Department of Medicine, University of Pittsburgh, Pittsburgh, PA.
Department of Epidemiology, University of Colorado, Denver, CO.
Chest. 2021 Sep;160(3):858-871. doi: 10.1016/j.chest.2021.04.066. Epub 2021 May 8.
Smokers manifest varied phenotypes of pulmonary impairment.
Which pulmonary phenotypes are associated with coronary artery disease (CAD) in smokers?
We analyzed data from the University of Pittsburgh COPD Specialized Center for Clinically Oriented Research (SCCOR) cohort (n = 481) and the Genetic Epidemiology of COPD (COPDGene) cohort (n = 2,580). Participants were current and former smokers with > 10 pack-years of tobacco exposure. Data from the two cohorts were analyzed separately because of methodologic differences. Lung hyperinflation was assessed by plethysmography in the SCCOR cohort and by inspiratory and expiratory CT scan lung volumes in the COPDGene cohort. Subclinical CAD was assessed as the coronary artery calcium score, whereas clinical CAD was defined as a self-reported history of CAD or myocardial infarction (MI). Analyses were performed in all smokers and then repeated in those with airflow obstruction (FEV to FVC ratio, < 0.70).
Pulmonary phenotypes, including airflow limitation, emphysema, lung hyperinflation, diffusion capacity, and radiographic measures of airway remodeling, showed weak to moderate correlations (r < 0.7) with each other. In multivariate models adjusted for pulmonary phenotypes and CAD risk factors, lung hyperinflation was the only phenotype associated with calcium score, history of clinical CAD, or history of MI (per 0.2 higher expiratory and inspiratory CT scan lung volume; coronary calcium: OR, 1.2; 95% CI, 1.1-1.5; P = .02; clinical CAD: OR, 1.6; 95% CI, 1.1-2.3; P = .01; and MI in COPDGene: OR, 1.7; 95% CI, 1.0-2.8; P = .05). FEV and emphysema were associated with increased risk of CAD (P < .05) in models adjusted for CAD risk factors; however, these associations were attenuated on adjusting for lung hyperinflation. Results were the same in those with airflow obstruction and were present in both cohorts.
Lung hyperinflation is associated strongly with clinical and subclinical CAD in smokers, including those with airflow obstruction. After lung hyperinflation was accounted for, FEV and emphysema no longer were associated with CAD. Subsequent studies should consider measuring lung hyperinflation and examining its mechanistic role in CAD in current and former smokers.
吸烟者表现出不同的肺部损伤表型。
哪些肺部表型与吸烟者的冠状动脉疾病（CAD）有关？
我们分析了来自匹兹堡大学 COPD 专门临床研究中心（SCCOR）队列（n=481）和 COPDGene 队列（n=2580）的数据。参与者为有>10 包年烟草暴露的当前和前吸烟者。由于方法学差异，两个队列的数据分别进行了分析。SCCOR 队列通过体积描记法评估肺过度充气，COPDGene 队列通过吸气和呼气 CT 扫描肺容积评估肺过度充气。亚临床 CAD 评估为冠状动脉钙评分，而临床 CAD 定义为 CAD 或心肌梗死（MI）的自述病史。所有吸烟者均进行了分析，然后在有气流受限（FEV/FVC 比值<0.70）的患者中重复分析。
包括气流受限、肺气肿、肺过度充气、弥散能力和气道重塑的放射学指标在内的肺表型彼此之间呈弱到中度相关（r<0.7）。在调整肺表型和 CAD 危险因素的多变量模型中，肺过度充气是唯一与钙评分、临床 CAD 病史或 MI 病史相关的表型（每增加 0.2 次呼气和吸气 CT 扫描肺容积；冠状动脉钙：比值比，1.2；95%CI，1.1-1.5；P=0.02；临床 CAD：比值比，1.6；95%CI，1.1-2.3；P=0.01；COPDGene 中的 MI：比值比，1.7；95%CI，1.0-2.8；P=0.05）。在调整 CAD 危险因素的模型中，FEV 和肺气肿与 CAD 风险增加相关（P<0.05）；然而，在调整肺过度充气后，这些关联减弱。在有气流受限的患者中，结果相同，并且在两个队列中均存在。
肺过度充气与吸烟者的临床和亚临床 CAD 密切相关，包括气流受限的吸烟者。在考虑到肺过度充气后，FEV 和肺气肿与 CAD 不再相关。随后的研究应考虑测量肺过度充气，并研究其在当前和前吸烟者中 CAD 的机制作用。
