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The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA)

Abstract Background and aims Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure. Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity w...

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Published in:Atherosclerosis 2017-03, Vol.258, p.119-130
Main Authors: Al Rifai, Mahmoud, DeFillippis, Andrew P, McEvoy, John W, Hall, Michael E, Acien, Ana Navas, Jones, Miranda R, Keith, Rachel, Magid, Hoda S, Rodriguez, Carlos J, Barr, Graham R, Benjamin, Emelia J, Robertson, Rose Marie, Bhatnagar, Aruni, Blaha, Michael J
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container_title Atherosclerosis
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creator Al Rifai, Mahmoud
DeFillippis, Andrew P
McEvoy, John W
Hall, Michael E
Acien, Ana Navas
Jones, Miranda R
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Barr, Graham R
Benjamin, Emelia J
Robertson, Rose Marie
Bhatnagar, Aruni
Blaha, Michael J
description Abstract Background and aims Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure. Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 & 2 (IL-2 & IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic & carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration. Results Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: -0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP. Conclusions Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.
doi_str_mv 10.1016/j.atherosclerosis.2017.01.021
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Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 &amp; 2 (IL-2 &amp; IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic &amp; carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration. Results Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: -0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP. Conclusions Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.</description><identifier>ISSN: 0021-9150</identifier><identifier>EISSN: 1879-1484</identifier><identifier>DOI: 10.1016/j.atherosclerosis.2017.01.021</identifier><identifier>PMID: 28237909</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Aged ; Aged, 80 and over ; Biomarkers - blood ; Biomarkers - urine ; Blood Coagulation ; C-Reactive Protein - analysis ; Cardiovascular ; Cardiovascular Diseases - diagnosis ; Cardiovascular Diseases - ethnology ; Cardiovascular Diseases - etiology ; Cardiovascular Diseases - physiopathology ; Chi-Square Distribution ; Cigarette smoking ; Cotinine - urine ; Cross-Sectional Studies ; Cytokines - blood ; Early Diagnosis ; Endothelial damage ; Female ; Fibrin Fibrinogen Degradation Products ; Fibrinogen ; Homocysteine - blood ; Humans ; Inflammation ; Inflammation Mediators - blood ; Linear Models ; Male ; Middle Aged ; Multivariate Analysis ; Myocardial injury ; Predictive Value of Tests ; Risk Assessment ; Risk Factors ; Smoking - adverse effects ; Smoking - ethnology ; Smoking - urine ; Smoking intensity ; Thrombosis ; Tobacco regulatory science ; Troponin T - blood ; United States - epidemiology ; Vascular dysfunction ; Vascular Stiffness ; Vasodilation</subject><ispartof>Atherosclerosis, 2017-03, Vol.258, p.119-130</ispartof><rights>2017 Elsevier B.V.</rights><rights>Copyright © 2017 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c554t-a604345441ac70a51bd3b2ef69a8abfe5cb79ffd1bf50e578fa76b38535a3dee3</citedby><cites>FETCH-LOGICAL-c554t-a604345441ac70a51bd3b2ef69a8abfe5cb79ffd1bf50e578fa76b38535a3dee3</cites><orcidid>0000-0003-4076-2336</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28237909$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Al Rifai, Mahmoud</creatorcontrib><creatorcontrib>DeFillippis, Andrew P</creatorcontrib><creatorcontrib>McEvoy, John W</creatorcontrib><creatorcontrib>Hall, Michael E</creatorcontrib><creatorcontrib>Acien, Ana Navas</creatorcontrib><creatorcontrib>Jones, Miranda R</creatorcontrib><creatorcontrib>Keith, Rachel</creatorcontrib><creatorcontrib>Magid, Hoda S</creatorcontrib><creatorcontrib>Rodriguez, Carlos J</creatorcontrib><creatorcontrib>Barr, Graham R</creatorcontrib><creatorcontrib>Benjamin, Emelia J</creatorcontrib><creatorcontrib>Robertson, Rose Marie</creatorcontrib><creatorcontrib>Bhatnagar, Aruni</creatorcontrib><creatorcontrib>Blaha, Michael J</creatorcontrib><title>The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA)</title><title>Atherosclerosis</title><addtitle>Atherosclerosis</addtitle><description>Abstract Background and aims Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure. Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 &amp; 2 (IL-2 &amp; IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic &amp; carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration. Results Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: -0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP. Conclusions Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biomarkers - blood</subject><subject>Biomarkers - urine</subject><subject>Blood Coagulation</subject><subject>C-Reactive Protein - analysis</subject><subject>Cardiovascular</subject><subject>Cardiovascular Diseases - diagnosis</subject><subject>Cardiovascular Diseases - ethnology</subject><subject>Cardiovascular Diseases - etiology</subject><subject>Cardiovascular Diseases - physiopathology</subject><subject>Chi-Square Distribution</subject><subject>Cigarette smoking</subject><subject>Cotinine - urine</subject><subject>Cross-Sectional Studies</subject><subject>Cytokines - blood</subject><subject>Early Diagnosis</subject><subject>Endothelial damage</subject><subject>Female</subject><subject>Fibrin Fibrinogen Degradation Products</subject><subject>Fibrinogen</subject><subject>Homocysteine - blood</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation Mediators - blood</subject><subject>Linear Models</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Multivariate Analysis</subject><subject>Myocardial injury</subject><subject>Predictive Value of Tests</subject><subject>Risk Assessment</subject><subject>Risk Factors</subject><subject>Smoking - adverse effects</subject><subject>Smoking - ethnology</subject><subject>Smoking - urine</subject><subject>Smoking intensity</subject><subject>Thrombosis</subject><subject>Tobacco regulatory science</subject><subject>Troponin T - blood</subject><subject>United States - epidemiology</subject><subject>Vascular dysfunction</subject><subject>Vascular Stiffness</subject><subject>Vasodilation</subject><issn>0021-9150</issn><issn>1879-1484</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNqNUsFq3DAUFKWl2Sb9haJLoTnYkSxrZRcaWMImDSTksOlZyPJzLMcrL5K8xdd-eWU2CU1OvUjiaWbe8OYh9JWSlBK6POtSFVpwg9f9fBqfZoSKlNCUZPQdWtBClAnNi_w9WpBYSkrKyRH65H1HCMkFLT6io6zImChJuUB_7lvADnoVzGB9a3a4gvAbwGK_HR6NfcDGBrDehAkrW2M_Vro31mjVY61cbYa98nrslYvAbnTTdzwr3o59MMk6tBGJN2GsJzw0ePXaOf52u96sTk_Qh0b1Hj4_3cfo1-X6_uJncnN3dX2xukk053lI1JLkLOd5TpUWRHFa1azKoFmWqlBVA1xXomyamlYNJ8BF0SixrFjBGVesBmDH6PyguxurLdQabHCqlztntspNclBGvv6xppUPw17yPHYuiijw4yCgo33voHnhUiLncGQn34Qj53AkoTImEflf_jXwwn5OIwKuDgCIY9gbcNJrA1ZDbRzoIOvB_Her8zdKz6k9wgS-G0Zn46wllT6TRG7mTZkXhQoWn4ywv9BnxKI</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Al Rifai, Mahmoud</creator><creator>DeFillippis, Andrew P</creator><creator>McEvoy, John W</creator><creator>Hall, Michael E</creator><creator>Acien, Ana Navas</creator><creator>Jones, Miranda R</creator><creator>Keith, Rachel</creator><creator>Magid, Hoda S</creator><creator>Rodriguez, Carlos J</creator><creator>Barr, Graham R</creator><creator>Benjamin, Emelia J</creator><creator>Robertson, Rose Marie</creator><creator>Bhatnagar, Aruni</creator><creator>Blaha, Michael J</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-4076-2336</orcidid></search><sort><creationdate>20170301</creationdate><title>The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA)</title><author>Al Rifai, Mahmoud ; DeFillippis, Andrew P ; McEvoy, John W ; Hall, Michael E ; Acien, Ana Navas ; Jones, Miranda R ; Keith, Rachel ; Magid, Hoda S ; Rodriguez, Carlos J ; Barr, Graham R ; Benjamin, Emelia J ; Robertson, Rose Marie ; Bhatnagar, Aruni ; Blaha, Michael J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c554t-a604345441ac70a51bd3b2ef69a8abfe5cb79ffd1bf50e578fa76b38535a3dee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biomarkers - blood</topic><topic>Biomarkers - urine</topic><topic>Blood Coagulation</topic><topic>C-Reactive Protein - analysis</topic><topic>Cardiovascular</topic><topic>Cardiovascular Diseases - diagnosis</topic><topic>Cardiovascular Diseases - ethnology</topic><topic>Cardiovascular Diseases - etiology</topic><topic>Cardiovascular Diseases - physiopathology</topic><topic>Chi-Square Distribution</topic><topic>Cigarette smoking</topic><topic>Cotinine - urine</topic><topic>Cross-Sectional Studies</topic><topic>Cytokines - blood</topic><topic>Early Diagnosis</topic><topic>Endothelial damage</topic><topic>Female</topic><topic>Fibrin Fibrinogen Degradation Products</topic><topic>Fibrinogen</topic><topic>Homocysteine - blood</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation Mediators - blood</topic><topic>Linear Models</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Multivariate Analysis</topic><topic>Myocardial injury</topic><topic>Predictive Value of Tests</topic><topic>Risk Assessment</topic><topic>Risk Factors</topic><topic>Smoking - adverse effects</topic><topic>Smoking - ethnology</topic><topic>Smoking - urine</topic><topic>Smoking intensity</topic><topic>Thrombosis</topic><topic>Tobacco regulatory science</topic><topic>Troponin T - blood</topic><topic>United States - epidemiology</topic><topic>Vascular dysfunction</topic><topic>Vascular Stiffness</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Al Rifai, Mahmoud</creatorcontrib><creatorcontrib>DeFillippis, Andrew P</creatorcontrib><creatorcontrib>McEvoy, John W</creatorcontrib><creatorcontrib>Hall, Michael E</creatorcontrib><creatorcontrib>Acien, Ana Navas</creatorcontrib><creatorcontrib>Jones, Miranda R</creatorcontrib><creatorcontrib>Keith, Rachel</creatorcontrib><creatorcontrib>Magid, Hoda S</creatorcontrib><creatorcontrib>Rodriguez, Carlos J</creatorcontrib><creatorcontrib>Barr, Graham R</creatorcontrib><creatorcontrib>Benjamin, Emelia J</creatorcontrib><creatorcontrib>Robertson, Rose Marie</creatorcontrib><creatorcontrib>Bhatnagar, Aruni</creatorcontrib><creatorcontrib>Blaha, Michael J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Atherosclerosis</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Al Rifai, Mahmoud</au><au>DeFillippis, Andrew P</au><au>McEvoy, John W</au><au>Hall, Michael E</au><au>Acien, Ana Navas</au><au>Jones, Miranda R</au><au>Keith, Rachel</au><au>Magid, Hoda S</au><au>Rodriguez, Carlos J</au><au>Barr, Graham R</au><au>Benjamin, Emelia J</au><au>Robertson, Rose Marie</au><au>Bhatnagar, Aruni</au><au>Blaha, Michael J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA)</atitle><jtitle>Atherosclerosis</jtitle><addtitle>Atherosclerosis</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>258</volume><spage>119</spage><epage>130</epage><pages>119-130</pages><issn>0021-9150</issn><eissn>1879-1484</eissn><abstract>Abstract Background and aims Modern tobacco regulatory science requires an understanding of which biomarkers of cardiovascular injury are most sensitive to cigarette smoking exposure. Methods We studied self-reported current smokers from the Multi-Ethnic Study of Atherosclerosis. Smoking intensity was defined by number of cigarettes/day and urinary cotinine levels. Subclinical cardiovascular injury was assessed using markers of inflammation [high-sensitivity C-reactive protein (hsCRP), interleukin 6 &amp; 2 (IL-2 &amp; IL-6), tumor necrosis factor alpha (TNF-α)], thrombosis (fibrinogen, D-dimer, homocysteine), myocardial injury (troponin T; TnT), endothelial damage (albumin: creatinine ratio), and vascular function [aortic &amp; carotid distensibility, flow-mediated dilation (FMD)]. Biomarkers were modeled as absolute and percent change using multivariable-adjusted linear regression models adjusted for cardiovascular risk factors and smoking duration. Results Among 843 current smokers, mean age was 58 (9) years, 53% were men, 39% were African American, mean number of cigarettes per day was 13 (10), and median smoking duration was 39 (15) years. Cigarette count was significantly associated with higher hsCRP, IL-6 and fibrinogen (β coefficients: 0.013, 0.011, 0.60 respectively), while ln-transformed cotinine was associated with the same biomarkers (β coefficients: 0.12, 0.04, 5.3 respectively) and inversely associated with aortic distensibility (β coefficient: -0.13). There was a limited association between smoking intensity and homocysteine, D-dimer, and albumin:creatinine ratio in partially adjusted models only, while there was no association with IL-2, TNF-α, carotid distensibility, FMD, or TnT in any model. In percent change analyses, relationships were strongest with hsCRP. Conclusions Smoking intensity was associated with early biomarkers of CVD, particularly, markers of systemic inflammation. Of these, hsCRP may be the most sensitive.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>28237909</pmid><doi>10.1016/j.atherosclerosis.2017.01.021</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0003-4076-2336</orcidid><oa>free_for_read</oa></addata></record>
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language eng
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source Elsevier
subjects Aged
Aged, 80 and over
Biomarkers - blood
Biomarkers - urine
Blood Coagulation
C-Reactive Protein - analysis
Cardiovascular
Cardiovascular Diseases - diagnosis
Cardiovascular Diseases - ethnology
Cardiovascular Diseases - etiology
Cardiovascular Diseases - physiopathology
Chi-Square Distribution
Cigarette smoking
Cotinine - urine
Cross-Sectional Studies
Cytokines - blood
Early Diagnosis
Endothelial damage
Female
Fibrin Fibrinogen Degradation Products
Fibrinogen
Homocysteine - blood
Humans
Inflammation
Inflammation Mediators - blood
Linear Models
Male
Middle Aged
Multivariate Analysis
Myocardial injury
Predictive Value of Tests
Risk Assessment
Risk Factors
Smoking - adverse effects
Smoking - ethnology
Smoking - urine
Smoking intensity
Thrombosis
Tobacco regulatory science
Troponin T - blood
United States - epidemiology
Vascular dysfunction
Vascular Stiffness
Vasodilation
title The relationship between smoking intensity and subclinical cardiovascular injury: The Multi-Ethnic Study of Atherosclerosis (MESA)
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