Dataset Information

Changes in carotid artery structure with smoking cessation.

ABSTRACT: Carotid artery grayscale ultrasound echogenicity and texture features predict cardiovascular disease events. We evaluated the longitudinal effects of smoking cessation on four grayscale ultrasound measures. This was a secondary analysis of data from 188 age, sex, and body mass index (BMI)-matched smokers (94 eventual abstainers [EA], 94 continued smokers [CS]) from a smoking cessation trial that had carotid ultrasound examinations at baseline and after 3 years. General linear models that included time, smoking group (EA or CS), and a time*smoking interaction term were used to examine the impact of smoking abstinence on carotid artery grayscale marker values at year 3. Participants were mean (SD) 50.3 (11.4) years old (57% female, 86% white). The baseline grayscale median value (GSM) was inversely correlated with age, BMI, insulin resistance, and smoking pack-years (r = -0.20 to -0.30, p < 0.007 for all). There was a significant time*smoking status interaction for predicting GSM at year 3: GSM decreased significantly in the EA group compared to the CS group (-3.63 [13.00] vs CS 0.39 [12.06] units; p = 0.029). BMI increased more in the EA than the CS group (2.42 [3.00] vs CS 0.35 [2.57] kg/m²; p < 0.001). After adjusting for changes in BMI, the time*smoking status interaction no longer was significant (p = 0.138). From baseline to year 3, contrast increased similarly in both groups. Entropy and angular second moment did not change significantly in either group. Changes in carotid ultrasound echogenicity and grayscale texture features during a smoking cessation attempt are modest and mostly related to weight gain. Clinicaltrials.gov Identifier: NCT01553084.

SUBMITTER: Mitchell C

PROVIDER: S-EPMC7552918 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Changes in carotid artery structure with smoking cessation.

Mitchell Carol C Piper Megan E ME Smith Stevens S SS Korcarz Claudia E CE Fiore Michael C MC Baker Timothy B TB Stein James H JH

Vascular medicine (London, England) 20190817 6

Carotid artery grayscale ultrasound echogenicity and texture features predict cardiovascular disease events. We evaluated the longitudinal effects of smoking cessation on four grayscale ultrasound measures. This was a secondary analysis of data from 188 age, sex, and body mass index (BMI)-matched smokers (94 eventual abstainers [EA], 94 continued smokers [CS]) from a smoking cessation trial that had carotid ultrasound examinations at baseline and after 3 years. General linear models that include ...[more]

PMID: 31422759

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Project description:Smoking has a well-documented detrimental effect on risk for myocardial infarction and stroke, but less information is available regarding peripheral artery disease (PAD), particularly among women.To prospectively assess the association of current smoking status, cumulative smoking exposure, and smoking cessation with incident symptomatic PAD in women.Prospective cohort study.U.S. female health care professionals in the Women's Health Study.39,825 women with no cardiovascular disease who were prospectively followed for a median of 12.7 years.Incidence of symptomatic PAD. Cox proportional hazards models were used to compare PAD risk across smoking categories.178 confirmed PAD events occurred. Across the 4 smoking categories (never, former, <15 cigarettes/d, and ?15 cigarettes/d), age-adjusted incidence rates were 0.12, 0.34, 0.95, and 1.63 per 1000 person-years of follow-up, respectively. Multivariate adjustment had little effect on this relationship (adjusted hazard ratios [HRs], 3.14 [95% CI, 2.01 to 4.90], 8.93 [CI, 5.02 to 15.89], and 16.95 [CI, 10.77 to 26.67], respectively, vs. women who never smoked). Additional adjustment for high-sensitivity C-reactive protein and soluble intercellular adhesion molecule-1 levels among women with available blood samples (28,314 participants, 117 events) attenuated risk estimates (HR, 5.58 [CI, 2.61 to 11.93] for smoking <15 cigarettes/d and 9.52 [CI, 5.17 to 17.53] for smoking ?15 cigarettes/d). Lifetime exposure showed a strong dose-response relationship; fully adjusted HRs for smoking abstinence of fewer than 10, 10 to 29, and 30 or more pack-years were 2.52 (CI, 1.49 to 4.25), 6.75 (CI, 4.33 to 10.52), and 11.09 (CI, 6.94 to 17.72), respectively. Compared with current smokers, the adjusted HRs for fewer than 10 years, 10 to 20 years, more than 20 years, or lifelong abstinence were 0.39 (CI, 0.24 to 0.66), 0.28 (CI, 0.17 to 0.46), 0.16 (CI, 0.10 to 0.26), and 0.08 (CI, 0.05 to 0.12), respectively.The use of symptomatic PAD as the a priori primary end point excludes asymptomatic disease.Among initially healthy women, smoking is a potent risk factor for symptomatic PAD and was associated with subclinical inflammation. Smoking cessation substantially reduces risk for PAD, but an increased occurrence of PAD persists even among former smokers who maintain abstinence.The National Heart, Lung, and Blood Institute and National Cancer Institute.

Project description:This study includes samples from two projects: Collaborative Genetic Study of Nicotine Dependence (COGEND; PI: Laura Bierut) and University of Wisconsin Transdisciplinary Tobacco Use Research Center (UW-TTURC; PI: Timothy Baker). Data are available for an additional 1420 COGEND subjects through the Study of Addiction: Genetics and Environment (SAGE), dbGaP study accession <a href="./study.cgi?study_id=phs000092">phs000092</a>. The majority of these subjects are independent from the current study, but there is a small amount of overlap between the two samples (n=29 subjects) for quality control purposes. It should be noted that the case definition in the SAGE study is DSM-IV alcohol dependence. The case definition in the current study is nicotine dependence by a current score of 4 or greater on the Fagerström Test for Nicotine Dependence (FTND). The overall goal of this project is to identify and characterize genetic variants that contribute to the development of nicotine dependence, related smoking behaviors, and smoking cessation. The COGEND sample includes unrelated cases and controls for a genetic association study of nicotine dependence. Cases are defined by a commonly used definition of nicotine dependence, a current score of 4 or more (maximum score of 10) on the Fagerström Test for Nicotine Dependence (FTND). Control status is defined as an individual who smoked at least 100 cigarettes during their lifetime, yet never became dependent (lifetime FTND=0). By selecting controls who smoked, those genetic effects that are specific to nicotine dependence can be examined. The UW-TTURC sample includes nicotine dependent smokers from three smoking cessation studies. Subjects had to smoke at least 10 cigarettes per day (confirmed smoking by an alveolar carbon monoxide (CO) level greater than 9) and report being motivated to quit smoking. Participants were excluded based on evidence of psychosis history, clinically significant depression symptoms, other severe mental illness, or contraindications to smoking cessation medications. COGEND: COGEND was initiated in 2001 as a three-part program project grant funded through the National Cancer Institute (NCI; PI: Laura Bierut). The three projects included a study of the familial transmission of nicotine dependence, a genetic study of nicotine dependence, and a study of the relationship of nicotine dependence with nicotine metabolism. The primary goal is to detect, localize, and characterize genes that predispose or protect an individual with respect to heavy tobacco consumption, nicotine dependence, and related phenotypes and to integrate these findings with the family transmission and nicotine metabolism findings. The primary design is a community based case-control family study. Nicotine dependent cases and non-dependent, smoking controls were identified and recruited from Detroit and St. Louis. In addition, one sibling for each case and control subject was recruited in a subset of the sample. More than 54,000 subjects aged 25-44 years were screened by telephone; more than 3,100 subjects were personally interviewed; and more than 2,900 subjects donated blood samples for genetic studies. UW-TTURC: The UW-TTURC was initiated in 2001 as a study of nicotine dependence and smoking cessation treatment. The second round of UW-TTURC was initiated in 2005 as a study of efficacy of smoking cessation and long term outcomes. Nicotine dependent smokers seeking cessation treatment were identified and recruited from Madison and Milwaukee, WI. Over 9,000 adult smokers were screened by telephone; 2,575 individuals were enrolled and randomized to treatment conditions that involved use of different smoking cessation medications. Participants from the UW-TTURC smoking cessation clinical trials had the option of participating in a genetic substudy, and approximately 2,000 donated blood samples for genetic studies. The goal of the genetic studies of smokers seeking cessation treatment is to detect, localize, and characterize genes that predispose or protect an individual with respect to heavy tobacco consumption, nicotine dependence, and related phenotypes including cessation, withdrawal, and relapse. Both studies (COGEND and UW-TTURC) include measures of basic socio-demographic variables, including age, sex, race/ethnicity, family income, and educational attainment. Information on nicotine dependence, as assessed by the Fagerström Test for Nicotine Dependence (FTND) is available for all subjects. In addition, participants also completed the Nicotine Dependence Syndrome Scale (NDSS; Shiffman et al., 2004) and the Wisconsin Inventory of Smoking Dependence Motives (WISDM-68; Piper et al, 2004). Coding for both individual variables and indices has been standardized across studies. All subjects were assessed in person by trained research assistants. This study is part of the Gene Environment Association Studies initiative (GENEVA, <a href="http://www.genevastudy.org" target="_blank">http://www.genevastudy.org</a>) funded by the trans-NIH Genes, Environment, and Health Initiative (GEI). The overarching goal is to identify novel genetic factors that contribute to the genetic architecture of smoking through large-scale genome-wide association studies of two well-characterized cohorts. Genotyping was performed at the Johns Hopkins University Center for Inherited Disease Research (CIDR). Data cleaning and harmonization were done at the GEI-funded GENEVA Coordinating Center at the University of Washington.

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Changes in carotid artery structure with smoking cessation.

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Changes in carotid artery structure with smoking cessation.

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