Hansen Kristina, Östling Gerd, Persson Margaretha, Nilsson Peter M, Melander Olle, Engström Gunnar, Hedblad Bo, Rosvall Maria
Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden.
Eur J Intern Med. 2016 Mar;28:74-9. doi: 10.1016/j.ejim.2015.10.018. Epub 2015 Nov 6.
The purpose of the study was to investigate the long-term associations between smoking habits, environmental tobacco smoke exposure (ETS), carotid intima-media thickness (IMT) progression rate, and rate of lumen diameter reduction in the carotid artery during a 16-year follow-up. Another objective was to investigate if an effect of smoking on progression rate could be explained by increased low grade inflammation.
The study population included 2992 middle-aged men and women in the 1991-1994 (baseline) and the 2007-2012 (re-examination) investigation of the Malmö Diet and Cancer Study cardiovascular cohort. Associations between smoking, progression of carotid IMT and lumen diameter reduction due to plaque protrusion were assessed by linear regression.
IMT progression rates and rate of lumen diameter reduction increased from never smokers with no ETS through former, moderate and heavy smokers, even after adjustment for traditional risk factors (e.g., differences in yearly progression rates (mm/year) of maximal IMT in the carotid bifurcation compared to never smokers; former smokers 0.0074 (95% CI: 0.0018-0.0129), moderate smokers 0.0106 (95% CI: 0.0038-0.0175), and heavy smokers 0.0146 (95% CI: 0.0061-0.0230)). Former smokers showed distinct lowering of progression rates after more than five years since smoking cessation. Smoking and former smoking was associated with increased low grade inflammation, however, the effect of smoking on atherosclerotic progression rate remained fairly unchanged after such adjustment.
The effect of smoking and former smoking on carotid IMT progression rates and change in lumen reduction due to plaque protrusion could not be explained by differences in traditional risk factors or low grade inflammation.
本研究旨在调查在16年随访期间吸烟习惯、环境烟草烟雾暴露（ETS）、颈动脉内膜中层厚度（IMT）进展率以及颈动脉管腔直径缩小率之间的长期关联。另一个目的是研究吸烟对进展率的影响是否可由低度炎症增加来解释。
研究人群包括参加马尔默饮食与癌症研究心血管队列1991 - 1994年（基线）和2007 - 2012年（重新检查）调查的2992名中年男性和女性。通过线性回归评估吸烟、颈动脉IMT进展与斑块突出导致的管腔直径缩小之间的关联。
即使在调整传统风险因素后，从无ETS的从不吸烟者到曾经吸烟者、中度吸烟者和重度吸烟者，IMT进展率和管腔直径缩小率均升高（例如，与从不吸烟者相比，颈动脉分叉处最大IMT的年进展率（mm/年）差异；曾经吸烟者0.0074（95%CI：0.0018 - 0.0129），中度吸烟者0.0106（95%CI：0.0038 - 0.0175），重度吸烟者0.0146（95%CI：0.0061 - 0.0230））。戒烟超过五年后，曾经吸烟者的进展率明显降低。吸烟和曾经吸烟与低度炎症增加相关，然而，调整后吸烟对动脉粥样硬化进展率的影响基本保持不变。
吸烟和曾经吸烟对颈动脉IMT进展率以及斑块突出导致的管腔缩小变化的影响，无法用传统风险因素或低度炎症的差异来解释。
