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INTRODUCTION: Currently, several studies have assessed the effect of yoga training on the management of chronic obstructive pulmonary disease (COPD), but these studies involved a wide variation of sample and convey inconclusive results. Hence, the present study was performed a systematic review and meta-analysis to investigate the efficacy of yoga training in COPD patients. METHODS: PubMed, EMBASE, the Cochrane Library, Google Scholar, and ClinicalTrials.gov databases were searched for relevant studies. The primary outcomes were forced expiratory volume in one second (FEV1), FEV1% predicted (% pred). Secondary outcomes included 6-min walking distance (6 MWD), arterial oxygen tension (PaO2), and arterial carbon dioxide tension (PaCO2). Weighted mean differences (WMDs) and 95% confidence intervals (CIs) were calculated, and heterogeneity was assessed with the I(2) test. RESULTS: Five randomized controlled trials (RCTs) involving 233 patients fulfilled the inclusion criteria. Yoga training significantly improved FEV1 (WMD: 123.57 mL, 95% CI: 4.12-243, P=0.04), FEV1% pred (WMD: 3.90%, 95% CI: 2.27-5.54, P<0.00001), and 6 MWD (WMD: 38.84 m, 95% CI: 15.52-62.16, P=0.001). However, yoga training had no significant effects on PaO2 (WMD: 1.29 mmHg, 95% CI: -1.21-3.78, P=0.31) and PaCO2 (WMD: -0.76 mmHg, 95% CI: -2.06-0.53, P=0.25). CONCLUSIONS: The current limited evidence suggested that yoga training has a positive effect on improving lung function and exercise capacity and could be used as an adjunct pulmonary rehabilitation program in COPD patients. However, further studies are needed to substantiate our preliminary findings and to investigate the long-term effects of yoga training.
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OBJECTIVE: To explore the role of soluble vascular cell adhesion molecule-1 (sVCAM-1) and soluble platelet endothelial cell adhesion molecular-1 (sPECAM-1) of prethrombotic state mediators in patients with chronic obstructive pulmonary disease (COPD). METHODS: The blood plasma levels of D-dimer (D-D), sVCAM-1 and sPECAM-1 in 20 healthy volunteers (control group) and 35 patients with acute exacerbation of COPD ( AECOPD) before and after treatment were measured by ELISA. The statistical analysis used Student' s t test of significance and Pearson linear correlation analysis. RESULTS: The level of D-D in patients before treatment [(4.49 +/- 1.47) mg/L] was significantly higher than that after treatment [(1.98 +/- 0.92) mg/L] and that of the control group [(0.44 +/- 0.14) mg/L] (t = 0.91, 13.10, both P < 0.001); the level of D-D in patients after treatment was also higher than that of the control group (t = 4.96, P < 0.001). The level of sVCAM-1 in patients before treatment [(11 +/- 5) nmol/L] was significantly higher than those of patients after treatment [(8 +/- 4) nmol/L] and control group [(7 +/- 4) nmol/L] (t = 2. 24, 2.75, both P < 0.001); but the difference of sVCAM-l between the post-treatment group and the control group was not significant (t = 0.75, P > 0.05). The level of sPECAM-1 in patients after treatment [(61 +/- 13) pmol/L] was significantly higher than that before treatment [(36 +/- 8) pmol/L] and that of the control group [(43 +/- 10) pmol/L] (t = 9.23, 5.91, both P < 0.001), and the level of the control group was also higher than that of patients before treatment (t = 2.35, P < 0.05). Before treatment, there was significant positive correlation between D-D and sVCAM-1 (r = 0.759, P < 0.01) but no correlation between sPECAM-1 and D-D or sVCAM-1 (r = 0.045, 0.078, both P > 0.05). After treatment, there was significant negative correlation between D-D and sPECAM-1 (r = -0.548, P < 0.01) but no correlation between sVCAM-land D-D or sPECAM-1 (r = -0.032, 0.143, both P > 0.05). There were no correlations among D-D and sPECAM-1 and sVCAM-1 respectively in the control group (r = 0.137, -0.121, 0.035, all P > 0.05). CONCLUSIONS: The levels of D-D and sVCAM-1 increase significantly during acute exacerbation of COPD, which suggests that prethrombotic state exists in acute exacerbation of COPD. The measurement of D-D and sVCAM-1 is useful to monitor prethrombotic state during acute exacerbation of COPD and may be useful in evaluating the severity. The significant increase of sPECAM-1 in plasma of patients after treatment suggests that sPECAM-1 may be a protective factor against prethrombotic state.
