University Medical Centre Utrecht and Utrecht University, Dept. Radiology, Utrecht, Netherlands.
Erasmus Medical Centre, Dept. Biostatistics, Rotterdam, Netherlands; Erasmus Medical Centre, Dept. Epidemiology, Rotterdam, Netherlands.
EBioMedicine. 2024 Oct;108:105366. doi: 10.1016/j.ebiom.2024.105366. Epub 2024 Sep 30.
In chronic obstructive pulmonary disease (COPD), vascular alterations have been shown to contribute to hypoxia and pulmonary hypertension, but the independent contribution of small vessel abnormalities to mortality remains unclear.
We quantified artery and vein dimensions on computed tomography (CT) down to 0.2 mm. Small vessel volumes (<1 mmᴓ) were normalized by body surface area. In 7903 current and former smokers of the COPDGene study (53.2% male) the independent contribution of small artery and small vein volume to all-cause mortality was tested in multivariable Cox models. Additionally, we calculated the 95 percentile of small arteries and veins in 374 never smokers to create two groups: normal and high small artery or vein volume. We describe clinical, physiological and imaging characteristics of subjects with a high small artery and high small vein volume.
Both high small artery and high small vein volumes were independently associated with mortality with an adjusted hazard ratio of 1.07 [1.01, 1.14] and 1.34 [1.21, 1.49] per mL/m increase, respectively. In COPDGene, 447 (5.7%) had high small artery volume and 519 (9.1%) subjects had high small vein volume and both had more emphysema, more air trapping and more severe coronary calcium.
In smokers, abnormally high volumes in small arteries and veins are both relevant for mortality, which urges investigations into the aetiology of small pulmonary vessels and cardiac function in smokers.
Award Number U01-HL089897 and U01-HL089856 from the NHLBI. COPD Foundation with contributions from AstraZeneca, Boehringer Ingelheim, Genentech, GlaxoSmithKline, Novartis, Pfizer, Siemens, and Sunovion.
在慢性阻塞性肺疾病(COPD)中,已经证明血管改变有助于缺氧和肺动脉高压,但小血管异常对死亡率的独立贡献仍不清楚。
我们在 CT 上量化了 0.2 毫米以下的动脉和静脉尺寸。用体表面积对小血管体积(<1 毫米³)进行归一化。在 COPDGene 研究中的 7903 名当前和以前的吸烟者(53.2%为男性)中,使用多变量 Cox 模型测试了小动脉和小静脉体积对全因死亡率的独立贡献。此外,我们计算了 374 名从不吸烟者中小动脉和小静脉的第 95 百分位数,以创建两个组:正常和高小动脉或小静脉体积。我们描述了小动脉和小静脉体积高的受试者的临床、生理和影像学特征。
高小动脉和高小静脉体积均与死亡率独立相关,调整后的危险比分别为 1.07[1.01,1.14]和 1.34[1.21,1.49]每毫升/毫升增加。在 COPDGene 中,447 名(5.7%)患者小动脉体积高,519 名(9.1%)患者小静脉体积高,两者均有更多的肺气肿、更多的空气滞留和更严重的冠状动脉钙化。
在吸烟者中,小动脉和小静脉体积异常增加都与死亡率相关,这促使人们对小肺血管和吸烟者心脏功能的病因进行研究。
NHLBI 的 U01-HL089897 和 U01-HL089856 奖。COPD 基金会得到了阿斯利康、勃林格殷格翰、基因泰克、葛兰素史克、诺华、辉瑞、西门子和山诺菲的贡献。