Arterial Intima-Media Thickness, Endothelial Function, and Apolipoproteins in Adolescents Frequently Exposed to Tobacco Smoke

Abstract

Background-Exposure to tobacco smoke is associated with markers of preclinical atherosclerosis in adults, but its effect on arterial structure in adolescents is unknown. Methods and Results-Healthy 13-year-old adolescents from the atherosclerosis prevention trial STRIP were studied.Maximum carotid and aortic intima-media thickness and brachial artery flow-mediated dilation were measured in 494 adolescents using high-resolution ultrasound. Serum lipid, lipoprotein, and apolipoprotein (Apo) A-I and B concentrations were determined using standard methods. Exposure to tobacco smoke was measured annually between ages 8 and 13 years using serum cotinine concentrations, analyzed with gas chromatography. To define longitudinal exposure, cotinine values of children having serum cotinine measured 2 to 6 times during follow-up were averaged and divided into tertiles (exposure groups): low (nϭ160), intermediate (nϭ171), and high (nϭ163 1 Passive smoking has been associated with attenuated endothelium-dependent dilation in young healthy adults. 2,3 We have previously shown in 11-year-old healthy children that tobacco smoke exposure is associated with endothelial dysfunction measured by flowmediated dilation (FMD) of the brachial artery. 4 In addition, both past and current passive smoking has been related with increased carotid intima-media thickness (cIMT) in adults. [5][6][7] Moreover, tobacco smoke exposure in pregnancy has recently been associated with increased aortic intima-media thickness (aIMT) in neonates 8 and increased cIMT in young adulthood. 9 Conventional cardiovascular risk factors have been related to early structural vascular wall changes in childhood, 10 -12 and exposure to cardiovascular risk factors in adolescence predicts increased adult cIMT. 13 However, none of the previous studies has examined the impact of exposure to tobacco smoke on IMT in healthy children or adolescents.Exposure to tobacco smoke may lead to alterations in serum lipid profile, especially to decrease in HDL cholesterol, in children 14,15 and adolescents. 16,17 In adults, heavy workplace exposure to tobacco smoke has been demonstrated to have an adverse influence on serum lipids. 18,19 Recently, it was indicated that maternal smoking in pregnancy is associ- 21 Exposure to tobacco smoke as indicated by objective measurement, serum cotinine concentration, has been frequently determined in school-aged children. The aim of the present study was to examine the effects of frequent exposure to tobacco smoke on vascular wall structure, endothelial function, and serum lipid profile in healthy 13-year-old adolescents. WHAT IS KNOWN• Exposure to environmental tobacco smoke is related to increased carotid intima-media thickness in adults, but this association has not been studied in children.• Exposure to environmental tobacco smoke may lead to alterations in serum lipid profile, but there are no data on the relations of tobacco smoke exposure and apolipoprotein levels in children. WHAT THE STUDY ADDS• This study shows that frequent exposure ...

Determinants of Blood Pressure in Preschool Children

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Association of Physical Activity With Vascular Endothelial Function and Intima-Media Thickness

“…[1][2][3] Impairment of endothelial vasodilatory function is associated with coronary atherosclerosis, 4 and it predicts cardiovascular events. 5 Flowmediated dilatation (FMD) of the brachial artery, assessed noninvasively by ultrasound, is a widely used marker of systemic arterial endothelial function.…”

Protection from cigarette smoke‐induced vascular injury by recombinant human relaxin‐2 (serelaxin)

“…There is conflicting evidence regarding regulation of endothelial nitric oxide synthase (eNOS) by CS extract (CSE) at the transcriptional/translational level in cellular models with some suggesting reduced eNOS mRNA/protein levels 14, 15, 16 while others demonstrating unchanged 17 or even increased eNOS levels 18: the latter possibly likely represents an attempt of endothelial cells to compensate for eNOS impairment. These functional alterations are accompanied by histological changes in vascular wall consisting in increase in the intima‐media wall thickness, a marker of early atherosclerosis, 4, 18, 19, elastic fibres damage, cytoplasmic vacuolation of smooth muscle cells of the intima‐media, and endothelial loss caused by disruption of the adhesion between endothelial cells and their basement membrane 20, 21.…”