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

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.