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Article: The mediating role of inflammation in the association between cigarette smoking and intima-media thickness

TitleThe mediating role of inflammation in the association between cigarette smoking and intima-media thickness
Authors
Keywordsatherosclerosis
cigarette smoking
inflammation
mediation analysis
Issue Date2020
PublisherLippincott, Williams & Wilkins: Various Creative Commons. The Journal's web site is located at http://journals.lww.com/md-journal/pages/default.aspx
Citation
Medicine, 2020, v. 99 n. 8, p. article no. e19207 How to Cite?
AbstractCigarette smoking is associated with thicker carotid intima-media thickness (IMT), probably partly through inflammatory pathways. However, to what extent does inflammation mediate the smoking-carotid atherosclerosis association is unclear. We investigated the mediating effect of inflammation on the association between cigarette smoking and carotid IMT, and quantified the respective contributions of inflammatory markers to this association. A total of 1752 participants from Guangzhou Biobank Cohort Study-Cardiovascular Disease Sub-cohort (GBCS-CVD) were included. Using causal mediation analysis under the counterfactual framework, we decomposed total effects of cigarette smoking on IMT into indirect effects (through inflammatory response) and direct effects (not through inflammatory response). After adjusting for traditional risk factors, the indirect effects of per 109/L increment in leukocyte and granulocyte, per mg/L increment in high-sensitivity C-reactive protein (hs-CRP), and per mg/dL increment in fibrinogen on carotid IMT was 0.0028 mm (95% confidence interval [CI], 0.0011–0.0047), 0.0019 mm (95% CI, 0.0006–0.0034), 0.0017 mm (95% CI, 0.0006–0.003), and 0.001 mm (95% CI, 0.0001–0.0021), respectively. No evidence for a mediating role of lymphocyte was found. The proportion of the smoking-IMT association mediated by leukocyte, granulocyte, hs-CRP, and fibrinogen was 12.57% (95% CI, 8.50%–22.11%), 8.50% (95% CI, 5.76%–15.09%), 7.64% (95% CI, 5.20%–13.79%), and 4.48% (95% CI, 3.04%–8.03%), respectively. Restricting data analysis to men showed similar results. The effects of cigarette smoking on IMT were partly mediated by leukocyte, hs-CRP, and fibrinogen. The mediating role of leukocyte was likely mainly driven by higher granulocyte.
Persistent Identifierhttp://hdl.handle.net/10722/281153
ISSN
2019 Impact Factor: 1.552
2015 SCImago Journal Rankings: 0.877

 

DC FieldValueLanguage
dc.contributor.authorWang, T-
dc.contributor.authorJiang, CQ-
dc.contributor.authorXu, L-
dc.contributor.authorZhang, WS-
dc.contributor.authorZhu, F-
dc.contributor.authorJin, YL-
dc.contributor.authorThomas, GN-
dc.contributor.authorCheng, KK-
dc.contributor.authorLam, TH-
dc.date.accessioned2020-03-09T09:50:53Z-
dc.date.available2020-03-09T09:50:53Z-
dc.date.issued2020-
dc.identifier.citationMedicine, 2020, v. 99 n. 8, p. article no. e19207-
dc.identifier.issn0025-7974-
dc.identifier.urihttp://hdl.handle.net/10722/281153-
dc.description.abstractCigarette smoking is associated with thicker carotid intima-media thickness (IMT), probably partly through inflammatory pathways. However, to what extent does inflammation mediate the smoking-carotid atherosclerosis association is unclear. We investigated the mediating effect of inflammation on the association between cigarette smoking and carotid IMT, and quantified the respective contributions of inflammatory markers to this association. A total of 1752 participants from Guangzhou Biobank Cohort Study-Cardiovascular Disease Sub-cohort (GBCS-CVD) were included. Using causal mediation analysis under the counterfactual framework, we decomposed total effects of cigarette smoking on IMT into indirect effects (through inflammatory response) and direct effects (not through inflammatory response). After adjusting for traditional risk factors, the indirect effects of per 109/L increment in leukocyte and granulocyte, per mg/L increment in high-sensitivity C-reactive protein (hs-CRP), and per mg/dL increment in fibrinogen on carotid IMT was 0.0028 mm (95% confidence interval [CI], 0.0011–0.0047), 0.0019 mm (95% CI, 0.0006–0.0034), 0.0017 mm (95% CI, 0.0006–0.003), and 0.001 mm (95% CI, 0.0001–0.0021), respectively. No evidence for a mediating role of lymphocyte was found. The proportion of the smoking-IMT association mediated by leukocyte, granulocyte, hs-CRP, and fibrinogen was 12.57% (95% CI, 8.50%–22.11%), 8.50% (95% CI, 5.76%–15.09%), 7.64% (95% CI, 5.20%–13.79%), and 4.48% (95% CI, 3.04%–8.03%), respectively. Restricting data analysis to men showed similar results. The effects of cigarette smoking on IMT were partly mediated by leukocyte, hs-CRP, and fibrinogen. The mediating role of leukocyte was likely mainly driven by higher granulocyte.-
dc.languageeng-
dc.publisherLippincott, Williams & Wilkins: Various Creative Commons. The Journal's web site is located at http://journals.lww.com/md-journal/pages/default.aspx-
dc.relation.ispartofMedicine-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectatherosclerosis-
dc.subjectcigarette smoking-
dc.subjectinflammation-
dc.subjectmediation analysis-
dc.titleThe mediating role of inflammation in the association between cigarette smoking and intima-media thickness-
dc.typeArticle-
dc.identifier.emailJiang, CQ: cqjiang@hkucc.hku.hk-
dc.identifier.emailXu, L: linxu@hku.hk-
dc.identifier.emailZhang, WS: zhangws9@hku.hk-
dc.identifier.emailThomas, GN: neilt@hkucc.hku.hk-
dc.identifier.emailCheng, KK: chengkk@hkucc.hku.hk-
dc.identifier.emailLam, TH: hrmrlth@hkucc.hku.hk-
dc.identifier.authorityXu, L=rp02030-
dc.identifier.authorityLam, TH=rp00326-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1097/MD.0000000000019207-
dc.identifier.pmid32080108-
dc.identifier.scopuseid_2-s2.0-85079813037-
dc.identifier.hkuros309293-
dc.identifier.volume99-
dc.identifier.issue8-
dc.identifier.spagearticle no. e19207-
dc.identifier.epagearticle no. e19207-
dc.publisher.placeUnited States-

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