Comment; Significant findings! Even nicotine-free vapor inhalation causes significant changes in major vessel circulation decreases, increased vessel wall stiffness and other problems. Adding nicotine will only increase the risk!
Alessandra
Caporale , Michael C.
Langham, Wensheng Guo, Alyssa Johncola, Shampa Chatterjee, Felix W. Wehrli
Published Online:Aug 20 2019https://doi.org/10.1148/radiol.2019190562
Background
Previous studies showed that nicotinized electronic cigarettes (hereafter, e-cigarettes) elicit systemic oxidative stress and inflammation. However, the effect of the aerosol alone on endothelial function is not fully understood.
Purpose
To quantify surrogate markers of endothelial function in nonsmokers after inhalation of aerosol from nicotine-free e-cigarettes.
Materials and Methods
In this prospective study (from May to September 2018), nonsmokers underwent 3.0-T MRI before and after inhaling nicotine-free e-cigarette aerosol. Peripheral vascular reactivity to cuff-induced ischemia was quantified by temporally resolving blood flow velocity and oxygenation (SvO2) in superficial femoral artery and vein, respectively, along with artery luminal flow-mediated dilation. Precuff occlusion, resistivity index, baseline blood flow velocity, and SvO2 were evaluated. During reactive hyperemia, blood flow velocity yielded peak velocity, time to peak, and acceleration rate (hyperemic index); SvO2 yielded washout time of oxygen-depleted blood, rate of resaturation, and maximum SvO2 increase (overshoot). Cerebrovascular reactivity was assessed in the superior sagittal sinus, evaluating the breath-hold index. Central arterial stiffness was measured via aortic pulse wave velocity. Differences before versus after e-cigarette vaping were tested with Hotelling T2 test.
Results
Thirty-one healthy never-smokers (mean age, 24.3 years ± 4.3; 14 women) were evaluated. After e-cigarette vaping, resistivity index was higher (0.03 of 1.30 [2.3%]; P < .05), luminal flow-mediated dilation severely blunted (−3.2% of 9.4% [−34%]; P < .001), along with reduced peak velocity (−9.9 of 56.6 cm/sec [−17.5%]; P < .001), hyperemic index (−3.9 of 15.1 cm/sec2 [−25.8%]; P < .001), and delayed time to peak (2.1 of 7.1 sec [29.6%]; P = .005); baseline SvO2 was lower (−13 of 65 %HbO2 [−20%]; P < .001) and overshoot higher (10 of 19 %HbO2 [52.6%]; P < .001); and aortic pulse wave velocity marginally increased (0.19 of 6.05 m/sec [3%]; P = .05). Remaining parameters did not change after aerosol inhalation.
Conclusion
Inhaling nicotine-free electronic cigarette aerosol transiently impacted endothelial function in healthy nonsmokers. Further studies are needed to address the potentially adverse long-term effects on vascular health.
Summary
Nicotine-free electronic cigarette aerosol inhalation in young, healthy nonsmokers resulted in transient impairment of vascular reactivity and endothelial function by using quantitative MRI metrics across multiple vascular beds.
Key Results
- ■ After inhalation of nicotine-free electronic cigarette aerosol, femoral artery flow-mediated dilation and reactive hyperemia acceleration were reduced (−34%, P < .001; −25.8%, P < .001, respectively), indicating acute endothelial dysfunction.
- ■ Inhalation of nicotine-free electronic cigarette aerosol was associated with hemoglobin saturation reduction (−20%; P < .001) in the superficial femoral vein, suggesting impaired microvascular function.
- ■ Inhalation of nicotine-free electronic cigarette aerosol was also associated with increase in aortic pulse wave velocity (3%; P = .05), suggesting acute aortic stiffening.
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