Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY.
Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY.
Chest. 2018 Jul;154(1):41-50. doi: 10.1016/j.chest.2017.11.031. Epub 2017 Dec 12.
Platelet activation reduces pulmonary microvascular blood flow and contributes to inflammation; these factors have been implicated in the pathogenesis of COPD and emphysema. We hypothesized that regular use of aspirin, a platelet inhibitor, would be associated with a slower progression of emphysema-like lung characteristics on CT imaging and a slower decline in lung function.
The Multi-Ethnic Study of Atherosclerosis (MESA) enrolled participants 45 to 84 years of age without clinical cardiovascular disease from 2000 to 2002. The MESA Lung Study assessed the percentage of emphysema-like lung below -950 Hounsfield units ("percent emphysema") on cardiac (2000-2007) and full-lung CT scans (2010-2012). Regular aspirin use was defined as 3 or more days per week. Mixed-effect models adjusted for demographics, anthropometric features, smoking, hypertension, angiotensin-converting enzyme inhibitor or angiotensin II-receptor blocker use, C-reactive protein levels, sphingomyelin levels, and scanner factors.
At baseline, the 4,257 participants' mean (± SD) age was 61 ± 10 years, 54% were ever smokers, and 22% used aspirin regularly. On average, percent emphysema increased 0.60 percentage points over 10 years (95% CI, 0.35-0.94). Progression of percent emphysema was slower among regular aspirin users compared with patients who did not use aspirin (fully adjusted model: -0.34% /10 years, 95% CI, -0.60 to -0.08; P = .01). Results were similar in ever smokers and with doses of 81 and 300 to 325 mg and were of greater magnitude among those with airflow limitation. No association was found between aspirin use and change in lung function.
Regular aspirin use was associated with a more than 50% reduction in the rate of emphysema progression over 10 years. Further study of aspirin and platelets in emphysema may be warranted.
血小板激活会减少肺微血管血流并促进炎症；这些因素与 COPD 和肺气肿的发病机制有关。我们假设，经常使用血小板抑制剂阿司匹林与 CT 成像上肺气肿样肺特征的进展较慢以及肺功能下降较慢有关。
动脉粥样硬化多民族研究（MESA）于 2000 年至 2002 年招募了无临床心血管疾病的 45 至 84 岁参与者。MESA 肺部研究评估了心脏（2000-2007 年）和全肺 CT 扫描（2010-2012 年）上低于-950 豪斯菲尔德单位的肺气肿样肺的百分比（“肺气肿百分比”）。经常使用阿司匹林定义为每周使用 3 天或以上。混合效应模型调整了人口统计学、人体测量特征、吸烟、高血压、血管紧张素转换酶抑制剂或血管紧张素 II 受体阻滞剂的使用、C 反应蛋白水平、神经鞘磷脂水平和扫描仪因素。
在基线时，4257 名参与者的平均（± SD）年龄为 61 ± 10 岁，54%为曾经吸烟者，22%经常使用阿司匹林。平均而言，10 年内肺气肿百分比增加了 0.60 个百分点（95%CI，0.35-0.94）。与未使用阿司匹林的患者相比，经常使用阿司匹林的患者肺气肿的进展速度较慢（完全调整模型：-0.34%/10 年，95%CI，-0.60 至-0.08；P =.01）。在曾经吸烟者和 81 毫克、300 至 325 毫克剂量中结果相似，在气流受限者中更为显著。阿司匹林使用与肺功能变化之间没有关联。
经常使用阿司匹林与 10 年内肺气肿进展率降低 50%以上有关。可能需要进一步研究阿司匹林和血小板在肺气肿中的作用。
