Golpe Rafael, Mateos-Colino Alfonso, Testa-Fernández Ana, Pena-Seijo Marta, Rodríguez-Enríquez Manuel, González-Juanatey Carlos, Martín-Vázquez Francisco J, Pose-Reino Antonio, Domínguez-Pin Nuria, Garnacho-Gayarre Nuria, Pérez-de-Llano Luis A
Respiratory Medicine Service, University Hospital Lucus Augusti, Lugo, Spain.
Internal Medicine Service, University Hospital Lucus Augusti, Lugo, Spain.
PLoS One. 2016 Jun 30;11(6):e0157932. doi: 10.1371/journal.pone.0157932. eCollection 2016.
Several studies suggest that there is a pathogenic link between chronic obstructive pulmonary disease (COPD) and cardiovascular diseases. On the other hand, increased sympathetic tone has been described in several respiratory diseases. Our objective was to determine whether hypertension mediated by sympathetic overactivity is a mechanism that explains the association between COPD and cardiovascular diseases.
Prospective nested case-control observational study; 67 COPD patients were matched 1:1 by sex and age to controls with smoking history. 24 hour-blood pressure monitoring, urinary catecholamines and their metabolites measurement, echocardiography, carotid ultrasound examination, nocturnal oximetry and retinography were performed.
classic cardiovascular risk factors and comorbidities were similarly distributed between cases and controls. No significant differences for blood pressure variables (difference for mean systolic blood pressure: -0·13 mmHg; 95% CI: -4·48,4·20; p = 0·94; similar results for all blood presssure variables) or catecholamines values were found between both groups. There was a tendency for lower left ventricle ejection fraction in the COPD cases, that approached statistical significance (64·8 ± 7·4 vs 67·1 ± 6·2, p = 0·05). There were no differences in the retinal arteriovenous ratio, the carotid intima-media thickness, or the number of carotid plaques, between cases and controls. Fibrinogen values were higher in the COPD group (378·4 ± 69·6 vs 352·2 ± 45·6 mg/dL, p = 0·01) and mean nocturnal oxygen saturation values were lower for COPD patients (89·0 ± 4·07 vs 92·3 ± 2·2%, p < 0·0001).
Hypertension induced by sympathetic overactivity does not seem to be a mechanism that could explain the association between COPD and cardiovascular disease.
多项研究表明,慢性阻塞性肺疾病(COPD)与心血管疾病之间存在致病联系。另一方面,在多种呼吸系统疾病中均有交感神经张力增加的描述。我们的目的是确定由交感神经过度活跃介导的高血压是否是解释COPD与心血管疾病之间关联的一种机制。
前瞻性巢式病例对照观察性研究;67例COPD患者按性别和年龄1:1匹配有吸烟史的对照。进行24小时血压监测、尿儿茶酚胺及其代谢产物测量、超声心动图、颈动脉超声检查、夜间血氧饱和度测定和视网膜造影。
经典心血管危险因素和合并症在病例组和对照组中分布相似。两组间血压变量(平均收缩压差异:-0.13 mmHg;95%可信区间:-4.48,4.20;p = 0.94;所有血压变量结果相似)或儿茶酚胺值无显著差异。COPD病例组左心室射血分数有降低趋势,接近统计学意义(64.8±7.4 vs 67.1±6.2,p = 0.05)。病例组和对照组在视网膜动静脉比、颈动脉内膜中层厚度或颈动脉斑块数量方面无差异。COPD组纤维蛋白原值较高(378.4±69.6 vs 352.2±45.6 mg/dL,p = 0.01),COPD患者夜间平均血氧饱和度值较低(89.0±4.07 vs 92.3±2.2%,p < 0.0001)。
交感神经过度活跃所致高血压似乎不是解释COPD与心血管疾病之间关联的一种机制。