From the Imaging Research Laboratories, Robarts Research Institute, 1151 Richmond St N, London, ON, Canada N6A 5B7 (D.P.I.C., N.Z., F.G., D.P., G.P.); Department of Medical Biophysics (D.P.I.C., D.P., G.P.), Graduate Program in Biomedical Engineering (F.G., G.P.), and Division of Respirology, Department of Medicine (D.G.M.), The University of Western Ontario, London, Ont, Canada; and Heart and Lung Institute, St Paul's Hospital, Vancouver, BC, Canada (M.K.).
Radiology. 2016 May;279(2):597-608. doi: 10.1148/radiol.2015151484. Epub 2016 Jan 8.
To directly compare magnetic resonance (MR) imaging and computed tomography (CT) parametric response map (PRM) measurements of gas trapping and emphysema in ex-smokers both with and without chronic obstructive pulmonary disease (COPD).
Participants provided written informed consent to a protocol that was approved by a local research ethics board and Health Canada and was compliant with the HIPAA (Institutional Review Board Reg. #00000940). The prospectively planned study was performed from March 2014 to December 2014 and included 58 ex-smokers (mean age, 73 years ± 9) with (n = 32; mean age, 74 years ± 7) and without (n = 26; mean age, 70 years ± 11) COPD. MR imaging (at functional residual capacity plus 1 L), CT (at full inspiration and expiration), and spirometry or plethysmography were performed during a 2-hour visit to generate ventilation defect percent (VDP), apparent diffusion coefficient (ADC), and PRM gas trapping and emphysema measurements. The relationships between pulmonary function and imaging measurements were determined with analysis of variance (ANOVA), Holm-Bonferroni corrected Pearson correlations, multivariate regression modeling, and the spatial overlap coefficient (SOC).
VDP, ADC, and PRM gas trapping and emphysema (ANOVA, P < .001) measurements were significantly different in healthy ex-smokers than they were in ex-smokers with COPD. In all ex-smokers, VDP was correlated with PRM gas trapping (r = 0.58, P < .001) and with PRM emphysema (r = 0.68, P < .001). VDP was also significantly correlated with PRM in ex-smokers with COPD (gas trapping: r = 0.47 and P = .03; emphysema: r = 0.62 and P < .001) but not in healthy ex-smokers. In a multivariate model that predicted PRM gas trapping, the forced expiratory volume in 1 second normalized to the forced vital capacity (standardized coefficients [βS] = -0.69, P = .001) and airway wall area percent (βS = -0.22, P = .02) were significant predictors. PRM emphysema was predicted by the diffusing capacity for carbon monoxide (βS = -0.29, P = .03) and VDP (βS = 0.41, P = .001). Helium 3 ADC values were significantly elevated in PRM gas-trapping regions (P < .001). The spatial relationship for ventilation defects was significantly greater with PRM gas trapping than with PRM emphysema in patients with mild (for gas trapping, SOC = 36% ± 28; for emphysema, SOC = 1% ± 2; P = .001) and moderate (for gas trapping, SOC = 34% ± 28; for emphysema, SOC = 7% ± 15; P = .006) COPD. For severe COPD, the spatial relationship for ventilation defects with PRM emphysema (SOC = 64% ± 30) was significantly greater than that for PRM gas trapping (SOC = 36% ± 18; P = .01).
In all ex-smokers, ADC values were significantly elevated in regions of PRM gas trapping, and VDP was quantitatively and spatially related to both PRM gas trapping and PRM emphysema. In patients with mild to moderate COPD, VDP was related to PRM gas trapping, whereas in patients with severe COPD, VDP correlated with both PRM gas trapping and PRM emphysema.
直接比较有和无慢性阻塞性肺疾病(COPD)的戒烟者的磁共振(MR)成像和计算机断层扫描(CT)参数响应图(PRM)测量的气体陷闭和肺气肿。
参与者书面同意参加一项协议,该协议得到了当地研究伦理委员会和加拿大卫生部的批准,并符合 HIPAA(机构审查委员会注册号 00000940)的规定。这项前瞻性研究于 2014 年 3 月至 2014 年 12 月进行,共纳入 58 名戒烟者(平均年龄 73 岁±9),其中 32 名(平均年龄 74 岁±7)有 COPD,26 名(平均年龄 70 岁±11)无 COPD。在 2 小时的就诊期间,进行了 MR 成像(功能残气量加 1 L)、CT(吸气和呼气完全)和肺量计或体描法,以生成通气缺陷百分比(VDP)、表观扩散系数(ADC)和 PRM 气体陷闭和肺气肿测量值。使用方差分析(ANOVA)、经 Holm-Bonferroni 校正的 Pearson 相关分析、多元回归模型和空间重叠系数(SOC)来确定肺功能与影像学测量值之间的关系。
在健康的戒烟者中,VDP、ADC 和 PRM 气体陷闭和肺气肿(ANOVA,P<.001)的测量值与 COPD 戒烟者的测量值有显著差异。在所有戒烟者中,VDP 与 PRM 气体陷闭(r = 0.58,P<.001)和 PRM 肺气肿(r = 0.68,P<.001)相关。VDP 与 COPD 戒烟者的 PRM 也有显著相关性(气体陷闭:r = 0.47,P =.03;肺气肿:r = 0.62,P<.001),但在健康的戒烟者中没有。在一个可以预测 PRM 气体陷闭的多元模型中,用力呼气量与用力肺活量的比值标准化系数(βS = -0.69,P =.001)和气道壁面积百分比(βS = -0.22,P =.02)是显著的预测因子。一氧化碳弥散量(βS = -0.29,P =.03)和 VDP(βS = 0.41,P =.001)可以预测 PRM 肺气肿。在 PRM 气体陷闭区域,氦 3 ADC 值显著升高(P<.001)。在轻度(气体陷闭时,SOC = 36%±28;肺气肿时,SOC = 1%±2;P =.001)和中度(气体陷闭时,SOC = 34%±28;肺气肿时,SOC = 7%±15;P =.006)COPD 患者中,通气缺陷的空间关系与 PRM 气体陷闭相比,与 PRM 肺气肿相比,差异有统计学意义。在严重 COPD 患者中,PRM 肺气肿的通气缺陷的空间关系(SOC = 64%±30)明显大于 PRM 气体陷闭(SOC = 36%±18;P =.01)。
在所有戒烟者中,PRM 气体陷闭区域的 ADC 值显著升高,VDP 与 PRM 气体陷闭和 PRM 肺气肿均具有定量和空间相关性。在轻度至中度 COPD 患者中,VDP 与 PRM 气体陷闭相关,而在重度 COPD 患者中,VDP 与 PRM 气体陷闭和 PRM 肺气肿均相关。