Key result
Current smoking is associated with ~44% higher augmentation index versus never smoking, partially reversible with cessation.
Why the study?
To assess the cross-sectional and longitudinal associations of smoking behaviour with central arterial haemodynamic measures in the Framingham Heart Study.
Does smoking behavior and cessation alter central arterial haemodynamic measures in a community-based cohort?
Observational (n=6,597)
Does smoking behavior and cessation alter central arterial haemodynamic measures in a community-based cohort?
Central arterial measures, particularly augmentation index, are sensitive to smoking status and intensity, but longer smoking cessation may partially revert these measures to levels seen in those with lower exposure.
May support smoking cessation counseling to improve central hemodynamics; extends observational data but remains hypothesis-generating.
AIMS: To assess the cross-sectional and longitudinal associations of smoking behaviour with central arterial haemodynamic measures in samples of the Framingham Heart Study. METHODS AND RESULTS: In 6597 participants [3606 (55%) women, 51.5% never smoked, 34.8% formerly quit, 4.3% recently quit, and 9.3% currently smoking], we assessed relations of smoking behaviour with central arterial measures using multivariable linear regression models. In cross-sectional models, central arterial measures were different across smoking behaviour groups. Particularly, augmentation index (AI) was higher among participants who formerly quit smoking (least squares mean ± standard error = 14.1 ± 0.4%; P < 0.001) and were currently smoking (18.1 ± 0.5%; P < 0.001) compared with participants who never smoked (12.6 ± 0.3%). Among participants currently smoking, higher cigarettes per day [B = 1.41; 95% confidence interval (CI), 0.47-2.34] were associated with higher AI. Among participants who had quit smoking, higher pack-years were associated with higher AI (B = 0.85; 95% CI, 0.60-1.14) and central pulse pressure (B = 0.84; 95% CI, 0.46-1.21). Using restricted cubic splines, we observed a negative linear association for AI, but non-linear associations for characteristic impedance and central pulse pressure, with higher time since quit (all P < 0.001). Additionally, we observed non-linear patterns of central arterial measures with smoking cessation by smoking burden (<20 vs. ≥20 pack-years). In longitudinal models, we observed higher increases in AI among participants who persistently quit (4.62 ± 0.41%; P < 0.001) and persistently smoked (5.48 ± 0.70%; P = 0.002) compared with participants who never smoked (3.45 ± 0.37%). CONCLUSION: Central arterial measures are sensitive to differences and changes in smoking behaviour. Longer cessation may revert central arterial measures to levels observed with lower smoking exposure.
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Cooper et al. (2025) conducted an observational in General population (n=6,597). Smoking behavior vs. Never smoked was evaluated on Augmentation index (p=<0.001). Current smoking was associated with a significantly higher augmentation index (18.1%) compared to never smoking (12.6%), reflecting increased central arterial wave reflection that partially reverses with cessation.
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