What is the clinical evidence from this study?

Study design: Cross-Sectional. Population: Healthy young adults (n=30). Intervention: Passive smoking exposure vs. Baseline (before exposure). Primary outcome: Coronary flow velocity reserve (CFVR) (p=<.001).

July 25, 2001

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

Q: What are the key findings of this study?

A 30-minute exposure to passive smoking significantly reduced mean coronary flow velocity reserve in healthy nonsmokers from 4.4 to 3.4 (P<.001).

Key Result

A 30-minute exposure to passive smoking significantly reduced mean coronary flow velocity reserve in healthy nonsmokers from 4.4 to 3.4 (P<.001).

Study Design

Type

Cross-Sectional (n=30)

Structured PICO

Does a 30-minute exposure to environmental tobacco smoke reduce coronary flow velocity reserve in healthy young men?

Population

30 Japanese men (mean age, 27 years; 15 healthy nonsmokers and 15 asymptomatic active smokers) without history of hypertension, diabetes mellitus, or hyperlipidemia.

Intervention

30-minute exposure to environmental tobacco smoke (passive smoking)

Comparator

Baseline (before exposure) and active smokers

Outcome

Coronary flow velocity reserve (CFVR), calculated as the ratio of hyperemic to basal coronary flow velocity induced by intravenous infusion of adenosine triphosphatesurrogate

A 30-minute exposure to passive smoking significantly reduces coronary flow velocity reserve in healthy nonsmokers, providing direct evidence of acute endothelial dysfunction.

Main Result

Absolute Event Rate: 3.4% vs 4.4%

p-value: p=<.001

Abstract

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.

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