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Medical Effects: Passive Tobacco Smoke Exposure causes early signs of hardening of the arteries.

[Wood Smoke has many of the same chemicals as tobacco smoke and is active in the body 40 times longer than tobacco. BI Editor]

Acute Effects of Passive Smoking on the Coronary Circulation in Healthy Young Adults

Journal of the American Medical Association
July 25, 2001 (Volume 286, Number 4)

Otsuka R, Watanabe H, Hirata K, et al.
JAMA. 2001;286:436-441

[The authors concluded that the decrease in coronary flow velocity reserve (CFVR) following passive smoking may be the result of endothelial dysfunction of the coronary circulation, an early process of atherosclerosis, and may explain, at least in part, why passive smoking is a risk for cardiac disease in nonsmokers.]

Ryo Otsuka, MD; Hiroyuki Watanabe, MD; Kumiko Hirata, MD; Kotaro Tokai, MD; Takashi Muro, MD; Minoru Yoshiyama, MD; Kazuhide Takeuchi, MD; Junichi Yoshikawa, MD

Author/Article Information: Author Affiliations: Department of Internal Medicine and Cardiology, Osaka City, University Medical School, Osaka, Japan.

Context: Recent studies have shown that passive smoking is a risk factor for ischemic heart disease and may be associated with vascular endothelial dysfunction. The acute effects of passive smoking on coronary circulation in nonsmokers are not known.

Objective To determine the acute effects of passive smoking on coronary circulation using coronary flow velocity reserve (CFVR), assessed by noninvasive transthoracic Doppler echocardiography.

Design, Setting, and Participants Cross-sectional study conducted from September 2000 to November 2000 among 30 Japanese men (mean age, 27 years; 15 healthy nonsmokers and 15 asymptomatic active smokers) without history of hypertension, diabetes mellitus, or hyperlipidemia.

Main Outcome Measures Coronary flow velocity reserve, calculated as the ratio of hyperemic to basal coronary flow velocity induced by intravenous infusion of adenosine triphosphate and measured in each participant before and after a 30-minute exposure to environmental tobacco smoke.

Results Heart rate and blood pressure responses to adenosine triphosphate infusion were not affected by passive smoking exposure in either group. Passive smoking exposure had no effect on basal coronary flow velocity in either group. Mean (SD) CFVR in nonsmokers was significantly higher than that in active smokers before passive smoking exposure (4.4 [0.91] vs 3.6 [0.88], respectively; P = .02), while CFVR after passive smoking exposure did not differ between groups (P = .83). Passive smoking exposure significantly reduced mean (SD) CFVR in nonsmokers (4.4 [0.91] vs 3.4 [0.73], respectively; P<.001).

Conclusions Passive smoking substantially reduced CFVR in healthy nonsmokers. This finding provides direct evidence that passive smoking may cause endothelial dysfunction of the coronary circulation in nonsmokers.

JAMA. 2001;286:436-441

Introduction

Exposure to environmental tobacco smoke (ETS) increases the risk of death due to heart disease by approximately 30%.[1] Exposure of nonsmokers to ETS breaks down the serum antioxidant defenses[2] and impairs the endothelium-dependent function of arterial walls.[3] The acute effects of exposure to ETS, or passive smoking, on the coronary circulation are not known. The current study was done to determine the acute effects of passive smoking on coronary circulation by measuring coronary flow velocity reserve (CFVR) using transthoracic Doppler echocardiography.

Methods

Thirty healthy Japanese men aged 27 +/- 4 years were recruited: 15 nonsmokers and 15 asymptomatic active smokers. Nonsmokers had no home or workplace smoke exposure and smokers regularly smoked at least 20 cigarettes per day. No exposure to ETS or active smoking occurred for more than 12 hours prior to study measurements.

Blood was drawn for plasma carboxyhemoglobin (HbCO) determination and lipid analyses. After baseline hemodynamics and echocardiographic assessment, all subjects spent 30 minutes in the smoking room of the hospital. Carbon monoxide concentration in the air of the smoking room and echocardiographic lab was measured.

Echocardiographic measurements were taken before and after passive smoking. Flow velocity in the distal left anterior descending artery was measured. Adenosine triphosphate was administered for 2 minutes to record signals during hyperemic conditions. Coronary flow velocity (CFV) was measured at baseline and peak hyperemic conditions. CFVR was calculated as the ratio of hyperemic to baseline CFV.

Results

Baseline characteristics did not differ significantly between nonsmokers and active smokers. Passive smoking did not affect baseline hemodynamic parameters (heart rate, blood pressure).

HbCO was significantly lower in nonsmokers vs active smokers at baseline. After passive smoking, there was a significant increase in the HbCO levels in nonsmokers but not in active smokers.

CFV was significantly higher in nonsmokers compared with smokers during hyperemia at baseline and was not significantly different after passive smoking. CFVR was significantly higher in nonsmokers at baseline (P = .02), but did not differ significantly between the 2 groups after passive smoking (P = .83). In nonsmokers, passive smoking significantly decreased the CFVR (P < .001).

Discussion

Cigarette smoking is a major risk factor for cardiovascular disease[4,5] and may be the result of structural[6] or functional[5,7] changes. Passive smoking has been linked to an excess risk for cardiac disease[1,8-12] and may be dose-related.[3]

The authors noted that impaired coronary flow reserve may be a marker for subclinical coronary atherosclerosis. Clinical studies have demonstrated that acutely, smoking can abruptly decrease CFVR[13] and that long-term, exposure to ETS impaired acetylcholine-induced coronary artery dilatation.[14] In this and other studies,[13,15]CFVR was lower in active smokers. Passive smoking in this study was shown to reduce CFVR to the same level as active smokers.

ETS includes many toxic substances, some of which may injure the arterial wall.[8-10] In this study, the demonstrated increase in HbCO in nonsmokers may account for the stronger adverse effect of passive smoking on CFVR in this group compared with active smokers. The authors acknowledged that a limitation of the current study was that the long-term effects of passive smoking and the duration of CFVR reduction were not assessed.

The authors concluded that the decrease in CFVR following passive smoking may be the result of endothelial dysfunction of the coronary circulation, an early process of atherosclerosis, and may explain, at least in part, why passive smoking is a risk for cardiac disease in nonsmokers.

References

1.Taylor AE, Johnson DC, Kazemi H. Environmental tobacco smoke and cardiovascular disease: a position paper from the Council on Cardiopulmonary and Critical Care, American Heart Association. Circulation. 1992;86:699-702.

2.Valkonen M, Kuusi T. Passive smoking induces atherogenic changes in low-density lipoprotein. Circulation. 1998;97:2012-2016.

3.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.

4.Holbrook JH, Grundy SM, Hennekens CH, et al. Cigarette smoking and cardiovascular diseases: a statement for health professionals by a task force appointed by the steering committee of the American Heart Association.
Circulation. 1984;70:1114A-1117A.

5.Zeiher AM, Schachinger V, Minners J. Long-term cigarette smoking impairs endothelium-dependent coronary arterial vasodilator function. Circulation. 1995;92:1094-1100.

6.Folkov B. "Structural factor" in primary and secondary hypertension. Hypertension. 1990;16:89-101.

7.Raij L, Nagy J, Jaimes E, et al. Mechanisms of cigarette smoke induced impairment of endothelium dependent
modulation of vascular tone [abstract]. Circulation. 1994;90(suppl 1):575.

8.Zhu B-Q, Sun Y-P, Sievers RE, et al. Passive smoking increases experimental atherosclerosis in cholesterol-fed rabbits. J Am Coll Cardiol. 1993;21:225-232.

9.Penn A, Snyder CA. Inhalation of sidestream cigarette smoke accelerates development of arteriosclerotic plaques.
Circulation. 1993;88:1820-1825.

10.Penn A, Chen L-C, Snyder CA. Inhalation of steady-state sidestream smoke from one cigarette promotes arteriosclerotic plaque development. Circulation. 1994;90:1363-1367.

11.Wells AJ. An estimate of adult mortality from passive smoking. Environ Int. 1988;14:249-265.
12.Steenland K. Passive smoking and the risk of heart disease. JAMA. 1992;267:94-99.

13.Tanaka T, Oka Y, Tawara I, et al. Acute effects of nicotine content in cigarettes on coronary flow velocity and coronary flow reserve in men. Am J Cardiol. 1998;82:1275-1278.

14.Sumida H, Watanabe H, Kugiyama K, et al. Does passive smoking impair endothelium-dependent coronary artery dilatation in women? J Am Coll Cardiol. 1998;31:811-815.

15.Kaufmann PA, Gnecchi-Ruscone T, Di Terlizzi M, et al. Coronary heart disease in smokers: vitamin C restores coronary microcirculatory function. Circulation. 2000;102:1233-1238.

Author/Article Information: Author Affiliations: Department of Internal Medicine and Cardiology, Osaka City University Medical School, Osaka, Japan.

Corresponding Author and Reprints: Hiroyuki Watanabe, MD, Department of Internal Medicine and Cardiology, Osaka City University Medical School, 1-4-3 Asahimachi Abeno-ku, Osaka City, Japan 545-8585 (e-mail: watanabe@med.osaka-cu.ac.jp).

Author Contributions: Study concept and design: Otsuka, Watanabe, Muro, Yoshiyama, Takeuchi, Yoshikawa.

Acquisition of data: Otsuka, Watanabe, Hirata, Tokai.

Analysis and interpretation of data: Otsuka, Watanabe.

Drafting of the manuscript: Otsuka, Watanabe, Hirata, Tokai, Muro.

Critical revision of the manuscript for important intellectual content: Otsuka, Watanabe, Hirata, Yoshiyama, Takeuchi, Yoshikawa.

Statistical expertise: Otsuka, Watanabe, Hirata.

Administrative, technical, or material support: Otsuka, Watanabe, Hirata, Tokai, Muro.

Study supervision: Watanabe, Yoshiyama, Takeuchi, Yoshikawa.

{Passive wood smoke exposure: wood smoke spewing from your neighbor's wood stove, fireplace, firepit, outdoor wood boiler or burn pile.}

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