Journal article
Centrilobular emphysema and coronary artery calcification: mediation analysis in the SPIROMICS cohort
Respiratory research, Vol.19(1), pp.257-257
12/18/2018
DOI: 10.1186/s12931-018-0946-1
PMCID: PMC6299495
PMID: 30563576
Abstract
BackgroundChronic obstructive pulmonary disease (COPD) is associated with a two-to-five fold increase in the risk of coronary artery disease independent of shared risk factors. This association is hypothesized to be mediated by systemic inflammation but this link has not been established.MethodsWe included 300 participants enrolled in the SPIROMICS cohort, 75 each of lifetime non-smokers, smokers without airflow obstruction, mild-moderate COPD, and severe-very severe COPD. We quantified emphysema and airway disease on computed tomography, characterized visual emphysema subtypes (centrilobular and paraseptal) and airway disease, and used the Weston visual score to quantify coronary artery calcification (CAC). We used the Sobel test to determine whether markers of systemic inflammation mediated a link between spirometric and radiographic features of COPD and CAC.ResultsFEV(1)/FVC but not quantitative emphysema or airway wall thickening was associated with CAC (p=0.036), after adjustment for demographics, diabetes mellitus, hypertension, statin use, and CT scanner type. To explain this discordance, we examined visual subtypes of emphysema and airway disease, and found that centrilobular emphysema but not paraseptal emphysema or bronchial thickening was independently associated with CAC (p=0.019). MMP3, VCAM1, CXCL5 and CXCL9 mediated 8, 8, 7 and 16% of the association between FEV1/FVC and CAC, respectively. Similar biomarkers partially mediated the association between centrilobular emphysema and CAC.ConclusionsThe association between airflow obstruction and coronary calcification is driven primarily by the centrilobular subtype of emphysema, and is linked through bioactive molecules implicated in the pathogenesis of atherosclerosis.Trial RegistrationClinicalTrials.gov: Identifier: NCT01969344.
Details
- Title: Subtitle
- Centrilobular emphysema and coronary artery calcification: mediation analysis in the SPIROMICS cohort
- Creators
- Richard C. BoucherRussell P. BowlerElizabeth E. CarrettaStephanie A. ChristensonAlejandro P. ComellasChristopher B. CooperDavid J. CouperGerard J. CrinerRonald G. CrystalJeffrey L. CurtisClaire M. DoerschukChristine M. FreemanNadia N. HanselAnnette T. HastieEric A. HoffmanR. Graham Barr - Columbia University Irving Medical CenterRobert J. KanerMark T. Dransfield - University of Alabama at BirminghamRichard E. KannerEric C. KleerupNeil E. AlexisJerry A. KrishnanWayne H. AndersonEugene R. BleeckerLisa M. LaVangeStephen C. LazarusSurya P. Bhatt - University of Alabama at BirminghamDeborah A. MeyersHrudaya P. Nath - University of Alabama at BirminghamYoung-il Kim - University of Alabama at BirminghamWendy C. MooreRekha Ramachandran - University of Alabama at BirminghamJohn D. NewellJubal R. Watts - University of Alabama at BirminghamLaura PaulinNina L. J. Terry - University of Alabama at BirminghamStephen PetersSushil Sonavane - University of Alabama at BirminghamWanda K. O'NealSwati P. Deshmane - University of Alabama at BirminghamVictor E. OrtegaPrescott G. Woodruff - University of California, San FranciscoRobert PaineNirupama PutchaElizabeth C. Oelsner - Columbia University Medical CenterSandeep Bodduluri - University of Alabama at BirminghamStephen I. RennardMeiLan K. Han - University of MichiganDonald P. TashkinWassim W. Labaki - University of MichiganMary Beth ScholandJ. Michael Wells - University of Alabama at BirminghamRobert A. WiseFernando J. Martinez - Weill Cornell MedicineSubPopulations and InteRmediate Outcome Measures In COPD Study (SPIROMICS) Investigators
- Resource Type
- Journal article
- Publication Details
- Respiratory research, Vol.19(1), pp.257-257
- DOI
- 10.1186/s12931-018-0946-1
- PMID
- 30563576
- PMCID
- PMC6299495
- NLM abbreviation
- Respir Res
- ISSN
- 1465-993X
- eISSN
- 1465-993X
- Publisher
- Springer Nature
- Number of pages
- 9
- Grant note
- Regeneron Pharmaceuticals, Inc.; Regeneron Takeda Pharmaceutical Company; Takeda Pharmaceutical Company Ltd Chiesi Farmaceutici S.p.A. HHSN268200900013C; HHSN268200900014C; HHSN268200900015C; HHSN268200900016C; HHSN268200900017C; HHSN268200900018C; HHSN268200900019C; HHSN268200900020C / NIH/NHLBI; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) Grifols Therapeutics, Inc. Foundation for the NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA ProterixBio Boehringer-Ingelheim Pharmaceuticals, Inc.; Boehringer Ingelheim K23HL133438 / NHLBI; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) Bellerophon Therapeutics GlaxoSmithKline Bayer; Bayer AG Novartis Pharmaceuticals Corporation; Novartis Sunovion Sanofi K24HL137013 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI) Ikaria, Inc. Nycomed GmbH COPD Foundation from AstraZeneca/MedImmune Forest Research Institute, Inc.
- Language
- English
- Date published
- 12/18/2018
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Radiology; Pulmonary, Critical Care, and Occupational Medicine; ICTS; Internal Medicine
- Record Identifier
- 9984318693802771
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