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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 |
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creator | 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 |
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 & 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.</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 & 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.</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 & 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.</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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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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