risk candidates

Current awareness: Pharmacoepidemiology and drug safety

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