Key result
Current cigarette smoking was significantly associated with higher odds of subclinical atherosclerosis, including an ankle-brachial index ≤1.0 (OR 2.52; 95% CI 2.06-3.08; P<0.001).
Why the study?
Does cigarette smoking increase markers of subclinical inflammation and atherosclerosis in adults without clinical cardiovascular disease?
Cross-Sectional (n=14,103)
Does cigarette smoking increase markers of subclinical inflammation and atherosclerosis in adults without clinical cardiovascular disease?
Cigarette smoking is strongly associated with increased markers of subclinical inflammation and atherosclerosis, including hsCRP, carotid intima-media thickness, abnormal ankle-brachial index, and coronary artery calcium, in adults without clinical cardiovascular disease.
Answers are grounded in this paper and cite their sources.
Smoking associated with subclinical atherosclerosis without clinical CVD; hypothesis-generating and requires prospective studies to assess causality.
Background There is a need to identify sensitive biomarkers of early tobacco‐related cardiovascular disease. We examined the association of smoking status, burden, time since quitting, and intensity, with markers of inflammation and subclinical atherosclerosis. Methods and Results We studied 14 103 participants without clinical cardiovascular disease in ELSA‐Brasil (Brazilian Longitudinal Study of Adult Health). We evaluated baseline cross‐sectional associations between smoking parameters and inflammation (high‐sensitivity C‐reactive protein [hs CRP ]) and measures of subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, and coronary artery calcium [ CAC ]). The cohort included 1844 current smokers, 4121 former smokers, and 8138 never smokers. Mean age was 51.7±8.9 years; 44.8% were male. After multivariable adjustment, compared with never smokers, current smokers had significantly higher levels of hs CRP (β=0.24, 0.19–0.29 mg/L; P <0.001) and carotid intima–media thickness (β=0.03, 0.02–0.04 mm; P <0.001) and odds of ankle‐brachial index ≤1.0 (odds ratio: 2.52; 95% confidence interval, 2.06–3.08; P <0.001) and CAC >0 (odds ratio: 1.83; 95% confidence interval, 1.46–2.30; P <0.001). Among former and current smokers, pack‐years of smoking (burden) were significantly associated with hs CRP ( P <0.001 and P =0.006, respectively) and CAC ( P <0.001 and P =0.002, respectively). Among former smokers, hs CRP and carotid intima–media thickness levels and odds of ankle‐brachial index ≤1.0 and CAC >0 were lower with increasing time since quitting ( P <0.01). Among current smokers, number of cigarettes per day (intensity) was positively associated with hs CRP ( P <0.001) and CAC >0 ( P =0.03) after adjusting for duration of smoking. Conclusions Strong associations were observed between smoking status, burden, and intensity with inflammation (hs CRP ) and subclinical atherosclerosis (carotid intima–media thickness, ankle‐brachial index, CAC ). These markers of early cardiovascular disease injury may be used for the further study and regulation of traditional and novel tobacco products.
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Kianoush et al. (2017) conducted a cross-sectional in Subclinical inflammation and atherosclerosis (n=14,103). Cigarette smoking vs. Never smokers was evaluated on ankle-brachial index ≤1.0 (OR 2.52, 95% CI 2.06-3.08, p=<0.001). Current cigarette smoking was significantly associated with higher odds of subclinical atherosclerosis, including an ankle-brachial index ≤1.0 (OR 2.52; 95% CI 2.06-3.08; P<0.001).
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