Key result
High cumulative smoking exposure linked to ~90% higher odds of silent atherosclerotic plaque.
Why the study?
Although smoking is an established risk factor for ASCVD, the dose-response relationship between cumulative smoking exposure and silent atherosclerosis remained poorly characterised.
Does cumulative lifetime smoking exposure increase the prevalence of imaging-defined silent atherosclerosis compared to never-smoking in asymptomatic adults?
Cross-Sectional (n=4,449)
Yes
Does cumulative lifetime smoking exposure increase the prevalence of imaging-defined silent atherosclerosis compared to never-smoking in asymptomatic adults?
Cumulative lifetime smoking exposure demonstrates a clear dose-response association with silent carotid, femoral, and coronary atherosclerosis independent of conventional risk factors, reinforcing smoking cessation as a vital primary prevention target.
Smoking linked to silent plaque; extends known ASCVD risk but hypothesis-generating for imaging in risk stratification.
Background Smoking is a well-established risk factor for atherosclerotic cardiovascular disease (ASCVD), yet the dose–response relationship between cumulative smoking exposure and silent atherosclerosis remains poorly characterised. Purpose We aimed to assess the association between lifetime smoking exposure and imaging-defined silent atherosclerosis. Methods We included asymptomatic participants aged 18-70 years at baseline in the cross-sectional multicentre prospective REACT cohort study in Spain and Denmark. Smoking status was obtained via a self-administered questionnaire. Cumulative smoking exposure was assessed as pack-years (continuous variable) and categorically using smoking status; never, former or current smoker, and among ever-smokers, tertiles of pack-years. The presence of atherosclerotic plaque was assessed bilaterally in the carotid and femoral arteries using 3D vascular ultrasound (3DVUS) and in the coronary arteries using CT angiography. Odds ratios (ORs) for silent atherosclerosis were estimated using multivariable logistic regression, adjusting for age, sex, physical activity, LDL-cholesterol and HbA1c. Results (preliminary) Information on smoking was available in 4,449 participants (mean age 47, SD = 13; 51 % men). Among these, 2,143 (48%) reported a history of smoking with a mean of 12 pack-years (SD = 12), and 550 (12 %) were current smokers. Ever-smoking was significantly associated with plaque presence compared to never-smokers (OR 1.24; 95% CI 1.0 - 1.4, p = 0.02). A dose-response relationship was observed for smoking burden expressed as tertiles of pack-years in adjusted analyses (Figure 1). Compared with never smokers (reference, n = 2,306), individuals in the highest tertile (T3, n = 672; range 14.0 - 133.0) had a significantly increased odds of plaque presence (OR 1.9; 95% CI 1.5 – 2.4, p < 0.001). Conclusion Cumulative smoking exposure was significantly associated with the presence of silent atherosclerosis after adjusting for conventional risk factors. These findings highlight the importance of cumulative smoking exposure being a driver of subclinical atherosclerosis, reinforcing smoking cessation as a key preventive target against developing atherosclerosis. Figure 1. Forest plot; Adjusted odds ratios (95% CI) for the presence of subclinical atherosclerosis by smoking burden (pack-year tertiles; T1-T3) versus never-smokers (reference group, OR = 1.0), adjusted for age, sex, physical activity, LDL cholesterol, and HbA1c.Figur 1.Forest plot
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Ahmad et al. (2026) conducted a cross-sectional in Silent atherosclerosis (n=4,449). Cumulative smoking exposure (highest tertile: 14.0-133.0 pack-years; or ever-smoking) vs. Never smokers was evaluated on Presence of imaging-defined silent atherosclerotic plaque in carotid, femoral, or coronary arteries (OR 1.9, 95% CI 1.5-2.4, p=<0.001). High cumulative smoking exposure (14-133 pack-years) was associated with increased odds of silent atherosclerotic plaque compared with never smoking (OR 1.9; 95% CI 1.5-2.4; p<0.001).
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