Validation for measurements of skeletal muscle areas using low-dose chest computed tomography

Various methods were suggested to measure skeletal muscle areas (SMAs) using chest low-dose computed tomography (chest LDCT) as a substitute for SMA at 3rd lumbar vertebra level (L3-SMA). In this study, four SMAs (L1-SMA, T12-erector spinae muscle areas, chest wall muscle area at carina level, pectoralis muscle area at aortic arch level) were segmented semi-automatically in 780 individuals taking concurrent chest and abdomen LDCT for healthcare screening. Four SMAs were compared to L3-SMA and annual changes were calculated from individuals with multiple examinations (n = 101). Skeletal muscle index (SMI; SMA/height2) cut-off for sarcopenia was determined by lower 5th percentile of young individuals (age ≤ 40 years). L1-SMA showed the greatest correlation to L3-SMA (men, R2 = 0.7920; women, R2 = 0.7396), and the smallest annual changes (0.3300 ± 4.7365%) among four SMAs. L1-SMI cut-offs for determining sarcopenia were 39.2cm2/m2 in men, and 27.5cm2/m2 in women. Forty-six men (9.5%) and ten women (3.4%) were found to have sarcopenia using L1-SMI cut-offs. In conclusion, L1-SMA could be a reasonable substitute for L3-SMA in chest LDCT. Suggested L1-SMI cut-offs for sarcopenia were 39.2cm2/m2 for men and 27.5cm2/m2 for women in Asian.

Chest wall muscle atrophy as a contributory factor for forced vital capacity decline in systemic sclerosis-associated interstitial lung disease

Objective To investigate the potential contribution of accessory respiratory muscle atrophy to the decline of forced vital capacity (FVC) in patients with SSc-associated interstitial lung disease (ILD). Methods This single-centre, retrospective study enrolled 36 patients with SSc-ILD who underwent serial pulmonary function tests and chest high-resolution CT (HRCT) simultaneously at an interval of 1–3 years. The total extent of ILD and chest wall muscle area at the level of the ninth thoracic vertebra on CT images were evaluated by two independent evaluators blinded to the patient information. Changes in the FVC, ILD extent, and chest wall muscle area between the two measurements were assessed in terms of their correlations. Multiple regression analysis was conducted to identify the independent contributors to FVC decline. Results Interval changes in FVC and total ILD extent were variable among patients, whereas chest wall muscle area decreased significantly with time (P=0.0008). The FVC change was negatively correlated with the change in ILD extent (r=−0.48, P=0.003) and was positively correlated with the change in the chest wall muscle area (r = 0.53, P=0.001). Multivariate analysis revealed that changes in total ILD extent and chest wall muscle area were independent contributors to FVC decline. Conclusion In patients with SSc-ILD, FVC decline is attributable not only to the progression of ILD but also to the atrophy of accessory respiratory muscles. Our findings call attention to the interpretation of FVC changes in patients with SSc-ILD.