Key result
Cigarette smoking was independently associated with severe carotid stenosis in patients with focal cerebral ischemia (OR 1.5 in NOMASS; OR 3.9 in BCID), with the greatest effect observed among whites.
Why the study?
Does cigarette smoking increase the risk of high-grade carotid artery stenosis in patients with stroke or transient ischemic attack?
Cross-Sectional (n=914)
Yes
Does cigarette smoking increase the risk of high-grade carotid artery stenosis in patients with stroke or transient ischemic attack?
Cigarette smoking is an independent, dose-dependent risk factor for severe carotid artery stenosis in patients with cerebral ischemia, with the strongest association observed in white patients.
Answers are grounded in this paper and cite their sources.
Reinforces smoking cessation as a critical secondary prevention target in cerebral ischemia; leaves open whether racial.
BACKGROUND AND PURPOSE: We sought to investigate the association of cigarette smoking with high-grade carotid artery stenosis in Hispanic, black, and white patients with cerebral ischemia in two independent samples. METHODS: Prospectively collected data from the Northern Manhattan Stroke Study (NOMASS) (n=431) and the Berlin Cerebral Ischemia Databank (BCID) (n=483) were used separately for a cross-sectional study estimating the association between cigarette smoking and high-grade carotid stenosis (defined as a luminal narrowing of > or =60%, diagnosed by duplex and/or Doppler ultrasound). In both studies, cerebral ischemia patients with normal sonographic findings or nonstenosing plaques of their carotid arteries served as a comparison group. Multivariate logistic regression models were used for statistical tests to determine the association between smoking and the dependent variable for high-grade carotid stenosis. Age, sex, hypertension, diabetes, hypercholesterolemia, and race/ethnicity were considered potential confounders. Further analyses of the NOMASS data estimated the effect of the amount of cigarette use and the impact of race/ethnicity. RESULTS: High-grade carotid stenoses were found in 14% of the NOMASS and in 21% of the Berlin patients. In Berlin the entire sample was white, whereas in New York only 19% of the cohort were white. In both samples, smoking was independently associated with severe carotid stenosis (NOMASS: odds ratio [OR], 1.5; 95% confidence interval [CI], 1.1 to 2.0; BCID: OR, 3.9; 95% CI, 2.4 to 6.4). Patients smoking 20 pack-years or more showed a significant association (OR, 2.0; 95% CI, 1.1 to 3.9), whereas no significant effect was found for lower amounts of cigarette use. In NOMASS, white smokers displayed a significant (OR, 3.2; 95% CI, 1.1 to 8.9) association with high-grade carotid stenosis, the association for black smokers was less strong, and no association was found among Hispanics. CONCLUSIONS: Smoking is an independent determinant of severe carotid artery stenosis in patients with focal cerebral ischemia. The association differs by race/ethnicity, with the greatest effect observed among whites.
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Mast et al. (1998) conducted a cross-sectional in Stroke or Transient Ischemic Attack (n=914). Cigarette smoking vs. Non-smokers or lower amounts of cigarette use was evaluated on High-grade carotid artery stenosis (luminal narrowing of ≥60%) (OR 1.5 (NOMASS), OR 3.9 (BCID), 95% CI 1.1-2.0 (NOMASS), 2.4-6.4 (BCID)). Cigarette smoking was independently associated with severe carotid stenosis in patients with focal cerebral ischemia (OR 1.5 in NOMASS; OR 3.9 in BCID), with the greatest effect observed among whites.
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