Delayed cardiotoxicity in venlafaxine and quetiapine overdose

Hertzog, Tatiana; Cetran, Laura; Labadie, Magali; Bragança, Coralie; Goncalves, Ruben

doi:10.1080/15563650.2021.1914341

Cited by 4 publications

(1 citation statement)

References 3 publications

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“…A venlafaxine overdose may result in encephalopathy, consciousness impairment, seizures, metabolic disturbances, rhabdomyolysis, and serotoninergic syndrome. Life-threatening cardiotoxicity may occur from sodium channel blockage (membrane stabilizing activity), leading to QT prolongation and QRS widening on the electrocardiogram, ventricular arrhythmia, and cardiac failure [ 12 , 13 , 14 , 15 ]. Besides gastrointestinal decontamination if indicated, its management relies on mechanical ventilation, 8.4% sodium bicarbonate, inotropic drugs, and vasopressors, and may require veno-arterial extracorporeal membrane oxygenation (ECMO) in the rare cases of refractory cardiac failure or arrest [ 16 , 17 , 18 , 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Life-Threatening Cardiogenic Shock Related to Venlafaxine Poisoning—A Case Report with Metabolomic Approach

et al. 2023

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Metabolomics in clinical toxicology aim at reliably identifying and semi-quantifying a broad array of endogenous and exogenous metabolites using dedicated analytical methods. Here, we developed a three-step-based workflow to investigate the metabolic impact of the antidepressant drug venlafaxine in a poisoned patient who developed life-threatening cardiac failure managed with extracorporeal membrane oxygenation. Both targeted quantitative and untargeted semi-quantitative metabolomic analyses using liquid chromatography hyphenated to high-resolution tandem mass spectrometry were performed to determine the plasma kinetics of venlafaxine, O-desmethyl-venlafaxine, and N-desmethyl-venlafaxine and to identify sixteen different venlafaxine-derived metabolites including one unknown (i.e., venlafaxine conjugated to a hexosyl-radical), respectively. Correlations between the quantitative metabolomic data and annotated endogenous metabolites suggested impaired amino acid and lipid metabolism, Krebs cycle, and kynurenine pathway. This preliminary study represents a first step towards a more extensive application of toxicometabolomics in clinical toxicology and a useful workflow to identify the biomarkers of toxicity.

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