e-Cigarette smoking associated with endothelial dysfunction

By Dr Timothy Swinn

Two recently published have shed light on the vascular damage caused by cigarettes and e-cigarettes. Flow-mediated dilatation (FMD) was used to measure endothelial function. FMD refers to the dilatation of an artery (brachial or femoral) following a period of ischaemia measured by ultrasound. Reduced FMD is a marker of endothelial dysfunction, which in turn may be a precursor to chronic vascular disease.

Nabavizadeh et al1, measured FMD in rats before and after acute exposure to a variety of cigarettes/substances. FMD was reduced in rats exposed to all experimental cigarettes (altering nicotine and menthol levels), as well as following inhalation of acrolein and acetaldehyde (both found in cigarette and e-cigarette smoke) and inert carbon nanoparticles (all at concentrations relevant to smoking). Higher nicotine content was associated with increased endothelial dysfunction, whereas increased menthol levels were associated with reduced endothelial dysfunction. It should be noted that this does not imply a protective role for menthol and crucially, no single ingredient was responsible for the endothelial dysfunction. Interestingly, reduced FMD was not seen in rats who had undergone bilateral cervical vagotomy prior to smoke exposure. The authors hypothesise that the endothelial dysfunction may be mediated by vagal stimulation following airway irritation from smoke inhalation rather than a single ingredient being responsible.

The second study, by Mohammadi et al2, studied FMD in 120 humans (aged 21-50, no known cardiovascular disease) that were grouped into “chronic cigarette smokers”, “chronic e-cigarette smokers”, and “non-smokers”. They found that FMD had a >5% relative reduction in both cigarette and e-cigarette smokers compared to non-smokers. Furthermore, they studied the effect that participants’ sera had on cultured endothelial cells. This showed that both cigarette and e-cigarette smokers’ sera impaired VEGF-induced nitric oxide release from cultured cells, but only e-cigarette smokers’ sera increased vascular permeability and hydrogen peroxide release. Both cigarette and e-cigarette smokers had higher circulating levels of inflammatory and pro-thrombotic cytokines compared to non-smokers, albeit with different profiles.

These papers complement each other and serve to shed light on health issues associated with vaping; a subject that has the potential to become a large public health issue. Long-term data regarding health-effects of vaping are lacking and hence investigating mechanisms of potential harm in this manner may help clinicians guide patients towards healthier lifestyles without having to wait to see long-term results.


  1. Nabavizadeh P, Liu J, Rao P, Ibrahim S, Han DD, Derakhshandeh R, et al. Impairment of Endothelial Function by Cigarette Smoke Is Not Caused by a Specific Smoke Constituent, but by Vagal Input From the Airway. Arterioscler Thromb Vasc Biol. 2022 Nov;42(11):1324–32.
  2. Mohammadi L, Han DD, Xu F, Huang A, Derakhshandeh R, Rao P, et al. Chronic E-Cigarette Use Impairs Endothelial Function on the Physiological and Cellular Levels. Arterioscler Thromb Vasc Biol. 2022 Nov;42(11):1333–50.