Electronic Cigarettes Impair Human Coronary Endothelial Function

Abstract

Electronic (e‐) cigarettes are claimed—but unproven—to be less harmful than standard tobacco cigarettes, which are well known to impair coronary endothelial function and constitute a major cardiovascular risk factor. To determine whether e‐cigarettes cause impairment in human coronary endothelial function, we compared effects of tobacco cigarette smoking and e‐cigarette use to blunt the normal increase in myocardial blood flow (MBF) quantified by contrast enhanced echocardiography perfusion imaging, induced by the exercise pressor reflex (post‐handgrip forearm vascular occlusion). The exercise pressor reflex is a reproducible stimulus to endothelial‐dependent coronary vasodilation while also increasing coronary sympathetic vasoconstrictor drive. The coronary endothelial function testing was performed in healthy young adult cigarette smokers (n=5) and age‐matched e‐cigarette users (n=8), ages 21–38 years: a) after overnight smoking/vaping abstinence; and b) immediately after smoking one Camel‐filtered cigarette or one standard use (15 puffs in 7 minutes) of a popular tank‐style e‐cigarette (Evod: battery 3.7 volts, nicotine content 18 mg). During tobacco abstinence in the young cigarette smokers, the exercise pressor reflex increased mean arterial pressure (MAP) by 21.6 ± 4 mmHg (mean ± SE) and increased MBF by 66 ± 20% over baseline (p<0.05), the latter indicating endothelial‐dependent vasodilation in the human coronary microcirculation. As expected, the MBF failed to increase when the exercise pressor reflex was elicited immediately after cigarette smoking (Δ MBF −2 ± 24%, p=n.s.), indicating acute impairment in coronary endothelial function. The surprising new findings of this study are that MBF also failed to increase and tended to decrease by −45 ± 20% (p=n.s.) when the exercise pressor reflex was elicited immediately after acute e‐cigarette use and by −16 ± 10% (p=n.s.) even when elicited during vaping abstinence (despite comparable mean reflex increases in MAP of 21.1 and 21.6 mm Hg, respectively). Thus, our data to date suggest that, in contrast to what has been widely assumed, e‐cigarette use in young adults causes an impairment in coronary endothelial function that appears to be more persistent than with traditional tobacco cigarettes. Further research is warranted to determine if specific oxidant nanoparticles in e‐cigarette vapor mediate the impaired coronary endothelial function.Support or Funding InformationFunded by Tobacco Related Disease Research Program; ClinicalTrials.gov NCT02612701This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.