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Am J Physiol Heart Circ Physiol. 2019 Jun 7. doi: 10.1152/ajpheart.00738.2018. [Epub ahead of print]

Chronic Intermittent Electronic Cigarette Exposure Induces Cardiac Dysfunction and Atherosclerosis in Apolipoprotein E (ApoE) Knockout Mice.

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Charles R. Drew University of Medicine and Science, United States.
Department of Neurobiology, David Geffen School of Medicine at UCLA, United States.
David Geffen School of Medicine at UCLA, United States.
Internal Medicine, Charles R. Drew University of Medicine and Science, United States.
Endocrinology, Metabolism & Molecular Medicine, Charles R. Drew University of Medicine & Science, UCLA School of Medicine, United States.
Physiology, David Geffen School of Medicine at University of California, United States.
Internal Medicine, Charles R. Drew Unversity, United States.
Charles R. Drew University of Medicine and Science and University of California, Los Angeles, United States.


Electronic cigarettes (e-cigarettes), also known as electronic nicotine delivery systems (ENDS) are a popular alternative to conventional nicotine cigarettes, both among smokers and those who have never smoked. In spite of the widespread use of e-cigarettes and the proposed detrimental cardiac and atherosclerotic effects of nicotine, the effects of e-cigarettes on these systems are not known. In this study, we investigated the cardiovascular and cardiac effects of e-cigarettes with and without nicotine in Apolipoprotein E knockout (ApoE-/-) mice. We developed an e-cigarettes exposure model that delivers nicotine in a manner similar to that of human e-cigarettes users. Using commercially available e-cigarettes, bluCig PLUS, ApoE-/- mice were exposed to saline, e-cigarette without nicotine [e-cigarette (0%)] and e-cigarette with 2.4% nicotine [e-cigarette (2.4%)] aerosol for 12 weeks. Echocardiographic data show that mice treated with e-cigarette (2.4%) had decreased left ventricular fractional shortening and ejection fraction compared to e-cigarette (0%) and saline. Ventricular transcriptomic analysis revealed changes in genes associated with metabolism, circadian rhythm and inflammation in e-cigarette (2.4%)-treated ApoE-/- mice. Transmission electron microscopy revealed that cardiomyocytes of mice treated with e-cigarette (2.4%) exhibited ultrastructural abnormalities indicative of cardiomyopathy. Additionally, we observed increased oxidative stress and mitochondrial DNA mutations in mice treated with e-cigarette (2.4%). ApoE-/- mice on e-cigarette (2.4%) had also increased atherosclerotic lesions compared to saline aerosol-treated mice. These results demonstrate adverse effects of e-cigarettes on cardiac function in mice.


Atherosclerosis; Cardiomyopathy; Cardiovascular Disease; Inflammation; Myocardial Biology

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