scholarly journals Cigarette Smoking Is Related to Endothelial Dysfunction of Resistance, but Not Conduit Arteries in the General Population—Results From the Gutenberg Health Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Omar Hahad ◽  
Natalie Arnold ◽  
Jürgen H. Prochaska ◽  
Marina Panova-Noeva ◽  
Andreas Schulz ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Cigarette Smoking ◽  
Endothelial Function ◽  
Smoking Status ◽  
Health Study ◽  
Computer Assisted ◽  
Resistance Arteries ◽  
Gutenberg Health Study ◽  
Quitting Smoking ◽  
Former Smokers

Aims: Cigarette smoking is one of the most complex and least understood cardiovascular risk factors. Importantly, differences in the tobacco-related pathophysiology of endothelial dysfunction, an early event in atherogenesis, between circulatory beds remain elusive. Therefore, this study evaluated how smoking impacts endothelial function of conduit and resistance arteries in a large population-based cohort.Methods and results: 15,010 participants (aged 35–74 years) of the Gutenberg Health Study were examined at baseline from 2007 to 2012. Smoking status, pack-years of smoking, and years since quitting smoking were assessed by a computer-assisted interview. Endothelial function of conduit and resistance arteries was determined by flow-mediated dilation (FMD) of the brachial artery, reactive hyperemia index (RHI) using peripheral arterial tonometry, as well as by reflection index (RI) derived from digital photoplethysmography, respectively. Among all subjects, 45.8% had never smoked, 34.7% were former smokers, and 19.4% were current smokers. Mean cumulative smoking exposure was 22.1 ± 18.1 pack-years in current smokers and mean years since quitting was 18.9 ± 12.7 in former smokers. In multivariable linear regression models adjusted for typical confounders, smoking status, pack-years of smoking, and years since quitting smoking were independently associated with RHI and RI, while no association was found for FMD. Overall, no clear dose-dependent associations were observed between variables, whereby higher exposure tended to be associated with pronounced resistance artery endothelial dysfunction.Conclusions: Cigarette smoking is associated with altered endothelial function of resistance, but not conduit arteries. The present results suggest that smoking-induced endothelial dysfunction in different circulatory beds may exhibit a differential picture.

scholarly journals Association of smoking status and smoking intensity with general and abdominal obesity in a sample of middle-aged men

2020 ◽  
Vol 19 (3) ◽  
pp. 2446
Author(s):  
A. A. Alexandrov ◽  
V. B. Rozanov ◽  
V. A. Dadaeva ◽  
M. B. Kotova ◽  
E. I. Ivanova ◽  
...  
Keyword(s):  
Linear Relationship ◽  
Abdominal Obesity ◽  
Smoking Status ◽  
Population Sample ◽  
Initial Population ◽  
Anthropometric Parameters ◽  
Waist To Hip Ratio ◽  
Smoking Intensity ◽  
Quitting Smoking ◽  
Former Smokers

Aim. To assess the association of smoking status and smoking intensity with general and abdominal obesity in a sample of middle-a ged men.Material and methods. This study was conducted as a part of the 32-year prospective cohort observation of males from childhood (11-12 years of age). The study included 301 (30,0%) representatives of the initial population sample aged 41-44 years. Age, anthropometric parameters, relationship of smoking status and smoking intensity with general (overweight/obesity) and abdominal obesity were analyzed.Results. Overweight/obesity were more common in former smokers (78,1%) compared with non-smokers (58,7%; p<0,01). Abdominal obesity, estimated by the waist circumference (WC), was detected more often among former (57,5%) and current smokers (50,7%), and abdominal obesity, estimated by the waist-to-hip ratio, was more common among current smokers, compared with non-smokers (37,0%; p<0,01, p<0,05 and p<0,05 respectively). A direct linear relationship was found between the intensity of current smoking and indicators of abdominal obesity in terms of waist-to-hip ratio (P for trend=0,004) and a direct linear relationship between intensity of former smoking and general obesity estimated by BMI (P for trend = 0,001), and abdominal obesity estimated by waist-tohip ratio (P for trend=0,004). The probability of developing abdominal obesity in current smokers with WC≥94,0 cm and with waist-to-hip ratio ≥0,9 was 1,8 and 2 times higher, respectively, than in non-smokers, but lower compared to former smokers. The risk of overweight/obesity and abdominal obesity in former smokers was 2,5 and 2,3 times higher, respectively, than in non-smokers. The 10-year risk of fatal CVD in nonsmokers and former smokers was lower than in current smokers (0,8% and 0,9% vs 1,8%; p<0,001 and p<0,001, respectively).Conclusion. High intensity of smoking among current smokers is associated with a higher probability of developing abdominal obesity, and in former smokers — with a higher probability of developing general and abdominal obesity. Former smokers, compared to current smokers, are at a lower risk of developing fatal cardiovascular diseases. Smoking cessation activities should be aimed at minimizing weight gain after quitting smoking and developing tobacco control programs.

Association of device type, flavours and vaping behaviour with tobacco product transitions among adult electronic cigarette users in the USA

2021 ◽  
pp. tobaccocontrol-2020-055999
Author(s):  
Alyssa F Harlow ◽  
Jessica L Fetterman ◽  
Craig S Ross ◽  
Rose Marie Robertson ◽  
Aruni Bhatnagar ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Multinomial Logistic Regression ◽  
Sociodemographic Factors ◽  
Tobacco Product ◽  
Electronic Cigarette ◽  
Health Study ◽  
Cigarette Use ◽  
Use Patterns ◽  
The Usa ◽  
Former Smokers

BackgroundFew studies assess whether electronic cigarette (e-cigarette) device characteristics or flavours impact longitudinal patterns of cigarette and e-cigarette use.DesignWe examined data from waves 2–4 of the Population Assessment of Tobacco and Health Study (2014–2018). Among adult (≥18 years) current e-cigarette users at wave 2 who were current smokers (dual users; n=1759) and former smokers (exclusive e-cigarette users; n=470), we classified participants into four use patterns at wave 3 (~12 months later) and wave 4 (~24 months later): (1) dual use of e-cigarettes and cigarettes; (2) exclusive cigarette smoking; (3) exclusive e-cigarette use; (4) non-use of both products. We used multinomial logistic regression to assess correlates of changing use patterns at 24 months, relative to no change, adjusting for sociodemographic factors.ResultsAt 24 months, 26.5% of baseline exclusive e-cigarette users, and 9% of baseline dual users, abstained from both vaping and smoking. Participants who vaped non-tobacco flavours (vs tobacco flavours), and used refillable tank or modifiable devices (vs disposable, cartridges and other devices) were less likely to transition to non-use of both products and to exclusive cigarette smoking. Baseline daily vaping (vs non-daily) was positively associated with exclusive e-cigarette use at 24 months for baseline daily cigarette smokers, but negatively associated with exclusive e-cigarette use and non-use of both products at 24 months for baseline non-daily smokers.ConclusionsNon-tobacco flavours, daily vaping and modifiable e-cigarette devices may help some smokers abstain from cigarette smoking via transitioning to exclusive e-cigarette use, but are also associated with ongoing exclusive e-cigarette use.

scholarly journals Smoking status and endothelial function in Japanese men

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haruki Hashimoto ◽  
Tatsuya Maruhashi ◽  
Takayuki Yamaji ◽  
Takahiro Harada ◽  
Yiming Han ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Vascular Function ◽  
Reference Group ◽  
Smoking Status ◽  
Critical Role ◽  
Heavy Smoker ◽  
Japanese Men ◽  
Light Smoker ◽  
Never Smoker

AbstractIt is established that smoking is a major risk factor of atherosclerosis. Endothelial dysfunction occurs in the initial step in the pathogenesis of atherosclerosis and plays a critical role in the development of atherosclerosis. The purpose of this study was to evaluate the association between smoking status and endothelial function in detail in men. We measured flow-mediated vasodilation (FMD) in 2209 Japanese men including 1181 men who had never smoked and 1028 current smokers. All of the participants were divided into five groups by smoking pack-years: never smoker group (= 0), light smoker group (> 0 to 10), moderate smoker group (> 10 to 20), heavy smoker group (> 20 to 30) and excessive smoker group (> 30). FMD significantly decreased in relation to pack-years (6.6 ± 3.4% in the never smoker group, 6.8 ± 3.0% in the light smoker group, 6.5 ± 2.9% in the moderate smoker group, 5.9 ± 2.9% in the heavy smoker group, and 4.9 ± 2.7% in the excessive smoker group; P < 0.001). After adjustment for age (≥ 65 years), body mass index, systolic blood pressure, low-density lipoprotein cholesterol, glucose, and year of recruitment, FMD was significantly smaller in the excessive smoker group than in the never smoker group as a reference group (OR 1.95, 95% CI 1.42 to 2.67; P < 0.001). These findings suggest that FMD decreases with an increase in the number of cigarettes smoked and that excessive smoking is associated with endothelial dysfunction. Cigarette smoking is harmful to vascular function in men who are heavy smokers.

scholarly journals Effect modification of the association between total cigarette smoking and ALS risk by intensity, duration and time-since-quitting: Euro-MOTOR

2019 ◽  
Vol 91 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Susan Peters ◽  
Anne E Visser ◽  
Fabrizio D'Ovidio ◽  
Jelle Vlaanderen ◽  
Lützen Portengen ◽  
...  
Keyword(s):  
Cigarette Smoking ◽  
Smoking Status ◽  
Disease Onset ◽  
Population Based ◽  
Pooled Analysis ◽  
Effect Modification ◽  
Case Control Studies ◽  
Alcohol Education ◽  
Logistic Regression Models ◽  
Quitting Smoking

BackgroundWe investigated the association between cigarette smoking and risk of amyotrophic lateral sclerosis (ALS) in a pooled analysis of population-based case–control studies and explored the independent effects of intensity, duration and time-since-quitting.MethodsALS cases and controls, matched by age, sex and region, were recruited in the Netherlands, Italy and Ireland (*Euro-MOTOR project). Demographics and detailed lifetime smoking histories were collected through questionnaires. Effects of smoking status, intensity (cigarettes/day), duration (years), pack-years and time-since-quitting (years) on ALS risk were estimated using logistic regression models, adjusting for age, sex, alcohol, education and centre. We further investigated effect modification of the linear effects of pack-years by intensity, duration and time-since-quitting using excess OR (eOR) models.ResultsAnalyses were performed on 1410 cases and 2616 controls. Pack-years were positively associated with ALS risk; OR=1.26 (95% CI: 1.03 to 1.54) for the highest quartile compared with never smokers. This association appeared to be predominantly driven by smoking duration (ptrend=0.001) rather than intensity (ptrend=0.86), although the trend for duration disappeared after adjustment for time-since-quitting. Time-since-quitting was inversely related to ALS (ptrend<0.0001). The eOR decreased with time-since-quitting smoking, until about 10 years prior to disease onset. High intensity smoking with shorter duration appeared more deleterious than lower intensity for a longer duration.ConclusionsOur findings provide further support for the association between smoking and ALS. Pack-years alone may be insufficient to capture effects of different smoking patterns. Time-since-quitting appeared to be an important factor, suggesting that smoking may be an early disease trigger.

scholarly journals Effect of an inhaled glucocorticoid on endothelial function in healthy smokers

2008 ◽  
Vol 105 (1) ◽  
pp. 54-57 ◽  
Author(s):  
Eliana S. Mendes ◽  
Gabor Horvath ◽  
Patricia Rebolledo ◽  
Maria Elena Monzon ◽  
S. Marina Casalino-Matsuda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Endothelial Dysfunction ◽  
Cigarette Smoking ◽  
Endothelial Function ◽  
Vascular Reactivity ◽  
Systemic Circulation ◽  
Sublingual Nitroglycerin ◽  
Proof Of Concept ◽  
Inhaled Corticosteroid ◽  
Clinical Investigations

Cigarette smoking is associated with attenuated endothelium-dependent vasodilation (endothelial dysfunction) in the systemic circulation, including the airway circulation. We wished to determine whether an inhaled corticosteroid could restore endothelial function in the airway of lung-healthy current smokers, ex-smokers, and nonsmokers. We measured baseline airway blood flow (Q̇aw) and Q̇aw reactivity to inhaled albuterol as an index of endothelium-dependent vasodilation and to sublingual nitroglycerin as an index of endothelium-independent vasodilation in lung-healthy current smokers, ex-smokers, and nonsmokers. Current smokers were then treated with inhaled fluticasone for 3 wk, and all measurements were repeated after fluticasone treatment and after a subsequent 3-wk fluticasone washout period. Baseline mean Q̇aw and endothelium-independent Q̇aw reactivity were similar in the three groups. Mean endothelium-dependent Q̇aw reactivity was 49.5% in nonsmokers, 42.7% in ex-smokers, and 10.8% in current smokers ( P < 0.05 vs. nonsmokers). In current smokers, mean baseline Q̇aw was unchanged after fluticasone treatment, but endothelium-dependent Q̇aw reactivity significantly increased to 34.9%. Q̇aw reactivity was again blunted after fluticasone washout. Endothelial dysfunction, as assessed by vascular reactivity, can be corrected with an inhaled corticosteroid in the airway of lung-healthy current smokers. This proof of concept can serve as the basis for future clinical investigations on the effect of glucocorticoids on endothelial function in smokers.

scholarly journals Receipt of tobacco direct mail/email discount coupons and trajectories of cigarette smoking behaviours in a nationally representative longitudinal cohort of US adults

2018 ◽  
Vol 28 (3) ◽  
pp. 282-288 ◽  
Author(s):  
Kelvin Choi ◽  
Julia Cen Chen ◽  
Andy S L Tan ◽  
Samir Soneji ◽  
Meghan B Moran
Keyword(s):  
Smoking Status ◽  
Smoking Initiation ◽  
Direct Mail ◽  
Health Study ◽  
Demographic Correlates ◽  
Former Smokers ◽  
Nationally Representative ◽  
Never Smokers ◽  
Study Participants ◽  
Smoking Behaviours

BackgroundWe assessed whether receipt of coupons—via direct mail or e-mail—was prospectively related to trajectories of smoking behaviours.MethodsData were from a cohort of US adults (n=26 447) who participated in wave 1 (2013–2014) and wave 2 (2014–2015) of the Population Assessment of Tobacco and Health Study. Participants reported receipt of tobacco direct mail/email coupons in the past 6 months in wave 1 and their smoking status in both waves. Weighted multiple logistic regressions were used to examine demographic correlates of receiving tobacco direct mail/email coupons at wave 1 and to examine the prospective effect of receiving tobacco coupons on trajectories of smoking behaviours.FindingsAt wave 1, 10.7% of never smokers, 13.9% of experimental smokers, 37.1% of current smokers and 16.5% of former smokers reported receiving tobacco direct mail/email coupons. Lower education and higher poverty adults and non-Hispanic white current smokers were more likely to have received these coupons (p<0.05). Receiving tobacco direct mail/email coupons at wave 1 was associated with increased odds of smoking initiation among never smokers (adjusted odds ratio (AOR)=2.28, 95% CI 1.36 to 3.83), becoming established smokers among experimenters (AOR=1.62, 95% CI 1.29 to 2.04), becoming daily smokers among non-daily smokers (AOR=1.56, 95% CI 1.23 to 1.99) and smoking relapse among former smokers between waves (AOR=1.91, 95% CI 1.39 to 2.65). Receiving these coupons at wave 1 was associated with reduced odds of smoking cessation ≥6 months among current smokers (AOR=0.71, 95% CI 0.58 to 0.88).ConclusionsTobacco direct mail/email coupons encourage and sustain smoking and disproportionately affect lower socioeconomic populations.

scholarly journals Maternal exposure to cigarette smoking induces immediate and durable changes in placental DNA methylation affecting enhancer and imprinting control regions

2019 ◽  
Author(s):  
Sophie Rousseaux ◽  
Emie Seyve ◽  
Florent Chuffart ◽  
Ekaterina Bourova-Flin ◽  
Meriem Benmerad ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cigarette Smoking ◽  
Smoking Status ◽  
Gene Clusters ◽  
Tobacco Exposure ◽  
Smoking During Pregnancy ◽  
Former Smokers ◽  
Genomic Regions ◽  
Methylation Patterns ◽  
Control Regions

AbstractObjectiveExposure to cigarette smoking during pregnancy has been robustly associated with cord blood DNA methylation. However, little is known about such effects on the placenta; in particular, whether cigarette smoking before pregnancy could also induce epigenetic alterations in the placenta of former smokers is unknown.Design and resultsPlacental DNA methylation levels were measured in 568 women and compared among non-smokers and women either smoking during their pregnancy or who had ceased smoking before pregnancy. An Epigenome Wide Association Study identified 344 Differentially Methylated Regions (DMRs) significantly associated with maternal smoking status. Among these 344 DMRs, 262 showed “reversible” alterations of DNA methylation, only present in the placenta of current smokers, whereas 44 were also found altered in former smokers, whose placenta had not been exposed directly to cigarette smoking. This observation was further supported by a significant demethylation of LINE-1 sequences in the placentas of both current (−0.43 (−0.83 to −0.02)) and former smokers (−0.55 (−1.02 to −0.08)) compared to nonsmokers. A comparative analysis of the epigenome landscape based on the ENCODE placenta data demonstrated an enrichment of all 344 DMRs in enhancers histone marks. Additionally, smoking-associated DMRs were found near and/or overlapping with 13 imprinting gene clusters encompassing 18 imprinted genes.ConclusionsDNA methylation patterns alterations were found in 344 genomic regions in the placenta of women smoking during their pregnancy, including 44 DMRs and LINE-1 elements, where methylation changes persisted in former smokers, supporting the hypothesis of an “epigenetic memory” of exposure to cigarette smoking before pregnancy. Enhancers regions, including imprinting control regions were also particularly affected by placenta methylation changes associated to smoking, suggesting a biological basis for the sensitivity of these regions to tobacco exposure and mechanisms by which fetal development could be impacted.

Abstract WP415: Cigarette Smoking as Risk Factor for Hematoma Expansion in Primary Intracerebral Hemorrhage: Analysis From a Randomized Clinical Trial

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Shahram Majidi ◽  
Lydia Foster ◽  
Christopher P Kellner ◽  
Jose I Suarez ◽  
Adnan I Qureshi ◽  
...  
Keyword(s):  
Risk Factor ◽  
Cigarette Smoking ◽  
Intracerebral Hemorrhage ◽  
Smoking Status ◽  
Hematoma Expansion ◽  
Primary Analysis ◽  
Significant Difference ◽  
Former Smokers ◽  
Gcs Score ◽  
The Impact

Background: Cigarette smoking is a well-known risk factor for ischemic and hemorrhagic stroke. We evaluated the impact of smoking status on hematoma expansion and clinical outcome in patients with primary intracerebral hemorrhage (ICH). Methods: This is a post hoc exploratory analysis of Antihypertensive Treatment at Acute Cerebral Hemorrhage(ATACH)-2 trial. Patients with ICH were randomized into intensive blood pressure lowering(SBP: <139 mmHg) versus Baseline characteristics were compared based on smoking status. Analysis of outcome measures was adjusted for covariates included in the ATACH-2 primary analysis or those associated with smoking status. Results: Of total of 914 patients in the trial with known smoking status, 439 (48%) patients were ever-smokers (264 current smokers and 175 former smokers). Current and former smokers were younger and more likely to be male. There was no difference in the baseline Glasgow Coma Scale(GCS) score and initial hematoma size based on smoking status. Ever-smokers had higher rate of thalamic hemorrhage (42% vs 34%) and intraventricular hemorrhage (29% vs 23%); this rate was highest among former smokers (49% and 35%, respectively). Ever-smokers had higher rate of hematoma expansion in 24 hour [adjusted RR (95% CI): 1.46; (1.05 -2.03)] compared to non-smokers after adjusting for confounding factors. There was no significant difference in the rate of death and disability at 90 days between the two groups [adjusted RR; (95% CI): 1.18; (0.93 -1.50)]. Conclusions: Our analysis demonstrates cigarette smoking as an independent predictor for hematoma expansion. There was no significant difference in death and disability based on smoking status.

Abstract 55: Hiv Viral Proteins Elevate Blood Pressure And Impairs Endothelial Function In Resistance Arteries Via Sex Specific, Immune And Nox1-dependent Mechanisms In Mice.

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Taylor Kress
Keyword(s):  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Viral Infection ◽  
Immune Cells ◽  
Vascular Reactivity ◽  
Radio Telemetry ◽  
Viral Proteins ◽  
Mesenteric Arteries ◽  
Resistance Arteries

Thanks to the onset of combination antiretroviral therapy (cART), patients living with HIV live longer but experience accelerated rates of hypertension. However, the etiology of HIV-associated hypertension remains ill defined, specifically the respective contributions of repressed viral infection and cART treatment. Herein, we took advantage of a transgenic model (Tg26) of repressed viral infection to investigate the contribution of HIV viral proteins to hypertension. Quantification of inflammatory cytokines revealed elevated circulating TNFα levels but also high aorta and intraperitoneal immune cells TNFα in male Tg26 mice leading to the hypothesis that HIV-associated hypertension involves immune-derived TNFα secretion and endothelial dysfunction in males and females Tg26 mice. Blood pressure (BP) was measured via radio telemetry and vascular reactivity studies performed via wire myography. BP analysis revealed increased mean arterial pressure (MAP: male: WT=112.3±1.3 vs Tg26=121.9±4.0 mmHg/ female: WT=110.6±3.01/ Tg26=120.3±6.9 mmHg) and heart rate in both sexes (P<0.05). However, blockade of TNFα action with etanercept restored BP and aortic endothelial function in male Tg26 mice only. Along with an increase in TNFα, male Tg26 aortas showed infiltration of Tcells and proinflammatory cytokines IL-18, and IL-6, which were not seen in females. However, scavenging of reactive oxygen species with the selective NOX1 inhibitor GKT771 restored aorta endothelial function in both sexes. A contributor to hypertension is impaired endothelial relaxation in resistance arteries. Mesenteric arteries showed impaired endothelial relaxation to acetylcholine in both male and female Tg26 mice (P<0.05) with no impairment in smooth muscle cell relaxation. This phenotype was reproduced in WT mice transplanted with Tg26 bone marrow (BM) and remarkably reversed in Tg26 mice receiving WT BM supporting a clear role for immune cells in endothelial dysfunction. Collectively, these data indicate that HIV-related hypertension involves immune and NOX1-dependent endothelial dysfunction in both sexes but TNFα-dependent mechanisms in males only providing evidence of sex specific mechanisms.

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