Could E-cigarette vaping contribute to heart disease?

ABSTRACT

Introduction

E-cigarettes have become a controversial topic. While their benefits are questioned by the scientific community, a part of the medical profession is still supporting them as an effective harm reduction tool for smoking cessation. The impact of E-cigarettes on the cardiovascular system is still elusive.

Areas covered

We assessed results from animal, pre(clinical), and epidemiological studies to critically evaluate and synthesize evidence relevant to the cardiovascular effects of E-cigarettes. Animal studies have demonstrated that E-cigarette vapor exposure can cause endothelial and cardiac dysfunction. However, there have also been reports on the less harmful effects of E-cigarette vapor exposure in comparison to classical tobacco cigarettes. Measurements of flow-mediated dilation in acute human exposure settings have mostly demonstrated that E-cigarettes cause vascular endothelial dysfunction. Epidemiological studies have shown that E-cigarette use is associated with an increased risk for cardiovascular disease, although switching from classical tobacco cigarettes to E-cigarettes can have beneficial cardiovascular effects. Misinterpretation of scientific data by activists on either side is another problem.

Expert opinion

In conclusion, we need more and better (pre)clinical data comparing the health effects of E-cigarette vaping as compared with tobacco cigarette smoking, in order to counsel the legislation for better health policies.

KEYWORDS:

• Electronic nicotine delivery system
• cardiovascular disease
• vaping
• endothelial dysfunction
• oxidative stress
• acrolein

Article highlights

• Literature on both short- and long-term cardiovascular effects of E-cigarette use is very limited and inconclusive.

• E-cigarette aerosol contains numerous toxic compounds including nicotine, aldehydes, volatile organic compounds, nitrosamines, particulates, and metals that can lead to alteration of inflammatory and oxidative stress pathways, ultimately resulting in vascular endothelial dysfunction, thrombogenesis, and atherosclerosis.

• Although current data suggest that E-cigarettes are not harm-free products, they are associated with less negative cardiovascular effects compared to conventional cigarettes.

• There is evidence indicating that switching from conventional to E-cigarettes may have beneficial effects on blood pressure regulation and endothelial function, however, their potential as a smoking cessation tool remains unclear.

• Cell culture studies in endothelial cells and cardiomyocytes as well as lung cells revealed potential cardiovascular damage associated with E-cigarette vapor and tobacco cigarette smoke extracts.

• Animal models of E-cigarette vapor exposure revealed endothelial and cardiac dysfunction as well as oxidative stress and inflammation that were comparable those found upon exposure to tobacco cigarette smoke.

• Our own studies identified the acrolein-NOX-2 axis as a potential key mechanism underlying E-cigarette vapor induced adverse health effects since NOX-2 deficient mice were largely protected.

• The major toxic compounds in E-cigarette vapor are reactive aldehydes. Acrolein seems to play a role for cardiovascular damage but potentially also for neurodegenerative and respiratory diseases as well as cancer.

• Prospective studies and randomized controlled trials evaluating the long-term and short-term cardiovascular effects of E-cigarette use along with the specific impact of toxic compounds are clearly warranted.

• Smoking cessation will remain the most powerful approach to prevent smoking-induced cardiovascular disease.

Author contributions

All authors revised the article critically for important intellectual content and approved its final version. All authors contributed equally to the study.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

A Daiber and T Münzel were supported by vascular biology research grants from the Boehringer Ingelheim Foundation for the collaborative research group ‘Novel and neglected cardiovascular risk factors: molecular mechanisms and therapeutics’. Our research was continuously supported by Foundation Heart of Mainz. T Münzel is PI of the DZHK (German Center for Cardiovascular Research), Partner Site Rhine-Main, Mainz, Germany. M.K. holds a stipend of the TransMed PhD program of the University Medical Center Mainz, Germany.