Smoking Behaviors and Arterial Stiffness Measured by Pulse Wave Velocity in Older Adults: The Atherosclerosis Risk in Communities (ARIC) Study

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Abstract

<div class="section"> <a class="named-anchor" id="d1466945e260">  </a> <h5 class="section-title" id="d1466945e261">BACKGROUND</h5> <p id="d1466945e263">Though smoking is strongly associated with peripheral vascular disease and arteriosclerosis, smoking’s association with arterial stiffness has been inconsistent and mostly limited to a single arterial segment. We examined the relationship between smoking behaviors with arterial stiffness in multiple arterial segments among community dwelling older adults. </p> </div><div class="section"> <a class="named-anchor" id="d1466945e265">  </a> <h5 class="section-title" id="d1466945e266">METHODS</h5> <p id="d1466945e268">The cross-sectional relationship between smoking behavior with carotid-femoral (cfPWV) and femoral-ankle pulse wave velocity (faPWV) was examined in 5,002 men and women, separately, of the Atherosclerosis Risk in Communities (ARIC) cohort study. Brachial-ankle PWV was also assessed and presented in <a data-untrusted="" href="http://ajh.oxfordjournals.org/lookup/suppl/doi:10.1093/ajh/hpv189/-/DC1" id="d1466945e270" target="xrefwindow">Supplementary Material</a>. Heckman selection models were used to control for selective attrition and death in the ARIC cohort. </p> </div><div class="section"> <a class="named-anchor" id="d1466945e273">  </a> <h5 class="section-title" id="d1466945e274">RESULTS</h5> <p id="d1466945e276">In women, faPWV was lower in current smokers compared to never smokers (−66.0cm/s; 95% confidence interval (95% CI): −94.6, −37.4), and was 1.0cm/s lower (95% CI: −1.8, −0.2) for every additional year a woman smoked, after adjustment for confounders. Among women, cfPWV was not associated with smoking status or cigarette pack-years. Additionally, no associations of smoking status and cigarette pack-years with PWV were observed among men. Years since smoking cessation was not associated with PWV in either gender. </p> </div><div class="section"> <a class="named-anchor" id="d1466945e278">  </a> <h5 class="section-title" id="d1466945e279">CONCLUSION</h5> <p id="d1466945e281">Both smoking status and cumulative smoking exposure were associated with lower peripheral arterial stiffness among women, but not among men. We did not observe an association between central arterial stiffness and smoking status in either gender. The profound and well-documented adverse effects of cigarette smoking on the vasculature may not include a sustained stiffening of the arteries measured at older age. </p> </div>

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Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review.

Julia A Critchley, Simon Capewell (2003)

As more interventions become available for the treatment of coronary heart disease (CHD), policy makers and health practitioners need to understand the benefits of each intervention, to better determine where to focus resources. This is particularly true when a patient with CHD quits smoking. To conduct a systematic review to determine the magnitude of risk reduction achieved by smoking cessation in patients with CHD. Nine electronic databases were searched from start of database to April 2003, supplemented by cross-checking references, contact with experts, and with large international cohort studies (identified by the Prospective Studies Collaboration). Prospective cohort studies of patients who were diagnosed with CHD were included if they reported all-cause mortality and had at least 2 years of follow-up. Smoking status had to be measured after CHD diagnosis to ascertain quitting. Two reviewers independently assessed studies to determine eligibility, quality assessment of studies, and results, and independently carried out data extraction using a prepiloted, standardized form. From the literature search, 665 publications were screened and 20 studies were included. Results showed a 36% reduction in crude relative risk (RR) of mortality for patients with CHD who quit compared with those who continued smoking (RR, 0.64; 95% confidence interval [CI], 0.58-0.71). Results from individual studies did not vary greatly despite many differences in patient characteristics, such as age, sex, type of CHD, and the years in which studies took place. Adjusted risk estimates did not differ substantially from crude estimates. Many studies did not adequately address quality issues, such as control of confounding, and misclassification of smoking status. However, restriction to 6 higher-quality studies had little effect on the estimate (RR, 0.71; 95% CI, 0.65-0.77). Few studies included large numbers of elderly persons, women, ethnic minorities, or patients from developing countries. Quitting smoking is associated with a substantial reduction in risk of all-cause mortality among patients with CHD. This risk reduction appears to be consistent regardless of age, sex, index cardiac event, country, and year of study commencement.

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Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults.

D S Celermajer, K Sorensen, D. Georgakopoulos … (1993)

Cigarette smoking is the most important modifiable risk factor for atherosclerosis. Endothelial dysfunction is an early event in atherogenesis, and we hypothesized that smoking might be associated with endothelial damage in the systemic arteries of otherwise healthy young adults. We studied noninvasively the brachial arteries of 200 subjects aged 15 to 57 years, all normotensive, nondiabetic with cholesterol level < or = 240 mg/dL and no family history of premature vascular disease: 80 control subjects aged 16 to 56 years (mean, 35), 80 current smokers aged 15 to 55 years (mean, 33), and 40 former smokers aged 25 to 57 years (mean, 38). Total lifetime amount smoked varied from 1 to 75 pack years in the smokers. Using high-resolution ultrasound, vessel diameter was measured at rest, during reactive hyperemia (with flow increase causing endothelium-dependent dilation), and after sublingual glyceryl trinitrate (GTN, an endothelium-independent vasodilator). Flow-mediated dilation (FMD) was observed in all the control subjects (10 +/- 3.3%; range, 4% to 22%) but was impaired or absent in the smokers (4 +/- 3.9%; range, 0% to 17%; P < .0001). FMD in the smokers was inversely related to lifetime dose smoked (6.6 +/- 4.0% in very light smokers, 4.0 +/- 3.1% in light smokers, 3.2 +/- 3.2% in moderate smokers, and 2.6 +/- 1.2% in heavy smokers; P < .01). FMD for the former smokers was 5.1 +/- 4.1% (range, 0% to 15%). In a multivariate model adjusting for age, sex, cholesterol, smoking history, and vessel size, former smoking was associated with a higher FMD than current smoking (P = .07); when only male former and current smokers were considered, the higher FMD was significant (P = .0001) but not for female smokers (P = .24). GTN caused dilation in all subjects (control subjects, 20 +/- 5.2%; smokers, 17 +/- 5.8%; former smokers, 17.4 +/- 5.4%). Vessel diameter, baseline flow, and degree of reactive hyperemia (Doppler estimated) were similar in all groups. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent arterial dilation in asymptomatic young adults, consistent with endothelial dysfunction.

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Novel proteolytic microvesicles released from human macrophages after exposure to tobacco smoke.

Chun-jun Li, Yu-Yu Liu, Yan Chen … (2013)

Cigarette smoking damages the extracellular matrix in a variety of locations, leading to atherosclerotic plaque instability and emphysematous lung destruction, but the underlying mechanisms remain poorly understood. Here, we sought to determine whether exposure of human macrophages, a key participant in extracellular matrix damage, to tobacco smoke extract (TSE) induces the release of microvesicles (MVs; or microparticles) with proteolytic activity; the major proteases involved; and the cellular mechanisms that might mediate their generation. We found that MVs released from TSE-exposed macrophages carry substantial gelatinolytic and collagenolytic activities that surprisingly can be predominantly attributed to a single transmembrane protease of the matrix metalloproteinase (MMP) superfamily (namely, MMP14). Flow cytometric counts revealed that exposure of human macrophages to TSE for 20 hours more than quadrupled their production of MMP14-positive MVs (control, 1112 ± 231; TSE-induced, 5823 ± 2192 MMP14-positive MVs/μL of conditioned medium; means ± SEM; n = 6; P < 0.01). Our results indicate that the production of these MVs by human macrophages relies on a series of regulated steps that include activation of two mitogen-activated protein kinases (MAPKs, i.e., the Jun N-terminal kinase and p38 MAPK), and then MAPK-dependent induction and maturation of cellular MMP14, a remarkable accumulation of MMP14 into nascent plasma membrane blebs, and finally caspase- and MAPK-dependent apoptosis and apoptotic microvesicle generation. Proteolytically active MVs induced by tobacco smoke may be novel mediators of clinical important matrix destruction in smokers.

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Author and article information

Journal

Title: American Journal of Hypertension

Abbreviated Title: AJHYPE

Publisher: Oxford University Press (OUP)

ISSN (Print): 0895-7061

ISSN (Electronic): 1941-7225

Publication date Created: October 08 2016

Publication date Created: November 2016

Publication date (Print): November 2016

Publication date (Electronic): December 10 2015

Volume: 29

Issue: 11

Pages: 1268-1275

Article

DOI: 10.1093/ajh/hpv189

PMC ID: 5055735

PubMed ID: 26657706

SO-VID: a73ce93e-8819-4236-84dc-5c1ae370bc18

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Smoking Behaviors and Arterial Stiffness Measured by Pulse Wave Velocity in Older Adults: The Atherosclerosis Risk in Communities (ARIC) Study

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Most cited references 27

Mortality risk reduction associated with smoking cessation in patients with coronary heart disease: a systematic review.

Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults.

Novel proteolytic microvesicles released from human macrophages after exposure to tobacco smoke.

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