Cardiac arrest associated with synthetic cannabinoid use and acquired prolonged QTc interval: A case report and review of literature

Ahmed, Talha; Khan, Ahmed; See, Vincent; Robinson, Shawn

doi:10.1016/j.hrcr.2020.02.002

Cited by 8 publications

(6 citation statements)

References 12 publications

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“…Also Ahmed et al . reached the same conclusions in their review, in which they explain that the prolongation of the QT interval is attributable to the blockage of the potassium channels hERG (human Ether-à-go-go-Related Gene) [ 18 ]. These data support the hypothesis that SCs can cause sudden, potentially lethal arrhythmias, acting at the receptor and myocardial ion channels level.…”

Section: Resultsmentioning

confidence: 80%

Synthetic Cannabinoids and Cathinones Cardiotoxicity: Facts and Perspectives

Radaelli

Manfredi

Zanon

et al. 2021

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: New psychoactive substances (NPS) constitute a group of psychotropic substances, designed to mimic the effects of traditional substances like cannabis, cocaine, MDMA, khat, which is not regulated by the 1961 United Nations Convention on Narcotics or the 1971 United Nations Convention on Psychotropic Substances. Illegal laboratories responsible for their production regularly develop new substances and place them on the market to replace the ones that have been banned; for this reason, during the last decade this class of substances has represented a great challenge for the public health and forensic toxicologists. The spectrum of side effects caused by the intake of these drugs of abuse is very wide since they act on different systems with various mechanisms of action. To date most studies have focused on the neurotoxic effects, very few works focus on cardiotoxicity. Specifically, both synthetic cannabinoids and synthetic cathinones appear to be involved in different cardiac events, including myocardial infarction and sudden cardiac death due to fatal arrhythmias. Synthetic cannabinoids and cathinones cardiotoxicity are mainly mediated through activation of the CB1 receptor present on cardiomyocyte and involved with reactive oxygen species production, ATP depletion and cell death. Concerns with the adrenergic over-stimulation induced by this class of substances and increasing oxidative stress are mainly reported. In this systematic review we aim to summarize the data from all the works analyzing the possible mechanisms through which synthetic cannabinoids and synthetic cathinones damage the myocardial tissue.

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Section: Resultsmentioning

confidence: 80%

Synthetic Cannabinoids and Cathinones Cardiotoxicity: Facts and Perspectives

Radaelli

Manfredi

Zanon

et al. 2021

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“…Torsade de pointes (TdP) is the principal type of arrhythmia associated with delayed ventricular repolarization, indicated by QT interval prolongation [ 93 ]. TdP was reported in a patient who abused K2 products [ 94 ]. Moreover, JWH-018 during the tachyarrhythmia period and, to a lesser extent, Δ 9 -THC also induced the PR interval prolongation that is attributable to a higher risk of atrial fibrillation [ 95 ], and this evidence was reported in a clinical case after SCs consumption [ 96 ].…”

Section: Discussionmentioning

confidence: 99%

The Old and the New: Cardiovascular and Respiratory Alterations Induced by Acute JWH-018 Administration Compared to Δ9-THC—A Preclinical Study in Mice

Marchetti

Bilel

Tirri

et al. 2023

IJMS

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Several new psychoactive substances (NPS) are responsible for intoxication involving the cardiovascular and respiratory systems. Among NPS, synthetic cannabinoids (SCs) provoked side effects in humans characterized by tachycardia, arrhythmias, hypertension, breathing difficulty, apnoea, myocardial infarction, and cardiac arrest. Therefore, the present study investigated the cardio-respiratory (MouseOx Plus; EMKA electrocardiogram (ECG) and plethysmography TUNNEL systems) and vascular (BP-2000 systems) effects induced by 1-naphthalenyl (1-pentyl-1H-indol-3-yl)-methanone (JWH-018; 0.3–3–6 mg/kg) and Δ9-tetrahydrocannabinol (Δ9-THC; 0.3–3–6 mg/kg), administered in awake CD-1 male mice. The results showed that higher doses of JWH-018 (3–6 mg/kg) induced deep and long-lasting bradycardia, alternated with bradyarrhythmia, spaced out by sudden episodes of tachyarrhythmias (6 mg/kg), and characterized by ECG electrical parameters changes, sustained bradypnea, and systolic and transient diastolic hypertension. Otherwise, Δ9-THC provoked delayed bradycardia (minor intensity tachyarrhythmias episodes) and bradypnea, also causing a transient and mild hypertensive effect at the tested dose range. These effects were prevented by both treatment with selective CB1 (AM 251, 6 mg/kg) and CB2 (AM 630, 6 mg/kg) receptor antagonists and with the mixture of the antagonists AM 251 and AM 630, even if in a different manner. Cardio-respiratory and vascular symptoms could be induced by peripheral and central CB1 and CB2 receptors stimulation, which could lead to both sympathetic and parasympathetic systems activation. These findings may represent a starting point for necessary future studies aimed at exploring the proper antidotal therapy to be used in SCs-intoxicated patient management.

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“…THC has been associated with different types of ventricular arrhythmias, including VF from QTc prolongation or Brugada syndrome and monomorphic VT attributed to ischemia [3,6,7]. This case highlights the importance of pharmacogenomics in the pathophysiology of arrhythmia associated with the relatively common practice of THC dabbing.…”

Section: Discussionmentioning

confidence: 89%

“…This form of cannabis is highly concentrated in THC (50%+) compared to the medicinal plant, which has a concentration of 4-8% [2]. With these shifts in the use and forms of THC come increasing evidence of associated adverse cardiac events including cardiac arrest, which may be related to prolongation of the QTc interval [3]. In this report, we discuss the case of a 19-year-old female who frequently used marijuana and suffered QTc prolongation-related ventricular fibrillation (VF) arrest at home followed by recurrent Tor-sades de pointes (Tdp) during hospitalization.…”

Section: Introductionmentioning

confidence: 99%

Torsades de Pointes due to Excessive Marijuana Use in a Susceptible Patient

Shah

Mohammad

Nandkeolyar

et al. 2021

Case Reports in Cardiology

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There are several recent reports of tetrahydrocannabinol vaping-related sudden cardiac arrest, and the mechanisms are unclear. We report a unique case of a 19-year-old female who suffered documented prolonged QTc leading to Torsades de pointes and cardiac arrest in the setting of frequent marijuana wax vaping. While she demonstrated normal baseline QTc measurements years earlier, she was found to have a genetic predisposition to QTc prolongation (genetic mutation, family history of prolonged QTc), suggesting that specific patient populations are at higher risk of these adverse events. The patient was acutely managed with isoproterenol to increase the heart rate and was discharged on nadolol after placement of an implantable cardioverter-defibrillator. Marijuana wax vaping and dabbing may cause fatal Torsades de pointes in susceptible patients, and further research is required to identify these patients a priori.

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Cardiac arrest associated with synthetic cannabinoid use and acquired prolonged QTc interval: A case report and review of literature

Cited by 8 publications

References 12 publications

Synthetic Cannabinoids and Cathinones Cardiotoxicity: Facts and Perspectives

Synthetic Cannabinoids and Cathinones Cardiotoxicity: Facts and Perspectives

The Old and the New: Cardiovascular and Respiratory Alterations Induced by Acute JWH-018 Administration Compared to Δ9-THC—A Preclinical Study in Mice

Torsades de Pointes due to Excessive Marijuana Use in a Susceptible Patient

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