GDF-15 plasma levels in chronic obstructive pulmonary disease are associated with subclinical coronary artery disease

Carlos H Martinez; Christine M Freeman; Joshua D Nelson; Susan Murray; Xin Wang; Matthew J Budoff; Mark T Dransfield; John E Hokanson; Ella A Kazerooni; Gregory L Kinney; Elizabeth A Regan; J Michael Wells; Fernando J Martinez; MeiLan K Han; Jeffrey L Curtis; COPDGene Investigators

doi:10.1186/s12931-017-0521-1

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GDF-15 plasma levels in chronic obstructive pulmonary disease are associated with subclinical coronary artery disease

Journal article

Open access

Peer reviewed

GDF-15 plasma levels in chronic obstructive pulmonary disease are associated with subclinical coronary artery disease

Carlos H Martinez, Christine M Freeman, Joshua D Nelson, Susan Murray, Xin Wang, Matthew J Budoff, Mark T Dransfield, John E Hokanson, Ella A Kazerooni, Gregory L Kinney, …

Respiratory research, Vol.18(1), pp.42-42

02/28/2017

DOI: 10.1186/s12931-017-0521-1

PMCID: PMC5331711

PMID: 28245821

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Abstract

Growth differentiation factor-15 (GDF-15), a cytokine associated with cardiovascular mortality, increases during chronic obstructive pulmonary disease (COPD) exacerbations, but any role in stable COPD is unknown. We tested associations between GDF-15 and subclinical coronary atherosclerosis, assessed by coronary artery calcium (CAC) score, in COPD subjects free of clinical cardiovascular disease (CVD). Cross-sectional analysis of COPD participants (GOLD stages 2-4) in the COPDGene cohort without CVD at enrollment, using baseline CAC (from non-EKG-gated chest computed tomography) and plasma GDF-15 (by custom ELISA). We used multinomial logistic modeling of GDF-15 associations with CAC, adjusting for demographics, baseline risk (calculated using the HEART: Personal Heart Early Assessment Risk Tool (Budoff et al. 114:1761-1791, 2006) score), smoking history, measures of airflow obstruction, emphysema and airway disease severity. Among 694 participants with COPD (47% women, mean age 63.6 years) mean GDF-15 was 1,304 pg/mL, and mean CAC score was 198. Relative to the lower GDF-15 tertile, higher tertiles showed bivariate association with increasing CAC score (mid tertile odds ratio [OR] 1.80, 95% confidence interval [CI] 1.29, 2.51; higher tertile OR 2.86, CI 2.04, 4.02). This association was maintained after additionally adjusting for baseline CVD risk, for co-morbidities and descriptors of COPD severity and impact, markers of cardiac stress (N-terminal pro-B-type natriuretic peptide, troponin T) and of inflammation (Interleukin-6), and in subgroup analysis excluding men, diabetics, current smokers or those with limited ambulation. In ever-smokers with COPD free of clinical CVD, GDF-15 contributes independently to subclinical coronary atherosclerosis. ClinicalTrials.gov, NCT00608764 . Registered 28 January 2008.

Comorbidity

Pulmonary Disease, Chronic Obstructive - diagnosis

Reproducibility of Results

Humans

Middle Aged

Risk Factors

Male

Asymptomatic Diseases

Biomarkers - blood

Coronary Artery Disease - blood

Pulmonary Disease, Chronic Obstructive - epidemiology

Incidence

Growth Differentiation Factor 15 - blood

Coronary Artery Disease - diagnosis

Sensitivity and Specificity

Pulmonary Disease, Chronic Obstructive - blood

Female

Aged

Coronary Artery Disease - epidemiology

Causality

Michigan - epidemiology

Details

Title: Subtitle: GDF-15 plasma levels in chronic obstructive pulmonary disease are associated with subclinical coronary artery disease
Creators: Carlos H Martinez - Division of Pulmonary & Critical Care Medicine, University of Michigan Health System, 2215 Fuller Road, Ann Arbor, MI, 48105-2303, USA
Christine M Freeman - Research Service, VA Ann Arbor Healthcare System, Ann Arbor, MI, USA
Joshua D Nelson - Division of Pulmonary & Critical Care Medicine, University of Michigan Health System, 2215 Fuller Road, Ann Arbor, MI, 48105-2303, USA
Susan Murray - Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, USA
Xin Wang - Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, USA
Matthew J Budoff - Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA, USA
Mark T Dransfield - Medical Service, Birmingham Veteran Affairs Medical Center, Birmingham, AL, USA
John E Hokanson - School of Public Health, University of Colorado, Aurora, CO, USA
Ella A Kazerooni - Radiology Department, University of Michigan Health System, Ann Arbor, MI, USA
Gregory L Kinney - School of Public Health, University of Colorado, Aurora, CO, USA
Elizabeth A Regan - Pulmonary & Critical Care Medicine Division, Department of Medicine, University of Colorado, Denver, CO, USA
J Michael Wells - Medical Service, Birmingham Veteran Affairs Medical Center, Birmingham, AL, USA
Fernando J Martinez - Pulmonary & Critical Care Medicine Division, Department of Medicine, Weill Cornell Medical College, New York, NY, USA
MeiLan K Han - Division of Pulmonary & Critical Care Medicine, University of Michigan Health System, 2215 Fuller Road, Ann Arbor, MI, 48105-2303, USA
Jeffrey L Curtis - Medical Service, VA Ann Arbor Healthcare System, 2215 Fuller Road, Ann Arbor, MI, 48105-2303, USA. jlcurtis@umich.edu
COPDGene Investigators
Contributors: Eric A Hoffman (Contributor) - University of Iowa, Radiology
Resource Type: Journal article
Publication Details: Respiratory research, Vol.18(1), pp.42-42
DOI: 10.1186/s12931-017-0521-1
PMID: 28245821
PMCID: PMC5331711
NLM abbreviation: Respir Res
ISSN: 1465-9921
eISSN: 1465-993X
Publisher: England
Grant note: U01 HL089856 / NHLBI NIH HHS I01 CX001553 / CSRD VA K23 HL128936 / NHLBI NIH HHS U01 HL089897 / NHLBI NIH HHS R01 HL089856 / NHLBI NIH HHS S10 OD018526 / NIH HHS I01 CX000911 / CSRD VA I01 BX001389 / BLRD VA R01 HL089897 / NHLBI NIH HHS R01 HL122438 / NHLBI NIH HHS R01 HL130883 / NHLBI NIH HHS
Language: English
Date published: 02/28/2017
Academic Unit: Roy J. Carver Department of Biomedical Engineering; Radiology; Psychiatry; Internal Medicine
Record Identifier: 9984051561602771

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