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Relationships among muscle oxidative capacity, coronary artery calcium, and hepatic steatosis in COPD: A pilot study

Nicholas Tiller, Harry Rossiter, Asghar Abbasi, April Kinninger, Matthew Budoff, Richard Casaburi, Alessandra Adami
European Respiratory Journal 2020 56: 930; DOI: 10.1183/13993003.congress-2020.930
Nicholas Tiller
1The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, United States of America
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  • For correspondence: nicholas.tiller@lundquist.org
Harry Rossiter
1The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, United States of America
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Asghar Abbasi
1The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, United States of America
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April Kinninger
1The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, United States of America
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Matthew Budoff
1The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, United States of America
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Richard Casaburi
1The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, United States of America
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Alessandra Adami
2University of Rhode Island, Kingston, United States of America
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Abstract

Introduction: COPD is characterized by inactivity and muscle deconditioning. We recently showed a negative association between muscle oxidative capacity and serum triglyceride concentrations in severe COPD. It is unclear whether these maladaptations contribute to increased cardiometabolic disease risk. Aim. To assess relationships among muscle oxidative capacity, coronary artery calcium (CAC), and hepatic steatosis (liver-to-spleen Hounsfield Unit ratio) in smokers with and without COPD. Methods. Data from 90 COPDGene subjects (GOLD 1/2/3/4=10/12/6/7; 55 smoking controls with normal spirometry) were retrospectively analyzed. CAC and L/S were assessed from chest CT. Muscle oxidative capacity was estimated from the O2 consumption recovery rate constant (k) using near-infrared spectroscopy. Results. k was lower in COPD than controls (1.31±0.44 vs. 1.67±0.45min-1; p<0.001, d=0.81). Total CAC and calcification in the independent coronary arteries were not different between COPD patients and controls (452±694 vs. 707±1503; p>0.05). L/S was greater in COPD (1.45±0.49 vs. 1.31±0.26; p=0.038, d=0.36), and the threshold for fatty liver disease (L/S<1.0) was met by 9% of COPD patients and 7% of controls. Age-adjusted regressions showed no correlation between k and L/S (r=-0.14, p=0.189) or CAC (r=-0.05, p=0.648). Conclusions. CAC was not different between COPD patients and controls and was not associated with muscle k, suggesting that factors other than muscle oxidative capacity contribute to CAC formation in COPD. The hypothesis that COPD patients with low k may have more echolucent (less calcified) plaque, and thus increased CVD risk, remains to be tested.

  • Comorbidities
  • Systemic effect
  • COPD - mechanism

Footnotes

Cite this article as: European Respiratory Journal 2020; 56: Suppl. 64, 930.

This abstract was presented at the 2020 ERS International Congress, in session “Respiratory viruses in the "pre COVID-19" era”.

This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).

  • Copyright ©the authors 2020
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Relationships among muscle oxidative capacity, coronary artery calcium, and hepatic steatosis in COPD: A pilot study
Nicholas Tiller, Harry Rossiter, Asghar Abbasi, April Kinninger, Matthew Budoff, Richard Casaburi, Alessandra Adami
European Respiratory Journal Sep 2020, 56 (suppl 64) 930; DOI: 10.1183/13993003.congress-2020.930

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Relationships among muscle oxidative capacity, coronary artery calcium, and hepatic steatosis in COPD: A pilot study
Nicholas Tiller, Harry Rossiter, Asghar Abbasi, April Kinninger, Matthew Budoff, Richard Casaburi, Alessandra Adami
European Respiratory Journal Sep 2020, 56 (suppl 64) 930; DOI: 10.1183/13993003.congress-2020.930
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