ENDS Cardiovascular System: Difference between revisions

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'''Studies, Surveys, Papers, and Case Studies'''

*Sometimes it's necessary to view the PDF version to access the full study.

Electronic Cigarette vaping for four months, has a neutral effect on platelet aggregation of healthy smokers.

Continuation of tobacco cigarette smoking further deteriorates platelet function during 4 months of use.

Endothelial dysfunction, as measured by flow mediated vasodilation(FMD) is a predictor of future atherosclerosis and adverse cardiovascular events, and is impaired in tobacco cigarette (TC) smokers.

FMD was significantly impaired after smoking one TC, but not after vaping an equivalent "dose"(estimated plasma nicotine) of an e-cigarette (EC), consistent with the notion that non-nicotine constituents in TC smoke mediate the impairment.

   

Switching to ENDS/NTPs and nicotine delivery with cigarette smoke’s harmful effects elimination does not interrupt blood oxygen transport function which allows to avoid vessels endothelial damage. The obtained results show significantly less harmful influence of ENDS/NTPs on cardio-vascular function if compared to tobacco smoke and confirm the possibility to consider them as harm reduction products for smokers who do not want or are not ready to quit smoking completely.

Poster that goes with the study

   

that debunks this study: Electronic Cigarette Use and Myocardial Infarction Among Adults in the US Population Assessment of Tobacco and Health  

   

Insights from the 2016 and 2017 National Health Interview Surveys  

The pooled analysis of the 2016 and 2017 NHIS showed no association between e-cigarette use and MI or CHD. The associations between established risk factors, including smoking, and both conditions were remarkably consistent. The inconsistent associations observed in single-year surveys and the cross-sectional design of the NHIS cannot substantiate any link between e-cigarette use and an elevated risk for MI or CHD. Longitudinal studies are needed to explore the effects of e-cigarette use on cardiovascular disease.

   

(Jacob George, MD, Muhammad Hussain, MSc, Thenmalar Vadiveloo, PhD, Sheila Ireland, BSc, Pippa Hopkinson, BSc, Allan D.Struthers, MD, Peter T. Donnan, PhD, Faisel Khan, PhD, Chim C.Lang, MD

E-cigarette (EC) use is increasing exponentially worldwide. The early cardiovascular effects of switching from tobacco cigarettes (TC) to EC in chronic smokers is unknown. Meta-analysis of flow-mediated dilation (FMD) studies indicate 13% lower pooled, adjusted relative risks of cardiovascular events with every 1% improvement in FMD.

Though they may not be as harmless as previously proposed, it seems likely that on the spectrum of tobacco products, ECs are less harmful than TCs, and there is increasing evidence that ECs may help promote TC cessation. As such, ECs may be helpful for risk reduction.

While not harmless, electronic cigarettes (e-cigarettes) have demonstrated a much more favourable toxicological profile than combustible cigarettes—the worldwide leading cause of preventable death. Average eCO levels (ppm) were significantly higher in smokers than in e-cigarette users. Compared with cigarettes, G2 and G3 e-cigarettes resulted in significantly lower levels of exposure to a potent lung carcinogen and cardiovascular toxicant.

Electronic cigarette smoking causes a smaller increase of arterial stiffness and oxidative stress, compared to a single normal cigarette in an acute setting. Replacement of normal cigarettes by a moderate nicotine concentration electronic cigarette results in improved aortic elasticity and oxidative stress within 1 month.

Human coronary artery endothelial cells show a biological response to cigarette smoke.

This response was not seen following exposure to e-cigarette aerosol.

A male Caucasian patient, born in 1977, presented in September 2005 with asymptomatic elevation of white blood cell and neutrophil count, and mildly-elevated C-reactive protein levels. He was a smoker since 1996 and was treated with 20 mg/day of simvastatin since 2003 due to hyperlipidemia. Clinical examination, and laboratory and imaging investigations ruled out any infectious, haematological, rheumatological, or endocrine conditions. He was followed-up regularly and was advised to stop smoking. He had 2 unsuccessful attempts to quit smoking; one was unassisted and the second was performed with the use of both varenicline and nicotine replacement therapy (patches). During the subsequent 6.5 years, his leukocyte and C-reactive protein levels were repeatedly elevated; the condition was consistent with chronic idiopathic neutrophilia. In February 2012, he started using electronic cigarettes and he managed to quit smoking within 10 days. After 6 months, laboratory examination showed normalized leukocyte count and C-reactive protein levels, confirmed immediately by a second laboratory and by repeated tests after 1 and 2 months.

Smoking cessation with the use of electronic cigarette led to reversal of chronic idiopathic neutrophilia. The daily use of electronic cigarette may help preserve the beneficial effects of smoking cessation.

Active and passive tobacco cigarette smoking increased white blood cell, lymphocyte, and granulocyte counts for at least one hour in smokers and never smokers. Active and passive tobacco cigarette smoking increase the secondary proteins of acute inflammatory load for at least one hour.

It is concluded that acute active and passive smoking using the e-cigarettes tested in the current study does not influence CBC indices in smokers and never smokers. The results demonstrated that CBC indices remained unchanged during the control session and the active and passive e-cigarette smoking sessions.

   

Heart rate increased from an average (SD) of 65.7 (10.4) bpm at baseline to a peak of 80.3 (10.9) bpm five minutes after the first administration under the tobacco cigarette condition. No significant changes in heart rate were observed for the e-cigarette or sham conditions.

Under these acute testing conditions, neither of the electronic cigarettes exposed users to measurable levels of nicotine or CO, although both suppressed nicotine/tobacco abstinence symptom ratings.  

*Our data indicate that flavorings typically present in e-cig refill liquids do not cause endothelial dysfunction that would result in impaired vasodilation upon acute exposure. In contrast, most of the tested compounds caused endothelium-independent vasorelaxation, albeit at fairly high concentrations that appear to exceed by far the plasma concentrations expected to occur upon vaping flavored liquids.

*[https://storage.googleapis.com/plos-corpus-prod/10.1371/journal.pone.0222152/1/pone.0222152.pdf?X-Goog-Algorithm=GOOG4-RSA-SHA256&X-Goog-Credential=wombat-sa%40plos-prod.iam.gserviceaccount.com%2F20210106%2Fauto%2Fstorage%2Fgoog4_request&X-Goog-Date=20210106T115250Z&X-Goog-Expires=3600&X-Goog-SignedHeaders=host&X-Goog-Signature=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 PDF Version]

*Smoking is an important risk factor for cardiovascular disease and cigarette smoke (CS) has well-established cytotoxic effects on myocardial cells. The purpose of this study was to evaluate the cytotoxic potential of the vapour of 20 EC (e-cigarette) liquid samples and a “base” liquid sample (50% glycerol and 50% propylene glycol, with no nicotine or flavourings) on cultured myocardial cells. Included were 4 samples produced by using cured tobacco leaves in order to extract the tobacco flavour. Methods: Cytotoxicity was tested according to the ISO 10993-5 standard.

*In conclusion, from 20 commercially-available EC liquids that were tested in vapour form, four were found to be cytotoxic on cultured cardiomyoblasts. Cytotoxicity was mainly observed in most (but not all) samples produced by using tobacco leaves, while one sample using food-approved flavoring was marginally cytotoxic. EC vapour production by using higher-voltage devices caused a decrease in cell survival. Overall, EC vapour extracts showed significantly higher cell viability compared to CS extract, based on a realistic-use rather than a standardized comparative level of exposure. This supports the concept that ECs may be useful as tobacco harm reduction products.

The acute sympathomimetic effect of e‐cigarettes is attributable to the inhaled nicotine, not to non‐nicotine constituents in e‐cigarette aerosol

Oxidative stress, as estimated by plasma paraoxonase, did not increase following any of the 3 exposures.

Studies of nicotine medications and smokeless tobacco indicate that the risks of nicotine without tobacco combustion products (cigarette smoke) are low compared to cigarette smoking, but are still of concern in people with cardiovascular disease.

Electronic cigarettes deliver nicotine without combustion of tobacco and appear to pose low-cardiovascular risk, at least with short-term use, in healthy users.

*Topic

*Year (list new to old) Name of Study (In link format to the study)

"proatherogenic" = promoting fatty plaques in the arteries (which is bad)

*Click on the category link below for more studies by topic on ENDS and Nicotine.

[[Category:Studies, Surveys, and Papers]]

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