Journal article
Cory Kucera, Anand R Ramalingam, Shweta Srivastava, Aruni Bhatnagar, A. Carll
Nicotine & Tobacco Research, 2023
Nicotine & Tobacco Research, 2023
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APA
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Kucera, C., Ramalingam, A. R., Srivastava, S., Bhatnagar, A., & Carll, A. (2023). Nicotine Formulation Influences the Autonomic and Arrhythmogenic Effects of Electronic Cigarettes. Nicotine &Amp; Tobacco Research.
Chicago/Turabian
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Kucera, Cory, Anand R Ramalingam, Shweta Srivastava, Aruni Bhatnagar, and A. Carll. “Nicotine Formulation Influences the Autonomic and Arrhythmogenic Effects of Electronic Cigarettes.” Nicotine & Tobacco Research (2023).
MLA
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Kucera, Cory, et al. “Nicotine Formulation Influences the Autonomic and Arrhythmogenic Effects of Electronic Cigarettes.” Nicotine &Amp; Tobacco Research, 2023.
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@article{cory2023a,
title = {Nicotine Formulation Influences the Autonomic and Arrhythmogenic Effects of Electronic Cigarettes.},
year = {2023},
journal = {Nicotine & Tobacco Research},
author = {Kucera, Cory and Ramalingam, Anand R and Srivastava, Shweta and Bhatnagar, Aruni and Carll, A.}
}
Abstract
INTRODUCTION Evidence is mounting that electronic cigarette (e-cig) use induces cardiac sympathetic dominance and electrical dysfunction conducive to arrhythmias and dependent upon nicotine. A variety of nicotine types and concentrations are available in e-cigs, but their relative cardiovascular effects remain unclear. Here we examine how different nicotine forms (racemic, free-base, and salt) and concentrations influence e-cig-evoked cardiac dysfunction and arrhythmogenesis and provide a mechanism for nicotine-salt-induced autonomic imbalance.
METHODS ECG-telemetered C57BL/6J mice were exposed to filtered air (FA) or e-cig aerosols from propylene glycol and vegetable glycerin solvents either without nicotine (vehicle) or with increasing nicotine concentrations (1%, 2.5%, and 5%) for three 9-min puff sessions per concentration. Spontaneous ventricular premature beat (VPB) incidence rates, heart rate, and heart rate variability (HRV) were compared between treatments. Subsequently, to test the role of β1-adrenergic activation in e-cig-induced cardiac effects, mice were pretreated with atenolol and exposed to either FA or 2.5% nicotine salt.
RESULTS During puffing and washout phases, ≥ 2.5% racemic nicotine reduced heart rate and increased HRV relative to FA and vehicle controls, indicating parasympathetic dominance. Relative to both controls, 5% nicotine salt elevated heart rate and decreased HRV during washout, suggesting sympathetic dominance, and also increased VPB frequency. Atenolol abolished e-cig-induced elevations in heart rate and declines in HRV during washout, indicating e-cig-evoked sympathetic dominance is mediated by β1-adrenergic stimulation.
CONCLUSIONS Our findings suggest that inhalation of e-cig aerosols from nicotine salt-containing e-liquids could increase the cardiovascular risks of vaping by inducing sympathetic dominance and cardiac arrhythmias.
IMPLICATIONS Exposure to e-cig aerosols containing commercially relevant concentrations of nicotine salts may increase nicotine delivery and impair cardiac function by eliciting β1-adrenoceptor-mediated sympathoexcitation and provoking ventricular arrhythmias. If confirmed in humans, our work suggests that regulatory targeting of nicotine salts through minimum pH standards or limits on acid additives in e-liquids may mitigate the public health risks of vaping.