From the Division of Pulmonary and Critical Care Medicine, Department of Medicine (S.Y.A., A.A.D., S.E.M., F.N.R., C.L.P., G.R.W.), Applied Chest Imaging Laboratory (S.Y.A., R.S.J.E., A.A.D., S.E.M., F.N.R., C.L.P., G.V.S.F., G.R.W.), and Department of Radiology (R.S.J.E., G.V.S.F.), Brigham and Women's Hospital, 75 Francis St, PBB, CA-3, Boston, MA 02130; Departments of Biomedical Engineering and Medical Physics, University of Wisconsin School of Medicine and Public Health, Madison, Wis (S.B.F.); COPD Foundation, Washington, DC (R.T.S., D.M.); Lung Investigation Unit, Medicine, University Hospitals Birmingham NHS Foundation Trust, Queen Elizabeth Hospital Birmingham, Birmingham, England (R.A.S.); Respiratory and Inflammation Therapy Area, Clinical Development, AstraZeneca, Mölndal, Sweden (L.H.N.); Section of Pulmonary and Critical Care Medicine, Department of Medicine, University of Nebraska Medical Center, Omaha, Neb (S.R.); Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich (M.K.H.); Department of Radiology, National Jewish Health, Denver, Colo (S.M.H., D.A.L.); and Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh Department of Medicine, University of Pittsburgh, Pittsburgh, Pa (F.C.S.).
Radiology. 2021 Apr;299(1):222-231. doi: 10.1148/radiol.2021203531. Epub 2021 Feb 16.
Background The relationship between emphysema progression and long-term outcomes is unclear. Purpose To determine the relationship between emphysema progression at CT and mortality among participants with emphysema. Materials and Methods In a secondary analysis of two prospective observational studies, COPDGene (, NCT00608764) and Evaluation of Chronic Obstructive Pulmonary Disease Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE; , NCT00292552), emphysema was measured at CT at two points by using the volume-adjusted lung density at the 15th percentile of the lung density histogram (hereafter, lung density perc15) method. The association between emphysema progression rate and all-cause mortality was analyzed by using Cox regression adjusted for ethnicity, sex, baseline age, pack-years, and lung density, baseline and change in smoking status, forced expiratory volume in 1 second, and 6-minute walk distance. In COPDGene, respiratory mortality was analyzed by using the Fine and Gray method. Results A total of 5143 participants (2613 men [51%]; mean age, 60 years ± 9 [standard deviation]) in COPDGene and 1549 participants (973 men [63%]; mean age, 62 years ± 8) in ECLIPSE were evaluated, of which 2097 (40.8%) and 1179 (76.1%) had emphysema, respectively. Baseline imaging was performed between January 2008 and December 2010 for COPDGene and January 2006 and August 2007 for ECLIPSE. Follow-up imaging was performed after 5.5 years ± 0.6 in COPDGene and 3.0 years ± 0.2 in ECLIPSE, and mortality was assessed over the ensuing 5 years in both. For every 1 g/L per year faster rate of decline in lung density perc15, all-cause mortality increased by 8% in COPDGene (hazard ratio [HR], 1.08; 95% CI: 1.01, 1.16; = .03) and 6% in ECLIPSE (HR, 1.06; 95% CI: 1.00, 1.13; = .045). In COPDGene, respiratory mortality increased by 22% (HR, 1.22; 95% CI: 1.13, 1.31; < .001) for the same increase in the rate of change in lung density perc15. Conclusion In ever-smokers with emphysema, emphysema progression at CT was associated with increased all-cause and respiratory mortality. © RSNA, 2021 See also the editorial by Lee and Park in this issue.
肺气肿进展与长期结局之间的关系尚不清楚。目的:确定 CT 检测到的肺气肿进展与肺气肿患者的死亡率之间的关系。材料与方法:在两项前瞻性观察性研究(COPDGene 研究[, NCT00608764]和慢性阻塞性肺疾病纵向评估以确定预测替代终点(ECLIPSE;, NCT00292552)的二次分析中),采用肺密度直方图第 15 百分位数的体积校正肺密度(以下简称肺密度 perc15)方法,在 CT 上两次测量肺气肿。使用 Cox 回归分析,校正种族、性别、基线年龄、吸烟包年数和肺密度、吸烟状态的基线和变化、第 1 秒用力呼气量和 6 分钟步行距离,分析肺气肿进展率与全因死亡率之间的关系。在 COPDGene 研究中,使用 Fine 和 Gray 法分析呼吸死亡。结果:共评估了 COPDGene 研究中的 5143 名参与者(2613 名男性[51%];平均年龄 60 岁 ± 9[标准差])和 ECLIPSE 研究中的 1549 名参与者(973 名男性[63%];平均年龄 62 岁 ± 8),其中分别有 2097 名(40.8%)和 1179 名(76.1%)患有肺气肿。COPDGene 研究的基线成像时间为 2008 年 1 月至 2010 年 12 月,ECLIPSE 研究的基线成像时间为 2006 年 1 月至 2007 年 8 月。COPDGene 研究的随访成像时间为 5.5 年 ± 0.6,ECLIPSE 研究的随访成像时间为 3.0 年 ± 0.2,之后在接下来的 5 年内对死亡率进行了评估。在 COPDGene 研究中,肺密度 perc15 每年每降低 1 g/L,全因死亡率增加 8%(风险比[HR],1.08;95%CI:1.01,1.16; =.03),ECLIPSE 研究中增加 6%(HR,1.06;95%CI:1.00,1.13; =.045)。在 COPDGene 研究中,肺密度 perc15 变化率相同的情况下,呼吸死亡率增加 22%(HR,1.22;95%CI:1.13,1.31; <.001)。结论:在患有肺气肿的持续吸烟者中,CT 检测到的肺气肿进展与全因死亡率和呼吸死亡率的增加相关。©RSNA,2021 请参阅本期 Lee 和 Park 的社论。