E-cigarette, tobacco smoking negatively impact vascular, respiratory function
Electronic (e-)cigarette and tobacco smoking have negative effects on vascular function, suggests a recent study. Tobacco smoking significantly elevates microparticle formation, showing a possible endothelial injury, whereas e-cigarette use induces vasoreactivity and decreases peak expiratory flow.
“[W]e have demonstrated that both electronic and tobacco cigarettes elicit differential effects on circulating microparticles. Our findings suggest that e-cigarette use induces vasoreactivity and that tobacco cigarette use causes an endothelial inflammatory response,” researchers said.
“Underlying mechanisms for these differential responses are unclear but should be investigated. With regard to e-cigarettes, the long-term effects of these phenomena and their potential association with atherogenesis and cardiovascular risk await further clarification,” they added.
E-cigarette use and tobacco smoking both increased heart rate (HR; p<0.001), but blood pressure (BP) remained unchanged (p>0.05). Use of e-cigarettes, but not tobacco smoking, resulted in increased reactive hyperaemia index (RHI, microvascular reactivity; p=0.006) and augmentation index (p=0.010) but not augmentation index standardized to HR 75 bpm (p>0.05). [J Hypertens 2019;37:154-166]
Total microparticles (p<0.001), endothelial microparticles (EMPs, biomarker of endothelial function; p<0.001) and platelet microparticles (PMPs, biomarker of haemostasis/thrombosis; p<0.001) significantly increased following tobacco smoking.
E-cigarettes, on the other hand, only correlated with an increase in PMPs (p<0.001), with no significant changes in the total microparticle fraction or EMPs (p>0.05 for all). Following e-cigarette use, there was a significant decrease in peak expiratory flow (p=0.019).
“We observed a significant increase in HR following the use of both interventions; the effect was more pronounced following exposure to tobacco smoking,” researchers said.
Nicotine was responsible for such haemodynamic response, as it is known to activate the sympathetic nervous system, leading to a transient rise in HR, BP and systemic vasoconstriction. [Trends Cardiovasc Med 2016;26:515-523]
A study by Grassi and colleagues supports this finding, demonstrating significant increases in HR, systolic and diastolic BP, as well as in plasma noradrenaline and adrenaline levels. [Circulation 1994;90:248-253]
“In our study, the significantly greater rise in HR following tobacco cigarette use, compared with electronic cigarette use, may be explained by a faster nicotine absorption rate from tobacco cigarettes in comparison with electronic cigarettes,” researchers said. [Sci Rep 2014;4:4133; Sci Rep 2015;5:11269; Cancer Epidemiol Biomarkers Prev 2010;19:1945-1953]
A total of 20 smokers were included in this study. Their HR, BP, RHI, augmentation index and respiratory function were assessed immediately before and after e-cigarette use and tobacco smoking. Researchers determined the number of microparticles by flow cytometry using counting beads as reference. Total microparticle fraction was detected using labelling with Annexin-V. EMPs were characterized as CD31+CD42− and PMPs as CD31+CD42+.