Aims: Smoking impairs endothelial function as an acute effect. However, few population-based studies have examined the association between smoking status and endothelial function or the dose-response and duration-response association of smoking with endothelial function. We examined whether smoking habits were associated with impaired endothelial function depending on smoking dose and duration.
Methods: We conducted a cross-sectional study of 910 men and women aged 30-79 years from 2013 to 2016. Statistical analyses of the data were conducted between 2016 and 2017. Endothelial function was assessed by brachial artery flow-mediated dilation (FMD) measurement. Low FMD was defined in two ways as the cutoff point based on the lowest quartile of %FMD (<5.1%) and median of %FMD (<6.8%), regarding as impaired endothelial function. We investigated the smoking status in terms of cigarettes consumed per day and the duration of smoking.
Results: Heavy and chronic smokers were associated with a high prevalence of impaired endothelial function. Those associations did not change substantially after adjustment for other cardiovascular risk factors. Among all participants, the multivariable-adjusted ORs (95% CIs) of low FMD (<5.1%) with reference to never smokers were 2.23 (1.00-5.14) for current heavy smokers of ≥ 30 cigarettes per day, 1.83 (1.04-3.20) for heavy smokers of ≥ 40 pack-years, and 2.16 (1.15-4.06) for chronic smokers of ≥ 40 years. For low FMD (<6.8%) those values was 2.17 (1.01-5.05), 1.70 (1.01-2.86), and 1.98 (1.07-3.69), respectively.
Conclusions: Similar associations were observed among only men. Heavy or long-term tobacco smoking may induce impaired endothelial function.
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http://dx.doi.org/10.5551/jat.42150 | DOI Listing |
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Department of Ultrasonography, Fuwai Yunnan Hospital, Chinese Academy of Medical, Sciences/Affiliated Cardiovascular Hospital of Kunming Medical University, Kunming, 650102, China. Electronic address:
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Department of Pulmonary Disease, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 200071, China.
Angiotensin-converting enzyme 2 (ACE2) has been reported to exert a protective effect in acute lung injury (ALI), though its underlying mechanism remains incompletely understood. In this study, ACE2 expression was found to be upregulated in a mouse model of ALI induced by lipopolysaccharide (LPS) injection. ACE2 knockdown modulated the severity of ALI, the extent of autophagy, and the mTOR pathway in this model.
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