Correspondence

Smoking and Impaired Endothelium-Dependent Dilatation

N Engl J Med 1996; 334:1674June 20, 1996

Article

To the Editor:

Celermajer et al. (Jan. 18 issue)1 reported that passive smoking is associated with a dose-related impairment of flow-mediated, endothelium-dependent arterial dilatation in healthy young subjects. Previous studies have shown that active cigarette smoking induces a reduction of flow-mediated arterial dilatation that is partially reversible on smoking cessation.2 However, it is not known whether the endothelial dysfunction induced by smoking is the consequence of chronic damage to the endothelium or whether some components of cigarette smoke acutely affect endothelial function.

We assessed the short-term effects of cigarette smoking on flow-mediated arterial dilatation in healthy young adults who were long-term smokers. We studied 11 active smokers (7 women and 4 men; age, 19 to 49 years; mean [±SD], 30±11) with self-reported smoking histories of 3 to 22.5 pack-years (mean, 11±7) and 11 healthy nonsmoking subjects (7 women and 4 men; age, 20 to 39 years; mean, 29±6). Active smokers were defined as subjects who had smoked at least 20 cigarettes per day for at least one year (1 pack-year) or the equivalent. All subjects gave their informed consent, and all were clinically healthy, with no history of diabetes, hypertension, or dyslipidemia and no family history of precocious ischemic cardiovascular disease. All subjects were studied in the morning, none had recently ingested beverages containing alcohol or methylxanthine, and none had taken drugs during the two weeks preceding the study.

We used B-mode ultrasonography with a 7.5-MHz linear-array transducer and a standard Acuson 128 XP5 system (Acuson, Mountain View, Calif.) to measure the diameter of the brachial artery of the subject's right arm 2 to 5 cm above the elbow.3 Subjects rested for 10 minutes before the basal diameter of the artery was measured; then, a sphygmomanometer cuff was placed on the forearm and inflated to 240 mm Hg for 3 minutes, and arterial diameter was measured again 40 seconds after the cuff was released. The transducer was kept in the same position throughout the procedure, and all the studies were carried out by the same operator.

Active smokers were studied after they had abstained from smoking for at least eight hours and then immediately after they had smoked a cigarette with a high nicotine content (1 mg) in less than five minutes. Smoking produced the expected significant increase in heart rate and blood pressure.

Our results (Table 1Table 1Flow-Mediated Dilatation in Nonsmoking Control Subjects and Active Smokers before and Immediately after They Smoked a Cigarette.) confirm that long-term smoking impairs flow-mediated arterial dilatation even in subjects who have abstained from smoking for at least eight hours. Smoking a cigarette does not produce further acute impairment in flow-mediated arterial dilatation in long-term smokers. Among the acute effects of cigarette smoking that can precipitate cardiovascular events in long-term smokers,4 worsening of nitrous oxide–dependent arterial vasodilatation does not appear to play a part.

Rino Migliacci, M.D.
Cortona Hospital, 52042 Cortona, Italy

Paolo Gresele, M.D., Ph.D.
University of Perugia, 06126 Perugia, Italy

4 References

1. 1

   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;334:150-154
   Full Text | Web of Science | Medline

2. 2

   Celermajer DS, Sorensen KE, Georgakopoulos D, et al. Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilatation in healthy young adults. Circulation 1993;88:2149-2155
   Web of Science | Medline

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   Celermajer DS, Sorensen KE, Gooch VM, et al. Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Lancet 1992;340:1111-1115
   CrossRef | Web of Science | Medline

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   Martin JL, Wilson JR, Ferraro N, Laskey WK, Kleaveland JP, Hirshfeld JW Jr. Acute coronary vasoconstrictive effects of cigarette smoking in coronary heart disease. Am J Cardiol 1984;54:56-60
   CrossRef | Web of Science | Medline

Citing Articles (4)

Citing Articles

1. 1

   P. Gresele, R. Migliacci, M.C. Vedovati, A. Ruffatti, C. Becattini, M. Facco, G. Guglielmini, E. Boscaro, A.M. Mezzasoma, S. Momi, V. Pengo. (2009) Patients with primary antiphospholipid antibody syndrome and without associated vascular risk factors present a normal endothelial function. Thrombosis Research 123:3, 444-451
   CrossRef

2. 2

   M. Tripathi, M. Pandey, U. Singh, S. Dwivedi. (2008) Non-smokers are more prone to pulmonary oedema than smokers during acute coronary syndrome. International Journal of Clinical Practice 62:12, 1880-1885
   CrossRef

3. 3

   B.W. Mays, J.A. Freischlag, M.T. Eginton, R.A. Cambria, G.R. Seabrook, J.B. Towne. (1999) Ascorbic Acid Prevents Cigarette Smoke Injury to Endothelium-Dependent Arterial Relaxation. Journal of Surgical Research 84:1, 35-39
   CrossRef

4. 4

   Robert W Stadler, Sherrif F Ibrahim, Robert S Lees. (1998) Measurement of the time course of peripheral vasoactivity: results in cigarette smokers. Atherosclerosis 138:1, 197-205
   CrossRef