Spectrum of cardiac manifestations from aconitine poisoning

Karturi, Swetha; Gudmundsson, Hjalti; Akhtar, Masood; Jahangir, Arshad; Choudhuri, Indrajit

doi:10.1016/j.hrcr.2016.05.007

Cited by 7 publications

(9 citation statements)

References 12 publications

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“…The binding of these alkaloids promotes persistent opening of the Na + channel through suppressing conformational changes to the inactive state [25,26]. Prolongation of the open state of Na + channels and late Na + current leads to an increase in intracellular Na + , with subsequent membrane depolarization and the duration of action potential, referred to as early afterdepolarization.…”

Section: Discussionmentioning

confidence: 99%

“…Prolongation of the open state of Na + channels and late Na + current leads to an increase in intracellular Na + , with subsequent membrane depolarization and the duration of action potential, referred to as early afterdepolarization. The increase in intracellular Na + favors an increase in intracellular Ca 2+ through the activation of the Ca 2+ /Na + bidirectional exchanger and the release of intracellular Ca 2+ stored in the sarcoplasmic reticulum [18,25,26]. Aconitine has also been shown to block the potassium channels responsible for rapid and ultra-rapid delayed rectifier currents, which can result in further prolongation of the action potential [15,25,27].…”

Section: Discussionmentioning

confidence: 99%

“…Higher concentrations of aconitine suppress action potential transmission by continuous opening of the Na + channel, which reduces the release of acetylcholine at the axonal end terminus and the vagotonic effects at the myocardium [18,25]. The bradycardia and hypotensive manifestations can be explained by activation of the ventromedial nucleus of the hypothalamus associated with depression of the circulatory system and inhibition of L-type calcium channel currents that serve as a major driver of pacemaker monocytes [18,21,25,26,27]. These complex electrophysiological mechanisms generate self-excitatory abnormal microcircuits within the cardiac and nervous systems, which can trigger cardiovascular features such as arrhythmia, conduction blocks, bradycardia and asystole [18,25].…”

Section: Discussionmentioning

confidence: 99%

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Bradycardia and Hypotension from Improper Use of Aconite Root: A Case Report and Brief Review

et al. 2018

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Background: Adverse reactions associated with Chinese herbal medicines (CHMs) are usually the result of unpredictable active/toxic ingredients, inaccurate or mistaken beliefs, or poor supervision. The herb that most commonly induces severe adverse effects in Hong Kong and China is aconite root. More than 200 species of Aconitum plants are used for medicinal purposes, with aconite roots producing analgesic, anti-inflammatory, cardiotonic, and anti-tumor effects. The active components are alkaloids; these can be toxic, but CHM processing methods lower their toxicity and increase the pharmacological efficacy. However, aconite poisoning can result from inadequate decoction time or exceeding the recommended dose. Case Report: Here we report the case of a 92-year-old woman who presented with life-threatening bradycardia and hypotension. This started 1 h after she inappropriately consumed a herbal decoction containing Fuzi for mood fluctuation and health maintenance; Fuzi, an aconite root, has known cardiotoxicity. Electrocardiography showed supraventricular abnormalities, including sinus bradycardia and low-amplitude P waves. After an infusion of normal saline and inotropic agents for 25 h, the clinical manifestations subsided, her sinus rhythm returned to normal, and she was discharged. At follow-up 2 weeks later, she was in good health and had ceased taking any CHM. Conclusions: Standardized processing methods, stringent regulations, and cooperation between health professions can ensure medication safety and establish a fully-fledged operating process for these valuable drugs. We hope this report will help establish correct attitudes toward CHM and will assist Traditional Chinese Medicine practitioners to become more familiar with Aconitum plants.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Bradycardia and Hypotension from Improper Use of Aconite Root: A Case Report and Brief Review

et al. 2018

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“…The risk substances of cardiotoxicity caused by CMM, such as arsenic trioxide, berberine, hypaconitine, aconitine, and strychnine, usually induce the prolongation of APD and QT/QTc interval, thus causing various arrhythmias, abnormal cardiac systolic, and other adverse reactions ( Wang et al, 2008 ; Chen et al, 2010 ; Zhang et al, 2014 ; Xie et al, 2015 ; Wang et al, 2018 ). Aconitine not only triggered sinus rhythm with low-amplitude P waves and junctional rhythm conducting with narrow QRS complex but also presented diffuse ST-segment depression and the prolongation of QT interval ( Karturi et al, 2016 ). Aconitine and Venenum Bufonis disrupted heart rhythm, influenced diastolic function, and significantly promoted ST-segment elevation ( Sun et al, 2014 ; Bi et al, 2016 ).…”

Section: Preclinical Evaluation Of Cmm-induced Cardiotoxicitymentioning

confidence: 99%

Risk Compounds, Preclinical Toxicity Evaluation, and Potential Mechanisms of Chinese Materia Medica–Induced Cardiotoxicity

Zhou

Cao

et al. 2021

Front. Pharmacol.

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Chinese materia medica (CMM) has been applied for the prevention and treatment of diseases for thousands of years. However, arrhythmia, myocardial ischemia, heart failure, and other cardiac adverse reactions during CMM application were gradually reported. CMM-induced cardiotoxicity has aroused widespread attention. Our review aimed to summarize the risk compounds, preclinical toxicity evaluation, and potential mechanisms of CMM-induced cardiotoxicity. All relevant articles published on the PubMed, Embase, and China National Knowledge Infrastructure (CNKI) databases for the latest twenty years were searched and manually extracted. The risk substances of CMM-induced cardiotoxicity are relatively complex. A single CMM usually contains various risk compounds, and the same risk substance may exist in various CMM. The active and risk substances in CMM may be transformed into each other under different conditions, such as drug dosage, medication methods, and body status. Generally, the risk compounds of CMM-induced cardiotoxicity can be classified into alkaloids, terpenoids, steroids, heavy metals, organic acids, toxic proteins, and peptides. Traditional evaluation methods of chemical drug-induced cardiotoxicity primarily include cardiac function monitoring, endomyocardial biopsy, myocardial zymogram, and biomarker determination. In the preclinical stage, CMM-induced cardiotoxicity should be systematically evaluated at the overall, tissue, cellular, and molecular levels, including cardiac function, histopathology, cytology, myocardial zymogram, and biomarkers. Thanks to the development of systematic biology, the higher specificity and sensitivity of biomarkers, such as genes, proteins, and metabolic small molecules, are gradually applied for evaluating CMM-induced cardiotoxicity. Previous studies on the mechanisms of CMM-induced cardiotoxicity focused on a single drug, monomer or components of CMM. The interaction among ion homeostasis (sodium, potassium, and calcium ions), oxidative damage, mitochondrial injury, apoptosis and autophagy, and metabolic disturbance is involved in CMM-induced cardiotoxicity. Clarification on the risk compounds, preclinical toxicity evaluation, and potential mechanisms of CMM-induced cardiotoxicity must be beneficial to guide new CMM development and post-marketed CMM reevaluation.

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“…Bidirectional ventricular tachycardia is a hallmark of severe digitalis toxicity, and immediate specific antidote treatment with FAB antibodies must be started. This type of ventricular tachycardia may occur in aconite poisoning too [51,52].…”

Section: Cholinomimetic: Organophosphatesmentioning

confidence: 99%

Poisoning in the Pediatric Intensive Care Unit

Nistor¹,

Frăsinariu²,

Rugină³

et al. 2019

Poisoning in the Modern World - New Tricks for an Old Dog?

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Poisonings during childhood (both accidental and voluntary) are a common cause of presentation in the emergency departments (EDs) and the pediatric intensive care unit (PICU). The admission to PICU is warranted both for treatment and for continuous monitoring, as sometimes the evolution of a poisoning could be unpredictable. Sometimes, complications arise that may prolong the patients' hospitalization and may contribute to lowering the survival rate. The staff in these departments must be well trained to ensure patient monitoring, early detection of complications, and rapid intervention. Supporting vital functions is the main objective of the management of a poisoned patient admitted in PICU. In recent years, staff competence and advanced medical technology have helped to improve the prognosis of the patients admitted to these departments, including of the poisoned patients.

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Spectrum of cardiac manifestations from aconitine poisoning

Cited by 7 publications

References 12 publications

Bradycardia and Hypotension from Improper Use of Aconite Root: A Case Report and Brief Review

Bradycardia and Hypotension from Improper Use of Aconite Root: A Case Report and Brief Review

Risk Compounds, Preclinical Toxicity Evaluation, and Potential Mechanisms of Chinese Materia Medica–Induced Cardiotoxicity

Poisoning in the Pediatric Intensive Care Unit

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