Kristina Hansen1, Gerd Östling2, Margaretha Persson3, Peter M Nilsson4, Olle Melander5, Gunnar Engström6, Bo Hedblad7, Maria Rosvall8. 1. Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden. Electronic address: Kristina.hansen@med.lu.se. 2. Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden. Electronic address: Gerd.ostling@med.lu.se. 3. Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden. Electronic address: Margaretha.M.Persson@skane.se. 4. Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden. Electronic address: Peter.nilsson@med.lu.se. 5. Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden. Electronic address: Olle.melander@med.lu.se. 6. Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden. Electronic address: Gunnar.engstrom@med.lu.se. 7. Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden. Electronic address: Bo.hedblad@med.lu.se. 8. Department of Clinical Sciences, Lund University, Skåne University Hospital, SE-205 02 Malmö, Sweden. Electronic address: Maria.rosvall@med.lu.se.
Abstract
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.
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