Wassim W Labaki1, Meng Xia2, Susan Murray2, Jeffrey L Curtis3, R Graham Barr4, Surya P Bhatt5, Eugene R Bleecker6, Nadia N Hansel7, Christopher B Cooper8, Mark T Dransfield5, J Michael Wells5, Eric A Hoffman9, Richard E Kanner10, Robert Paine10, Victor E Ortega11, Stephen P Peters11, Jerry A Krishnan12, Russell P Bowler13, David J Couper14, Prescott G Woodruff15, Fernando J Martinez16, Carlos H Martinez17, MeiLan K Han17. 1. Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, USA. Electronic address: wlabaki@med.umich.edu. 2. Department of Biostatistics, University of Michigan, Ann Arbor, MI, USA. 3. Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, USA; Medical Service, VA Ann Arbor Healthcare System, Ann Arbor, MI, USA. 4. Division of Pulmonary, Allergy and Critical Care Medicine, Columbia University, New York, NY, USA. 5. Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, USA. 6. Division of Genetics, Genomics and Precision Medicine, University of Arizona, Tucson, AZ, USA. 7. Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA. 8. Departments of Medicine and Physiology, University of California Los Angeles, Los Angeles, CA, USA. 9. Department of Radiology, University of Iowa, Iowa City, IA, USA. 10. Division of Pulmonary Medicine, University of Utah, Salt Lake City, UT, USA. 11. Section on Pulmonary, Critical Care, Allergy and Immunologic Diseases, Wake Forest Baptist Health, Winston-Salem, NC, USA. 12. Division of Pulmonary, Critical Care, Sleep and Allergy, University of Illinois at Chicago, Chicago, IL, USA. 13. Department of Medicine, National Jewish Health, Denver, CO, USA. 14. Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA. 15. Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, University of California San Francisco, San Francisco, CA, USA. 16. Division of Pulmonary and Critical Care Medicine, Weill Cornell Medical College, New York, NY, USA. 17. Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI, USA.
Abstract
BACKGROUND: High N-terminal pro-brain natriuretic peptide (NT-proBNP) during COPD exacerbations is associated with worse clinical outcomes. The prognostic value of NT-proBNP measured during clinical stability has not been well characterized. METHODS: We studied SPIROMICS participants 40-80 years of age with COPD GOLD spirometric stages 1-4. The association between baseline NT-proBNP and incident COPD exacerbations within one year of follow-up was tested using zero-inflated Poisson regression models adjusted for age, gender, race, body mass index, current smoking status, smoking history, FEV1 percent predicted, COPD Assessment Test score, exacerbation history, total lung capacity on chest CT and cardiovascular disease (any of coronary artery disease, myocardial infarction or congestive heart failure). RESULTS: Among 1051 participants (mean age 66.1 years, 41.4% women), mean NT-proBNP was 608.9 pg/ml. Subjects in GOLD stage D had the highest mean NT-proBNP. After one year of follow-up, 268 participants experienced one or more COPD exacerbations. One standard deviation increase in baseline NT-proBNP was associated with a 13% increase in the risk of incident exacerbations (incident risk ratio 1.13; 95% CI 1.06-1.19; p < 0.0001). This association was maintained in participants with and without cardiovascular disease. CONCLUSION: Baseline NT-proBNP in COPD is an independent predictor of respiratory exacerbations, even in individuals without overt cardiac disease. The impact of detection and treatment of early cardiovascular dysfunction on COPD exacerbation frequency warrants further investigation.
BACKGROUND: High N-terminal pro-brain natriuretic peptide (NT-proBNP) during COPD exacerbations is associated with worse clinical outcomes. The prognostic value of NT-proBNP measured during clinical stability has not been well characterized. METHODS: We studied SPIROMICS participants 40-80 years of age with COPD GOLD spirometric stages 1-4. The association between baseline NT-proBNP and incident COPD exacerbations within one year of follow-up was tested using zero-inflated Poisson regression models adjusted for age, gender, race, body mass index, current smoking status, smoking history, FEV1 percent predicted, COPD Assessment Test score, exacerbation history, total lung capacity on chest CT and cardiovascular disease (any of coronary artery disease, myocardial infarction or congestive heart failure). RESULTS: Among 1051 participants (mean age 66.1 years, 41.4% women), mean NT-proBNP was 608.9 pg/ml. Subjects in GOLD stage D had the highest mean NT-proBNP. After one year of follow-up, 268 participants experienced one or more COPD exacerbations. One standard deviation increase in baseline NT-proBNP was associated with a 13% increase in the risk of incident exacerbations (incident risk ratio 1.13; 95% CI 1.06-1.19; p < 0.0001). This association was maintained in participants with and without cardiovascular disease. CONCLUSION: Baseline NT-proBNP in COPD is an independent predictor of respiratory exacerbations, even in individuals without overt cardiac disease. The impact of detection and treatment of early cardiovascular dysfunction on COPD exacerbation frequency warrants further investigation.
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