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Original research
CT pectoralis muscle area is associated with DXA lean mass and correlates with emphysema progression in a tobacco-exposed cohort
  1. Michael Emmet O'Brien1,
  2. Richard H Zou1,
  3. Nathan Hyre2,
  4. Joseph K Leader3,
  5. Carl R Fuhrman3,
  6. Frank C Sciurba1,
  7. Mehdi Nouraie1,
  8. Jessica Bon1
  1. 1 Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA
  2. 2 University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
  3. 3 Radiology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA
  1. Correspondence to Dr Jessica Bon, Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA; bonjm{at}


Introduction Muscle loss is an important extrapulmonary manifestation of COPD. Dual energy X-ray absorptiometry (DXA) is the method of choice for body composition measurement but is not widely used for muscle mass evaluation. The pectoralis muscle area (PMA) is quantifiable by CT and predicts cross-sectional COPD-related morbidity. There are no studies that compare PMA with DXA measures or that evaluate longitudinal relationships between PMA and lung disease progression.

Methods Participants from our longitudinal tobacco-exposed cohort had baseline and 6-year chest CT (n=259) and DXA (n=164) data. Emphysema was quantified by CT density histogram parenchymal scoring using the 15th percentile technique. Fat-free mass index (FFMI) and appendicular skeletal mass index (ASMI) were calculated from DXA measurements. Linear regression model relationships were reported using standardised coefficient (β) with 95% CI.

Results PMA was more strongly associated with DXA measures than with body mass index (BMI) in both cross-sectional (FFMI: β=0.76 (95% CI 0.65 to 0.86), p<0.001; ASMI: β=0.76 (95% CI 0.66 to 0.86), p<0.001; BMI: β=0.36 (95% CI 0.25 to 0.47), p<0.001) and longitudinal (ΔFFMI: β=0.43 (95% CI 0.28 to 0.57), p<0.001; ΔASMI: β=0.42 (95% CI 0.27 to 0.57), p<0.001; ΔBMI: β=0.34 (95% CI 0.22 to 0.46), p<0.001) models. Six-year change in PMA was associated with 6-year change in emphysema (β=0.39 (95% CI 0.23 to 0.56), p<0.001) but not with 6-year change in airflow obstruction.

Conclusions PMA is an accessible measure of muscle mass and may serve as a useful clinical surrogate for assessing skeletal muscle loss in smokers. Decreased PMA correlated with emphysema progression but not lung function decline, suggesting a difference in the pathophysiology driving emphysema, airflow obstruction and comorbidity risk.

  • emphysema
  • imaging/CT MRI etc
  • respiratory muscles
  • tobacco and the lung

Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information.

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Data availability statement

All data relevant to the study are included in the article or uploaded as supplementary information.

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  • MEO'B and RHZ are joint first authors.

  • Twitter @zou_richard

  • MEO'B and RHZ contributed equally.

  • Contributors MEO'B, RHZ, MN and JB were responsible for study concept and design. CRF provided semiquantitative radiographic emphysema scores. MEO'B, RHZ and NH performed data acquisition. MEO'B, RHZ and MN performed the statistical analyses. JKL, FCS, MN and JB provided intellectual input and edited the manuscript. MEO'B, RHZ, NH, JKL, FCS, MN and JB were responsible for the decision to submit the manuscript. JB was the guarantor and accepts full responsibility for the work and conduct of the study, had access to the data, and controlled the decision to publish.

  • Funding The study was funded by National Institutes of Health (NIH) and National Heart, Lung, and Blood Institute (NHLBI) grants R01 HL12828901, P50 HL084948 and P50 CA90440, and by CHEST Foundation Research Grant in Chronic Obstructive Pulmonary Disease.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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