Otsuka R, Watanabe H, Hirata K, et al.
Acute Effects of Passive Smoking on the Coronary
Circulation in Healthy Young Adults
[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.]
Ryo Otsuka, MD; Hiroyuki Watanabe, MD; Kumiko Hirata, MD; Kotaro Tokai, MD;
Takashi Muro, MD; Minoru Yoshiyama, MD; Kazuhide Takeuchi, MD; Junichi
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
Design, Setting, and Participants Cross-sectional study conducted
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
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
This finding provides direct evidence that passive smoking may cause endothelial
dysfunction of the coronary circulation in nonsmokers.
Exposure to environmental tobacco smoke (ETS) increases the risk of death due to heart disease by approximately 30%. Exposure of nonsmokers to ETS breaks down the serum antioxidant defenses and impairs the endothelium-dependent function of arterial walls. 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 oncoronary circulation by measuring coronary flow velocity reserve (CFVR) using transthoracic Doppler echocardiography.
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
was calculated as the ratio of hyperemic to baseline CFV.
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).
Cigarette smoking is a major risk factor for cardiovascular disease[4,5] and may be the result of structural 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.
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 and that long-term, exposure to ETS impaired acetylcholine-induced coronary artery dilatation. 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.
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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: email@example.com).
Author Contributions: Study concept and design: Otsuka, Watanabe,
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.
July 2001 (Volume 120, Number 1)
Journal of the American Medical Association
July 25, 2001 (Volume 286, Number 4)
Acute Effects of Passive Smoking on the Coronary Circulation in
Healthy Young Adults
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