Recurrent Ventricular Arrhythmia Caused by Ingestion of <i>Aconitum</i> (Monkshood) Flowers

Adami, Fernando; Paganussi, Peter; Perone, Giovanna; Bera, Paola; Braga, Giosuè; Concoreggi, C.

doi:10.1016/j.wem.2018.05.001

Cited by 5 publications

(5 citation statements)

References 11 publications

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“…Aconitum is a genus of over 300 species of plants that produce toxic alkaloids, including aconitine, mesaconitine, and hypaconitine, that can be found throughout the plant but are most abundant in the roots and root tubers. 1,2 Toxic effects of aconitine are due to effects on voltage-sensitive sodium channels on myocardial and neuronal cell membranes. Aconitine binds the open gates of these channels, leading to sustained sodium influx and delayed repolarization; this initiates premature excitation and can induce tachydysrhythmias.…”

Section: Discussionmentioning

confidence: 99%

Stir Fry with a Side of Extracorporeal Membrane Oxygen: Management of Cardiogenic Shock Secondary to Unintentional Aconitine Ingestion

Goumeniouk,

Maclean,

Howie

et al. 2023

Wilderness & Environmental Medicine

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Plant exposures leading to systemic or topical toxicity are common presentations seen in the emergency department. While often nonfatal, certain highly toxic plants result in cardiovascular or respiratory failure requiring invasive management. We describe a 65-y-old patient who presented with a refractory ventricular dysrhythmia secondary to an unintentional ingestion of an aconitine-containing plant after incorrect identification. Despite aggressive treatment with vasopressors, intravenous fluids, antiarrhythmics, as well as electrolyte correction and multiple attempted synchronized cardioversions, the patient remained in a refractory dysrhythmia with cardiogenic shock. Venoarterial extracorporeal membrane oxygen (ECMO) therapy was initiated successfully and resulted in rapid resolution of the unstable dysrhythmia. The patient was weaned from ECMO in under 48 h and was discharged without neurological or cardiovascular sequelae. This case highlights management options available to clinicians who encounter toxicity associated with aconitine ingestion. Fatal consequences were averted, and caution is required with the use of plant-identifying applications and resources.

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Section: Discussionmentioning

confidence: 99%

Stir Fry with a Side of Extracorporeal Membrane Oxygen: Management of Cardiogenic Shock Secondary to Unintentional Aconitine Ingestion

Goumeniouk,

Maclean,

Howie

et al. 2023

Wilderness & Environmental Medicine

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“…4,5 The aconite toxidrome typically begins within 2 hours after oral ingestion and progresses to include symptoms that predominantly involve the cardiovascular, 1). [5][6][7] It is believed to cause potentially lethal toxicity by binding to and maintaining the sodium channels in an open position, which renders them refractory to repolarization. The cardiotoxicity of aconitine is significantly associated with increased mortality, with most deaths occurring secondary to refractory ventricular arrhythmias and asystole.…”

Section: Discussionmentioning

confidence: 99%

Aconite Poisoning–Induced Ventricular Arrhythmia

Gupta¹,

Alcantara²,

Ranchal³

et al. 2020

American Journal of Therapeutics

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“…However, its severe toxicity limits the clinical use even after being processed (He et al, 2023). Heart is the most vulnerable organ suffering from Fuzi with 5.5% mortality caused by ventricular arrhythmia (Adami et al, 2018; Chan, 2009). In order to alleviate its toxicity, Fuzi is often combined with Glycyrrhiza uralensis Fisch.…”

Section: Introductionmentioning

confidence: 99%

“…caused by ventricular arrhythmia (Adami et al, 2018;Chan, 2009). In order to alleviate its toxicity, Fuzi is often combined with Glycyrrhiza uralensis Fisch.…”

mentioning

confidence: 99%

Physiologically based pharmacokinetic modeling for confirming the role of CYP3A1/2 and P‐glycoprotein in detoxification mechanism between glycyrrhizic acid and aconitine in rats

Jin,

Xu,

et al. 2024

J of Applied Toxicology

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Fuzi, an effective common herb, is often combined with Gancao to treat disease in clinical practice with enhancing its efficacy and alleviating its toxicity. The major toxic and bioactive compounds in Fuzi and Gancao are aconitine (AC) and glycyrrhizic acid (GL), respectively. This study aims to elucidate detoxification mechanism between AC and GL from pharmacokinetic perspective using physiologically based pharmacokinetic (PBPK) model. In vitro experiments exhibited that AC was mainly metabolized by CYP3A1/2 in rat liver microsomes and transported by P‐glycoprotein (P‐gp) in Caco‐2 cells. Kinetics assays showed that the Km and Vmax of AC towards CYP3A1/2 were 2.38 μM and 57.3 pmol/min/mg, respectively, whereas that of AC towards P‐gp was 11.26 μM and 147.1 pmol/min/mg, respectively. GL markedly induced the mRNA expressions of CYP3A1/2 and MDR1a/b in rat primary hepatocytes. In vivo studies suggested that the intragastric and intravenous administration of GL significantly reduced systemic exposure of AC by 27% and 33%, respectively. Drug–drug interaction (DDI) model of PBPK predicted that co‐administration of GL would decrease the exposure of AC by 39% and 45% in intragastric and intravenous dosing group, respectively. The consistency between predicted data and observed data confirmed that the upregulation of CYP3A1/2 and P‐gp was the crucial detoxification mechanism between AC and GL. Thus, this study provides a demonstration for elucidating the compatibility mechanisms of herbal formula using PBPK modeling and gives support for the clinical co‐medication of Fuzi and Gancao.

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Recurrent Ventricular Arrhythmia Caused by Ingestion of Aconitum (Monkshood) Flowers

Cited by 5 publications

References 11 publications

Stir Fry with a Side of Extracorporeal Membrane Oxygen: Management of Cardiogenic Shock Secondary to Unintentional Aconitine Ingestion

Stir Fry with a Side of Extracorporeal Membrane Oxygen: Management of Cardiogenic Shock Secondary to Unintentional Aconitine Ingestion

Aconite Poisoning–Induced Ventricular Arrhythmia

Physiologically based pharmacokinetic modeling for confirming the role of CYP3A1/2 and P‐glycoprotein in detoxification mechanism between glycyrrhizic acid and aconitine in rats

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