The effect of pulmonary rehabilitation on cardiovascular risk, oxidative stress and systemic inflammation in patients with COPD.

PURPOSE: Chronic obstructive pulmonary disease (COPD) is a leading cause of death, and cardiovascular (CV) comorbidities play a role. Evidence of the pulmonary rehabilitation (PR) effect in reducing the CV risk (CVR) in COPD patients is limited. In this study, we aimed to determine the impact of an 8-week PR program (PRP) on the CVR of the overall population and to compare the impact on the exacerbator versus non-exacerbator patients. PATIENTS AND METHODS: This was a prospective study that included adults who had post-bronchodilator forced expiratory volume in 1 s (FEV1) to forced vital capacity (FVC) (FEV1/FVC) ratio <70 % and FEV1 <80 % predicted, had quit smoking for at least 1 year and had a history of tobacco consumption greater than 10 packs/year, and were clinically stable in the last 8 weeks. Pre- and post-PRP assessments included respiratory function evaluation, laboratory tests, and exercise capacity assessment (6-min walking test [6MWT]). CVR was assessed using different risk prediction models. RESULTS: A total of 50 patients (28 exacerbators and 22 non-exacerbators) completed the PRP (median age: 64.5 years, men: 72 %; arterial hypertension: 70 %, dyslipidemia: 30 %, diabetes: 20 %; CV disease (CVD): 24 %. After the PRP, exacerbator patients showed a significant decrease in the CVR calculated by the COPDCoRi model (p < 0.001); patients with ≥30-m increase on the 6MWT showed statistically significant lower levels of glucose (p = 0.004), HbA1c (p = 0.004) and BODE index score (p = 0.026) compared to patients with <30-m increase. CONCLUSIONS: PR reduced certain modifiable CVR factors and CVD risk, especially in exacerbator patients.

High risk of subclinical atherosclerosis in COPD exacerbator phenotype.

It is not known whether COPD exacerbations contribute to an increased vascular risk already associated with the disease. For this reason, we prospectively evaluated 127 patients referred for a monographic COPD consultation. We classify as exacerbators those who had experienced two or more moderate exacerbations in the previous year, or who had had a hospital admission. All underwent a blood analysis, respiratory function tests, global cardiovascular and coronary risk estimates (with four of the most frequently used scores, and the Chronic Obstructive Pulmonary Disease Coronaropathy Risk (COPDCoRi) score, respectively); and an EcoDoppler to measure carotid intima-media thickness and the ankle-brachial index. Finally, we included 50 patients with exacerbator phenotypes and 57 with non-exacerbator phenotypes, ranging from 63 ±â€¯7 years old, 74% of whom were male. The exacerbator phenotype increased the risk of carotid intima-media thickness above the 75th percentile range by a factor of almost three, independently of the severity of COPD and global cardiovascular risk. The association between the exacerbator phenotype and high c-IMT was more evident in patients under 65. In conclusion, the presence of subclinical atherosclerosis is independently associated with the exacerbator phenotype, with more pronounced differences in younger patient; which suggests that we should intensify control of vascular risk factors in these groups of patients.