Basic Cardiac Electrophysiology and Common Drug-induced Arrhythmias

Lee, Aimee; Pickham, David

doi:10.1016/j.cnc.2016.04.007

Cited by 11 publications

(8 citation statements)

References 36 publications

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“…Sudden cardiac death (SCD) occurs in about 800,000 people every year, abnormal ventricular repolarisation-induced malignant centricular arrhythmia (MVA) is the most common reason for SCD in clinical practice [20]. Numerous drugs can trigger MVA including antibiotics [5]. Milberg et al [21] suggested that all antibiotics can trigger abnormal ventricular repolarisation and prolong the QT interval [21].…”

Section: Discussionmentioning

confidence: 99%

“…Easily affected by HR, QT is generally represented by using a corrected QT (QTc) interval [14]. QT or QTc interval prolongation is frequently used to evaluate the risk of endogenous TdP with various drugs [5, 14]. When depolarisation is prolonged (QRS ≥120 ms), the QT interval is also prolonged so that a single prolongation of repolarisation time cannot cause arrhythmia [24].…”

Section: Discussionmentioning

confidence: 99%

“…It is reported that antibiotics can prolong QT and QTc intervals [4–6]. Prolongation of the QT interval increases transmural dispersion of repolarisation (TDR) of the ventricle, probably increasing the risk of arrhythmia risk [5]. A case report indicates that antibiotics can lead to torsade de pointes [7].…”

Section: Introductionmentioning

confidence: 99%

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A Comparison of the Effect of Sevoflurane and Propofol on Ventricular Repolarisation after Preoperative Cefuroxime Infusion

Gao

Wang

et al. 2019

BioMed Research International

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The aim of this study is to investigate the changes in QT, QTc, and Tp-e intervals and Tp-e/QT ratio on surface electrocardiogram (ECG) signals during anaesthesia induction using propofol or sevoflurane after preoperative cefuroxime infusion. Some 120 cases of gynaecological patients are randomly divided into propofol (P) and sevoflurane (S) groups (n=60). After cefuroxime (1.5 g) was infused in the two groups of patients, propofol target controlled infusion (TCI) was conducted in the P group for 5 min to realise a plasma concentration of 4 μg/ml while patients in the S group inhaled anaesthesia by infusing 1.3 MAC sevoflurane for 6 min. The 12-lead ECGs were separately collected before infusing cefuroxime (T1), after infusing cefuroxime (T2), and after infusing propofol or sevoflurane (T3) to measure QT and Tp-e intervals, calculate QTc and Tp-e/QT, and record MAP and HR. Finally, we demonstrated that QT, QTc, and Tp-e intervals and Tp-e/QT ratio had no change (P > 0.05) after cefuroxime infusion in the two groups of patients compared with that before infusing antibiotics. Moreover, after conducting preoperative cefuroxime infusion, using propofol and sevoflurane had no influence on Tp-e interval, but sevoflurane can significantly prolong QT and QTc intervals (P < 0.05).

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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A Comparison of the Effect of Sevoflurane and Propofol on Ventricular Repolarisation after Preoperative Cefuroxime Infusion

Gao

Wang

et al. 2019

BioMed Research International

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“…During the plateau phase (phase 2) of the AP, characterized by a balance between inward calcium and outward potassium ions, a high concentration of intracellular calcium contributes to a cascade of actions that generate the mechanical contraction of myocardial cells [27]. The outward potassium current (I to ) can modulate contractility by regulating calcium ion transient amplitudes and kinetics [28].…”

Section: Discussionmentioning

confidence: 99%

The protective effect of Er-Xian decoction against myocardial injury in menopausal rat model

Zhang

Xiang

Zhao

et al. 2018

BMC Complement Altern Med

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BackgroundEr-Xian decoction (EXD), a formula of Chinese medicine, is often used to treat menopausal syndrome in China. The aim of the present study was to explore the potential cardioprotective mechanism of EXD against myocardial injury in an ovariectomy-induced menopausal rat model.MethodsWe divided the female Wistar rats into ovariectomy group and sham operation group (SHAM group). The ovariectomized (OVX) rats received treatment of vehicle (OVX group), EXD (EXD group) or 17β-estradiol (E2 group). After 12-week of treatment, the level of estradiol in serum was detected using an electrochemiluminescence immunoassay, and electrophysiologic changes in myocardial action potentials (AP) were evaluated using intracellular microelectrode technique. Changes in the histopathology of the left ventricle and the ultrastructure of the cardiomyocytes were observed by hematoxylin and eosin (HE) staining and transmission electronmicroscopy to assess myocardial injury. Microarrays were applied for the evaluation of gene expression profiles in ventricular muscle of the OVX and EXD rats. Further pathway analyses of the differential expression genes were carried out using the Kyoto Encyclopedia of Genes and Genomes (KEGG). And real-time quantitative RT-PCR (qRT-PCR) was used for verification of the key findings.ResultsThe results from electrophysiological and histomorphological observations demonstrated that EXD had a substantial myocardial protective effect. The EXD-treated rats, in comparison with the OVX rats, demonstrated up-regulated expression of 28 genes yet down-regulated expression of 157 genes in the ventricular muscle. The qRT-PCR assay validated all selected differential expression genes. The KEGG pathway analysis showed that the down-regulated genes were relevant to cardiomyopathy and myocardial contractility. EXD could decrease the mRNA expressions of cardiac myosin (Myh7, Myl2) and integrin (Itgb5) in the ventricular myocardium.ConclusionEXD had a protective effect against myocardial injury in OVX rats, and this cardioprotective effect may be associated with modulation of the expression of cardiac myosin or integrin at the mRNA level.Electronic supplementary materialThe online version of this article (10.1186/s12906-018-2311-9) contains supplementary material, which is available to authorized users.

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“…1,3,5 En 1966 el cardiólogo francés Dessertenne describió el patrón electrocardiográfico de la TV al cual nombró torsión de puntas y lo asoció con prolongación del intervalo QT; después en 1970 y 1980 se asoció con agentes antiarrítmicos como la quinidina, disopiramida y procainamida, hasta los medicamentos actuales que conforman grupos como antihistamínicos, antibióticos, opiáceos, antifúngicos, quimioterapéuticos e hipolipemiantes. 1,6,7 La agencia europea de medicamentos (EMA) y la administración de alimentos y medicamentos de EE.UU (FDA) encontraron que 38 medicamentos son reconocidos por su potencial de causar TdP, mientras que 72 prolongan el intervalo QT 1 , dividiéndolos en cuatro categorías con potencial "torsadogénico", las cuales son: con riesgo conocido de TdP, posible riesgo de TdP, riesgo condicional de TdP y medicamentos que se deben evitar en pacientes con síndrome de QT largo (tabla 1). 4,6…”

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Cardiotoxicidad inducida por fármacos: síndrome de QT prolongado con potencial arritmogénico

Benavides

2020

Repert. Med. Cir.

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Introducción: el uso de medicamentos que prolonguen el QT aumenta el riesgo de arritmias cardiacas especialmente taquicardia ventricular polimórfica tipo torsión de puntas (TdP) provocando estancias hospitalarias prolongadas, consulta a servicios de urgencias o incluso la muerte; lo que hace importante conocerlos para prevenir este tipo de reacciones adversas incluso antes de la prescripción del medicamento. Objetivo: esta revisión está enfocada en medicamentos de uso común tanto hospitalaria como ambulatoriamente que puedan producir prolongación del QT y TdP, el mecanismo por el cual se desarrollan este tipo de comorbilidades, los factores de riesgo en el paciente, el enfoque para su prevención y en caso de que se presenten como debe ser su manejo. Conclusión: los medicamentos que pueden causar prolongación del QT deben ser identificados y debidamente estudiados por parte del personal hospitalario y ambulatorio para de esta manera evitar reacciones adversas.

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Basic Cardiac Electrophysiology and Common Drug-induced Arrhythmias

Cited by 11 publications

References 36 publications

A Comparison of the Effect of Sevoflurane and Propofol on Ventricular Repolarisation after Preoperative Cefuroxime Infusion

A Comparison of the Effect of Sevoflurane and Propofol on Ventricular Repolarisation after Preoperative Cefuroxime Infusion

The protective effect of Er-Xian decoction against myocardial injury in menopausal rat model

Cardiotoxicidad inducida por fármacos: síndrome de QT prolongado con potencial arritmogénico

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