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Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults.
N Engl J Med 1996; 334(3):150-4NEJM

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 men and 39 women) 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.

Authors+Show Affiliations

Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

8531969

Citation

Celermajer, D S., et al. "Passive Smoking and Impaired Endothelium-dependent Arterial Dilatation in Healthy Young Adults." The New England Journal of Medicine, vol. 334, no. 3, 1996, pp. 150-4.
Celermajer DS, Adams MR, Clarkson P, et al. Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults. N Engl J Med. 1996;334(3):150-4.
Celermajer, D. S., Adams, M. R., Clarkson, P., Robinson, J., McCredie, R., Donald, A., & Deanfield, J. E. (1996). Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults. The New England Journal of Medicine, 334(3), pp. 150-4.
Celermajer DS, et al. Passive Smoking and Impaired Endothelium-dependent Arterial Dilatation in Healthy Young Adults. N Engl J Med. 1996 Jan 18;334(3):150-4. PubMed PMID: 8531969.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Passive smoking and impaired endothelium-dependent arterial dilatation in healthy young adults. AU - Celermajer,D S, AU - Adams,M R, AU - Clarkson,P, AU - Robinson,J, AU - McCredie,R, AU - Donald,A, AU - Deanfield,J E, PY - 1996/1/18/pubmed PY - 1996/1/18/medline PY - 1996/1/18/entrez SP - 150 EP - 4 JF - The New England journal of medicine JO - N. Engl. J. Med. VL - 334 IS - 3 N2 - 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 men and 39 women) 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. SN - 0028-4793 UR - https://www.unboundmedicine.com/medline/citation/8531969/Passive_smoking_and_impaired_endothelium_dependent_arterial_dilatation_in_healthy_young_adults_ L2 - http://www.nejm.org/doi/full/10.1056/NEJM199601183340303?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -