Pulmonary Microvascular Blood Flow in Mild Chronic Obstructive Pulmonary Disease and Emphysema The MESA COPD Study
Pulmonary Microvascular Blood Flow in Mild Chronic Obstructive Pulmonary Disease and Emphysema The MESA COPD Study
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DOI：
10.1164/rccm.201411-2120oc
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发表时间：
2015-09-01
影响因子：
24.7
通讯作者：
Barr, R. Graham
中科院分区：
文献类型：
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作者：
Hueper, Katja;Vogel-Claussen, Jens;Barr, R. Graham
原理：吸烟相关的微血管损失会导致肾脏、心脏和大脑的终末器官损伤。基础研究表明肺中也有类似的过程，但没有大规模的研究评估早期慢性肺疾病的肺微血管血流量（PMBF）。目的：研究轻度和重度慢性阻塞性肺疾病（COPD）和肺气肿患者的PMBF是否减少。方法：使用钆增强磁共振成像（MRI）测量COPD吸烟者和年龄50 - 79岁无临床心血管疾病的对照受试者的PMBF。COPD严重程度由标准标准定义。计算机断层扫描（CT）上的肺气肿由低于-950 Hounsfield单位（-950 HU）的肺区域百分比和放射科医生使用标准方案定义。我们调整了潜在的混杂因素，包括吸烟、氧合和左心室心输出量。测量和主要结果：在144名参与者中，轻度COPD患者的PMBF减少了30%，中度COPD患者减少了29%，重度COPD患者减少了52%（所有P <0.01与对照受试者相比）。肺气肿（-950 HU）和放射科医生定义的肺气肿（特别是全小叶和小叶中心肺气肿）百分比更高时，PMBF降低（所有P vi 0.01）。MRI和CT图像的配准显示，轻度COPD患者的非肺气肿和肺气肿肺区的PMBF均降低。PMBF的协会是独立的CT和气体捕获的小气道疾病的措施，很大程度上是因为肺气肿和小气道疾病发生在不同的smokers.Conclusions：PMBF减少轻度COPD，包括在肺部没有弗兰克肺气肿的地区，并可能代表一个不同的病理过程，从小气道疾病。PMBF可以为针对肺部微血管的治疗策略提供成像生物标志物。
Rationale: Smoking-related microvascular loss causes end-organ damage in the kidneys, heart, and brain. Basic research suggests a similar process in the lungs, but no large studies have assessed pulmonary microvascular blood flow (PMBF) in early chronic lung disease.Objectives: To investigate whether PMBF is reduced in mild as well as more severe chronic obstructive pulmonary disease (COPD) and emphysema.Methods: PMBF was measured using gadolinium-enhanced magnetic resonance imaging (MRI) among smokers with COPD and control subjects age 50 to 79 years without clinical cardiovascular disease. COPD severity was defined by standard criteria. Emphysema on computed tomography (CT) was defined by the percentage of lung regions below -950 Hounsfield units ( -950 HU) and by radiologists using a standard protocol. We adjusted for potential confounders, including smoking, oxygenation, and left ventricular cardiac output.Measurements and Main Results: Among 144 participants, PMBF was reduced by 30% in mild COPD, by 29% in moderate COPD, and by 52% in severe COPD (all P < 0.01 vs. control subjects). PMBF was reduced with greater percentage emphysema(-950HU) and radiologist-defined emphysema, particularly panlobular and centrilobular emphysema (all P vi 0.01). Registration of MRI and CT images revealed that PMBF was reduced in mild COPD in both nonemphysematous and emphysematous lung regions. Associations for PMBF were independent of measures of small airways disease on CT and gas trapping largely because emphysema and small airways disease occurred in different smokers.Conclusions: PMBF was reduced in mild COPD, including in regions of lung without frank emphysema, and may represent a distinct pathological process from small airways disease. PMBF may provide an imaging biomarker for therapeutic strategies targeting the pulmonary microvasculature.