title: Pulmonary abnormalities and carotid atherosclerosis in ex-smokers without airflow limitation.
abstract: It is well-established that COPD patients have a burden of vascular disease that cannot be fully-explained by smoking history but the mechanistic links between atherosclerosis and pulmonary disease in COPD patients are not well-understood. Moreover, in ex-smokers without symptoms or other evidence of COPD, subclinical pulmonary and vascular disease, although potentially present, has not been described or evaluated. Hence our aim was to use sensitive three-dimensional (3D) pulmonary and carotid imaging to quantify pulmonary airway/parenchyma abnormalities and atherosclerosis in ex-smokers without airflow limitation or symptoms consistent with COPD. We evaluated 61 subjects without airflow limitation including 34 never- (72 ± 6 years) and 27 ex-smokers (73 ± 9 years), who provided written informed consent to spirometry, plethysmography, (3)He magnetic resonance imaging (MRI) and carotid ultrasound (US) and, for ex-smokers alone, thoracic X-ray computed tomography (CT). Ex-smokers had significantly greater (3)He ventilation defect percent (VDP = 7%, p = 0.001) and carotid total plaque volume (TPV = 250 mm(3), p = 0.002) than never-smokers, although there were no significant differences for spirometry or plethysmography, and CT airway and emphysema measurements were normal. There were univariate relationships for (3)He VDP with carotid intima media thickness (IMT, r = 0.42, p = 0.004), TPV (r = 0.41, p = 0.006) and vessel wall volume (VWV, r = 0.40, p = 0.007). Multivariate models that included age, BMI, FEV1, DLCO and VDP showed that only VDP significantly predicted IMT (β = 0.41, p = 0.001), VWV (β = 0.45, p = 0.003) and TPV (β = 0.38, p = 0.005). In summary, there was imaging evidence of mild airways disease and carotid plaque burden that were related and significantly greater in ex-smokers without airflow limitation than in never-smokers.
authors.affiliation: 1Imaging Research Laboratories, Robarts Research Institute, Department of Medical Biophysics, The University of Western Ontario , London, Ontario , Canada.
authors.forename: Damien
authors.initials: D
authors.lastname: Pike
authors.forename: Miranda
authors.initials: M
authors.lastname: Kirby
authors.forename: Tamas J
authors.initials: TJ
authors.lastname: Lindenmaier
authors.forename: Khadija
authors.initials: K
authors.lastname: Sheikh
authors.forename: Casey E
authors.initials: CE
authors.lastname: Neron
authors.forename: Daniel G
authors.initials: DG
authors.lastname: Hackam
authors.forename: J David
authors.initials: JD
authors.lastname: Spence
authors.forename: Aaron
authors.initials: A
authors.lastname: Fenster
authors.forename: Nigel A M
authors.initials: NA
authors.lastname: Paterson
authors.forename: Don D
authors.initials: DD
authors.lastname: Sin
authors.forename: Harvey O
authors.initials: HO
authors.lastname: Coxson
authors.forename: David G
authors.initials: DG
authors.lastname: McCormack
authors.forename: Grace
authors.initials: G
authors.lastname: Parraga
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002340:Carotid Artery Diseases / Q000175:diagnosis / Q000209:etiology*; D059168:Carotid Intima-Media Thickness; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D021621:Imaging, Three-Dimensional; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010991:Plethysmography; D029424:Pulmonary Disease, Chronic Obstructive / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology; D012044:Regression Analysis; D012307:Risk Factors; D012720:Severity of Illness Index; D012907:Smoking / Q000009:adverse effects*; D016540:Smoking Cessation; D013147:Spirometry; D014057:Tomography, X-Ray Computed
keywords: COPD; atherosclerosis; magnetic resonance imaging; tobacco; ultrasound