Age at quitting smoking as a predictor of risk of cardiovascular disease incidence independent of smoking status, time since quitting and pack-years

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dc.contributor.authorMannan, Haider R
dc.contributor.authorStevenson, Christopher E
dc.contributor.authorPeeters, Anna
dc.contributor.authorWalls, Helen L
dc.contributor.authorMcNeil, John J
dc.date.accessioned2015-12-15T02:48:37Z
dc.date.available2015-12-15T02:48:37Z
dc.date.issued2011
dc.date.updated2016-02-24T11:08:28Z
dc.description.abstractBACKGROUND Risk prediction for CVD events has been shown to vary according to current smoking status, pack-years smoked over a lifetime, time since quitting and age at quitting. The latter two are closely and inversely related. It is not known whether the age at which one quits smoking is an additional important predictor of CVD events. The aim of this study was to determine whether the risk of CVD events varied according to age at quitting after taking into account current smoking status, lifetime pack-years smoked and time since quitting. FINDINGS We used the Cox proportional hazards model to evaluate the risk of developing a first CVD event for a cohort of participants in the Framingham Offspring Heart Study who attended the fourth examination between ages 30 and 74 years and were free of CVD. Those who quit before the median age of 37 years had a risk of CVD incidence similar to those who were never smokers. The incorporation of age at quitting in the smoking variable resulted in better prediction than the model which had a simple current smoker/non-smoker measure and the one that incorporated both time since quitting and pack-years. These models demonstrated good discrimination, calibration and global fit. The risk among those quitting more than 5 years prior to the baseline exam and those whose age at quitting was prior to 44 years was similar to the risk among never smokers. However, the risk among those quitting less than 5 years prior to the baseline exam and those who continued to smoke until 44 years of age (or beyond) was two and a half times higher than that of never smokers. CONCLUSIONS Age at quitting improves the prediction of risk of CVD incidence even after other smoking measures are taken into account. The clinical benefit of adding age at quitting to the model with other smoking measures may be greater than the associated costs. Thus, age at quitting should be considered in addition to smoking status, time since quitting and pack-years when counselling individuals about their cardiovascular risk.
dc.description.sponsorshipThis research was supported by an NHMRC health services research grant (no. 465130), an NHMRC/NHF PhD scholarship and a Vichealth Fellowship.en_AU
dc.format9 pages
dc.identifier.issn1756-0500en_AU
dc.identifier.urihttp://hdl.handle.net/1885/95022
dc.publisherBioMed Central
dc.relationhttp://purl.org/au-research/grants/nhmrc/465130
dc.rights© 2011 Mannan et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.sourceBMC Research Notes
dc.subjectcardiovascular disease CVD
dc.subjectrisk
dc.subjectsmoking
dc.subjectage
dc.subjectpack-years
dc.subjectlifetime
dc.subjecttime
dc.subjectquitting
dc.subjectCox
dc.subjectproportional
dc.subjecthazards
dc.subjectmodel
dc.subjectFramingham
dc.subjectOffspring
dc.subjectHeart
dc.subjectStudy
dc.titleAge at quitting smoking as a predictor of risk of cardiovascular disease incidence independent of smoking status, time since quitting and pack-years
dc.typeJournal article
dcterms.dateAccepted2011-02-15
local.bibliographicCitation.issue39
local.bibliographicCitation.startpage39en_AU
local.contributor.affiliationMannan, Haider R, Monash University, Australiaen_AU
local.contributor.affiliationStevenson, C, Monash University, Australiaen_AU
local.contributor.affiliationPeeters, Anna, Monash University, Australiaen_AU
local.contributor.affiliationWalls, Helen, College of Medicine, Biology and Environment, CMBE Research School of Population Health, Natl Centre for Epidemiology & Population Health, The Australian National Universityen_AU
local.contributor.affiliationMcNeil, John J, Monash University, Australiaen_AU
local.contributor.authoremailhelen.walls@anu.edu.auen_AU
local.contributor.authoruidu4320141en_AU
local.description.notesImported from ARIES.en_AU
local.identifier.absfor111716en_AU
local.identifier.absseo920412en_AU
local.identifier.ariespublicationu4468094xPUB207en_AU
local.identifier.citationvolume4en_AU
local.identifier.doi10.1186/1756-0500-4-39en_AU
local.identifier.essn1756-0500en_AU
local.identifier.scopusID2-s2.0-79851507906
local.identifier.uidSubmittedByu3488905en_AU
local.publisher.urlhttp://www.biomedcentral.com/en_AU
local.type.statusPublished Versionen_AU

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