Relationship between Emphysema Progression at CT and Mortality in Ever-Smokers: Results from the COPDGene and ECLIPSE Cohorts.
Relationship between Emphysema Progression at CT and Mortality in Ever-Smokers: Results from the COPDGene and ECLIPSE Cohorts.
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DOI：
10.1148/radiol.2021203531
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发表时间：
2021-04
期刊：
影响因子：
19.7
通讯作者：
COPDGene Investigators and the COPD Biomarker Qualification Consortium
中科院分区：
文献类型：
--
作者：
Ash SY;San José Estépar R;Fain SB;Tal-Singer R;Stockley RA;Nordenmark LH;Rennard S;Han MK;Merrill D;Humphries SM;Diaz AA;Mason SE;Rahaghi FN;Pistenmaa CL;Sciurba FC;Vegas-Sánchez-Ferrero G;Lynch DA;Washko GR;COPDGene Investigators and the COPD Biomarker Qualification Consortium
肺气肿进展与长期结果之间的关系尚不清楚。确定 CT 肺气肿进展与肺气肿参与者死亡率之间的关系。在两项前瞻性观察性研究 COPDGene（clinicaltrials.gov，NCT00608764）和纵向评估慢性阻塞性肺疾病以识别预测替代终点（ECLIPSE；clinicaltrials.gov.NCT00292552）的二次分析中，使用肺密度第 15 个百分位数的体积调整肺密度在 CT 上测量两个点的肺气肿直方图（以下简称肺密度 perc15）方法。使用 Cox 回归分析肺气肿进展率与全因死亡率之间的关联，并根据种族、性别、基线年龄、包装年数和肺密度、基线和吸烟状况变化、1 秒用力呼气量和 6 分钟步行距离进行调整。在 COPDGene 中，使用 Fine and Gray 方法分析呼吸系统死亡率。 COPDGene 中共有 5143 名参与者（2613 名男性 [51%]；平均年龄，60 岁 ± 9 [标准差]）和 ECLIPSE 中的 1549 名参与者（973 名男性 [63%]；平均年龄，62 岁 ± 8）进行了评估，其中分别有 2097 名（40.8%）和 1179 名（76.1%）患有肺气肿。 COPDGene 的基线成像于 2008 年 1 月至 2010 年 12 月进行，ECLIPSE 的基线成像于 2006 年 1 月至 2007 年 8 月进行。 COPDGene 中 5.5 年±0.6 年后进行随访成像，ECLIPSE 中 3.0 年±0.2 年后进行随访成像，并评估随后 5 年的死亡率。肺密度 perc15 每年下降速度每加快 1 g/L，COPDGene 中的全因死亡率就会增加 8%（风险比 [HR], 1.08; 95% CI: 1.01, 1.16; P = .03），而 ECLIPSE 中的全因死亡率会增加 6%（HR, 1.06; 95% CI: 1.00, 1.13; P = .045）。在 COPDGene 中，肺密度 perc15 变化率同样增加，呼吸系统死亡率增加 22%（HR，1.22；95% CI：1.13，1.31；P < .001）。在患有肺气肿的曾经吸烟者中，CT 发现的肺气肿进展与全因死亡率和呼吸系统死亡率增加相关。
The relationship between emphysema progression and long-term outcomes is unclear. To determine the relationship between emphysema progression at CT and mortality among participants with emphysema. In a secondary analysis of two prospective observational studies, COPDGene (clinicaltrials.gov, NCT00608764) and Evaluation of Chronic Obstructive Pulmonary Disease Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE; clinicaltrials.gov. 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. 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; P = .03) and 6% in ECLIPSE (HR, 1.06; 95% CI: 1.00, 1.13; P = .045). In COPDGene, respiratory mortality increased by 22% (HR, 1.22; 95% CI: 1.13, 1.31; P < .001) for the same increase in the rate of change in lung density perc15. In ever-smokers with emphysema, emphysema progression at CT was associated with increased all-cause and respiratory mortality.
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影响因子：
39.2
作者：
Moyer, Virginia A.
通讯作者：
Moyer, Virginia A.
影响因子：
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作者：
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DOI：
10.1164/rccm.201705-0860oc
发表时间：
2018-01-15
影响因子：
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影响因子：
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作者：
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Vestbo, Jorgen