Right ventricular outflow tract tachycardia after an initial dose of amantadine

Kocas, Cuneyt; Türkmen, Yusuf; Çetinkal, Gökhan; Doğan, Sait Mesut

doi:10.5543/tkda.2015.32885

Cited by 3 publications

(3 citation statements)

References 8 publications

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“…There has only been one case of cardiac arrhythmia caused by 200 mg of amantadine in which the patient developed right ventricular outflow tract tachycardia. In this case, the authors attributed the tachycardia to amantadine and its possible effects on the ventricular muscle and sympathetic nervous system [15]. Previously reported cases of cardiac arrhythmias induced by amantadine were all attributed to high doses, with the lowest and highest doses being 600 mg and 12 g, respectively.…”

Section: Discussionmentioning

confidence: 75%

Amantadine-Induced Cardiac Arrest in a Patient With COVID-19

Bakhati¹,

Sibi²,

Mekala³

et al. 2022

Cureus

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Amantadine, which is known for its antiviral activity, is presently used as therapy for Parkinson's disease. Adverse effects, such as cardiac arrhythmias, have been described in patients after ingestion of amantadine. Here, we present a patient who suffered a cardiac arrest following ingestion of a low dose of amantadine.A 71-year-old man was admitted to the emergency department for a witnessed cardiac arrest. He had developed an upper respiratory tract infection the preceding week and was prescribed 100 mg of amantadine. Within half an hour of taking the first dose, the patient collapsed. He was found to be in asystole by emergency medical services, and advanced cardiac life support protocols were initiated, including cardiopulmonary resuscitation and intubation for airway protection. However, he sustained multiple recurrences of cardiac arrest, and despite all resuscitation efforts, the patient expired.

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Section: Discussionmentioning

confidence: 75%

Amantadine-Induced Cardiac Arrest in a Patient With COVID-19

Bakhati¹,

Sibi²,

Mekala³

et al. 2022

Cureus

View full text Add to dashboard Cite

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“…Amantadine hydrochloride is an antagonist of the N -methyl-D-aspartate receptor used to treat influenza A virus, Parkinson’s disease, and dyskinesia. However, cases of acute cardiotoxicity manifested by cardiac arrhythmia such as right ventricular outflow tract tachycardia and QT elongation had been reported in patients after amantadine overdose ( 19 – 21 ). In addition, cases of newborns with complex cardiovascular lesions and ToF and tibial hemimelia associated with maternal exposure to amantadine were also reported ( 6 ).…”

Section: Discussionmentioning

confidence: 99%

An EGFP Knock-in Zebrafish Experimental Model Used in Evaluation of the Amantadine Drug Safety During Early Cardiogenesis

Ouyang

Qin

Niu

et al. 2022

Front. Cardiovasc. Med.

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BackgroundDrug exposure during gestation or in prematurely born children represents a significant risk to congenital heart disease (CHD). Amantadine is an antiviral agent also effective in the treatment of Parkinson’s disease. However, while its potential side effects associated with tetralogy of fallot (ToF) and birth defects were implicated, its underlying etiologic mechanisms of action remain unknown. Here, we report teratogenic effects of amantadine drug during early cardiogenesis through developing a novel zebrafish (Danio rerio) knock-in (KI) animal model and explore the underlying mechanisms.MethodsHomologous recombination (HR) pathway triggered by CRISPR/Cas9 system was utilized to generate an enhanced green fluorescent protein (EGFP) KI zebrafish animal model. Dynamic fluorescence imaging coupled with a whole-mount in-situ hybridization (WISH) assay was employed to compare the spatial and temporal expression patterns of the EGFP reporter in the KI animal model with the KI-targeted endogenous gene. Heart morphology and EGFP expression dynamics in the KI animal models were monitored to assess cardiac side effects of different doses of amantadine hydrochloride. Expression of key genes required for myocardium differentiation and left–right (LR) asymmetry was analyzed using WISH and quantitative reverse transcription-PCR (RT-PCR).ResultsA novel EGFP KI line targeted at the ventricular myosin heavy chain (vmhc) gene locus was successfully generated, in which EGFP reporter could faithfully recapitulate the endogenous expression dynamics of the ventricle chamber-specific expression of the vmhc gene. Amantadine drug treatment-induced ectopic expression of vmhc gene in the atrium and caused cardiac-looping or LR asymmetry defects to dose-dependently during early cardiogenesis, concomitant with dramatically reduced expression levels of key genes required for myocardium differentiation and LR asymmetry.ConclusionWe generated a novel zebrafish KI animal model in which EGFP reports the ventricle chamber-specific expression of vmhc gene dynamics that is useful to effectively assess drug safety on the cardiac morphology in vivo. Specifically, this study identified teratogenic effects of amantadine drug during early cardiogenesis dose dependent, which could be likely conveyed by inhibiting expression of key genes required for cardiac myocardium differentiation and LR asymmetry.

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“…Even though amantadine is considered as a relatively safe drug, it should be used with caution. Amantadine has a potency to cause side effects, sometimes life-threatening [ 19 , 20 ]. Amantadine is frequently self-administered in belief of antiviral effect.…”

Section: Introductionmentioning

confidence: 99%