This commentary refers to ‘Short-term e-cigarette vapour exposure causes vascular oxidative stress and dysfunction: evidence for a close connection to brain damage and a key role of the phagocytic NADPH oxidase (NOX-2)’, by M. Kuntic et al., doi: 10.1093/eurheartj/ehz772.

I read with particular interest the study by Kuntic et al. who reported the acute adverse effects of e-cigarette use on endothelial function and arterial stiffness.1 The authors concluded that e-cigarettes have the potential to induce marked adverse cardiovascular, pulmonary, and cerebrovascular consequences. However, I am concerned that their findings have questionable clinical relevance for long-term cardiovascular risk.

While endothelial function and arterial stiffness are prognostic markers, this is applicable only when measured under strict resting conditions and when refraining from stimulant intake for several hours, as recommended in published guidelines.2 There is no evidence that changes in vascular function after an acute intervention have any prognostic value. Acute adverse effects on vascular function have been observed immediately after intake of caffeine and approved nicotine replacement therapies (NRTs),3  ,  4 both of which are not considered risk factors for cardiovascular disease. In fact, quitting smoking with NRTs results in rapid improvement in vascular function when measurements were performed according to guidelines. Very recently, a study identified rapid (within 4 weeks) improvement in vascular function (measured at rest) when switching from smoking to e-cigarette use.5 Remarkably, no difference was observed between nicotine-containing and nicotine-free e-cigarettes, while improvement was observed even in those smokers who did not completely quit smoking but reduced their cigarette consumption. The study did not compare e-cigarettes with pharmacological smoking cessation products or with quitting without any aid; however, it suggests that at least for smokers unable or unwilling to quit by themselves or with current approved methods, e-cigarettes may reduce the future risk for cardiovascular disease when used as smoking substitutes. This is contradictory to the interpretation of the acute effects of e-cigarette as presented by Kuntic et al.

In conclusion, while more research is certainly needed to identify the long-term effects of switching from smoking to e-cigarette use on the cardiovascular system, the acute effects of delivering a stimulant (nicotine) on vascular function cannot be used as a prognostic marker for cardiovascular risk. Therefore, the findings by Kuntic et al. have questionable clinical value on future disease risk and should be interpreted with caution.

Conflict of interest: none declared.

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