The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Original Article
PreviousPrevious
Volume 334:150-155 January 18, 1996 Number 3
NextNext

Passive Smoking and Impaired Endothelium-Dependent Arterial Dilatation in Healthy Young Adults
David S. Celermajer, Ph.D., Mark R. Adams, M.B., B.S., Peter Clarkson, M.B., B.S., Jacqui Robinson, R.N., Robyn McCredie, B.Sc., Ann Donald, and John E. Deanfield, M.B., Ch.B.

 Sign up for free e-toc
 

This Article
-Full Text
- PDF

Commentary
-Letters

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited

More Information
-PubMed Citation
ABSTRACT

Background Passive smoking has been linked to an increased risk of dying from atherosclerotic heart disease. Since endothelial dysfunction is an early feature of atherogenesis and occurs in young adults who actively smoke cigarettes, we hypothesized that passive smoking might also be associated with endothelial damage in healthy young-adult nonsmokers.

Methods We studied 78 healthy subjects (39 male and 39 female) 15 to 30 years of age (mean ±SD, 22±4): 26 control subjects who had never smoked or had regular exposure to environmental tobacco smoke, 26 who had never smoked but had been exposed to environmental tobacco smoke for at least one hour daily for three or more years, and 26 active smokers. Using ultrasonography, we measured the brachial-artery diameter under base-line conditions, during reactive hyperemia (with flow increase causing endothelium-dependent dilatation), and after sublingual administration of nitroglycerin (an endothelium-independent dilator).

Results Flow-mediated dilatation was observed in all control subjects (8.2±3.1 percent; range, 2.1 to 16.7) but was significantly impaired in the passive smokers (3.1±2.7 percent; range, 0 to 9; P<0.001 for the comparison with the controls) and in the active smokers (4.4±3.1 percent; range, 0 to 10; P<0.001 for the comparison with the controls; P = 0.48 for the comparison with the passive smokers). In the passive smokers, there was an inverse relation between the intensity of exposure to tobacco smoke and flow-mediated dilatation (r = -0.67, P<0.001). In contrast, dilatation induced by nitroglycerin was similar in all groups.

Conclusions Passive smoking is associated with dose-related impairment of endothelium-dependent dilatation in healthy young adults, suggesting early arterial damage.


Source Information

From the Department of Cardiology, Royal Prince Alfred Hospital (D.S.C., M.R.A., J.R., R.M.), and the Heart Research Institute (D.S.C., J.R., R.M.), Sydney, Australia; and the Cardiothoracic Unit, Hospital for Sick Children, London (P.C., A.D., J.E.D.).

Address reprint requests to Dr. Celermajer at the Department of Cardiology, Royal Prince Alfred Hospital, Missenden Rd., Camperdown 2050, Sydney, Australia.

Full Text of this Article


Related Letters:

Smoking and Impaired Endothelium-Dependent Dilatation
Migliacci R., Gresele P.
Extract | Full Text  
N Engl J Med 1996; 334:1674, Jun 20, 1996. Correspondence

This article has been cited by other articles:



HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2008 Massachusetts Medical Society. All rights reserved.