Does passive smoking impair endothelium-dependent coronary artery dilation in women?

J Am Coll Cardiol. 1998 Mar 15;31(4):811-5. doi: 10.1016/s0735-1097(98)00010-2.

Abstract

Objectives: This study sought to examine whether passive smoking is associated with endothelial dysfunction in the coronary arteries.

Background: Long-term exposure to cigarette smoking has been reported to suppress endothelium-dependent arterial dilation in humans. Endothelial dysfunction is an early feature of atherogenesis, and the impairment of acetylcholine (ACh)-induced coronary artery dilation indicates coronary endothelial dysfunction.

Methods: We studied 38 women (40 to 60 years old) who had no known risk factors for coronary artery disease other than tobacco smoking: 11 nonsmokers who had never smoked and had never been regularly exposed to environmental tobacco smoke; 19 passive smokers with self-reported histories of exposure to environmental tobacco smoke of > or = 1 h/day for > or = 10 years; and 8 active smokers. We examined the response of the epicardial coronary artery diameters (proximal and distal segments of the left anterior descending [LAD] and left circumflex [LCx] coronary arteries) to the intracoronary injection of ACh into the left coronary artery by means of quantitative coronary angiography.

Results: ACh significantly dilated the distal segment in nonsmokers (percent change from baseline diameter: LAD 13.7+/-3.4%, p < 0.05; LCx 18.8+/-2.9%, p < 0.01) but not the proximal segment (LAD 7.4+/-3.5%; LCx 3.1+/-5.0%). ACh significantly constricted all segments of the left coronary artery in passive smokers (LAD: proximal -20.3+/-3.7%, p < 0.05; distal -22.3+/-4.1%, p < 0.01; LCx: proximal -20.8+/-3.1%, p < 0.05; distal -17.3+/-2.9%, p < 0.01) and active smokers (LAD: proximal -14.8+/-3.4%, p < 0.05; distal -27.2+/-6.0%, p < 0.01; LCx: proximal -14.5+/-6.6%, p < 0.05; distal -22.4+/-4.0%, p < 0.01). Thus, ACh constricted most coronary arteries in both passive and active smokers and dilated the coronary arteries in nonsmokers.

Conclusions: Impairment of ACh-induced coronary artery dilation, indicating coronary endothelial dysfunction, may occur diffusely in passive smokers as well as in active smokers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / pharmacology
  • Adult
  • Cholesterol / blood
  • Coronary Angiography
  • Coronary Artery Disease / etiology
  • Coronary Vessels / drug effects
  • Coronary Vessels / physiopathology*
  • Endothelium, Vascular / physiopathology*
  • Female
  • Humans
  • Middle Aged
  • Risk Factors
  • Smoking / adverse effects
  • Tobacco Smoke Pollution / adverse effects*
  • Vasoconstriction
  • Vasodilation* / drug effects

Substances

  • Tobacco Smoke Pollution
  • Cholesterol
  • Acetylcholine