Systemic Inflammation And Pulmonary Hypertension In COPD Patients

Author(s):  
Hong Joon Shin ◽  
Yong Soo Kwon ◽  
Yu Il Kim ◽  
Sung Chul Lim ◽  
Young Chul Kim ◽  
...  
2018 ◽  
Vol 17 (2) ◽  
pp. 24-28
Author(s):  
O. M. Polikutina ◽  
Y. S. Slepynina ◽  
E. D. Bazdyrev ◽  
V. N. Karetnikova ◽  
O. L. Barbarach

Aim. To evaluate the structural and functional changes in the lungs of ST elevation myocardial infarction (STEMI) patients with absence or presence of chronic obstructive lung disease (COPD), and the relation with myocardial dysfunction and systemic inflammation.Material and methods. Totally, 189 STEMI patients included: group 1 — STEMI with COPD of moderate and mild grade, 2 — STEMI with no lung pathology. Groups were comparable by clinical and anamnestic parameters. Assessment of lung function and blood collection were done at 10­12 day of STEMI. For comparison of the parameters representing structural and functional changes in the lungs and comparison of C­reactive protein (CRP), N­terminal pro­brain natriuretic peptide (NT­proBNP) concentration, a control group was formed with no pulmonary pathology, comparable by age and sex with the STEMI patients.Results. In COPD patients, higher values revealed of the parameters representing the part of residual volumes in pulmonary structure. Higher residual volume (RV) was found also in STEMI and no COPD comparing to controls, however the relation RV/TLC (total lung capacity) was not higher than normal range. In both groups there were lower values of diffusion lung capacity (DLCO) comparing to controls. The lowest DLCO found in COPD patients. Concentration of NT­proBNP (H=41,6; p<0,001) and CRP (H=38,6; p<0,001) in COPD was significantly higher in STEMI with no COPD patients than in controls. The negative correlations found for NT­proBNP and CRP with forced expiratory volume 1 sec, FEV/FVC1, DLCO, and positive — with the values of thoracic volume, RV/TLC.Conclusion. In STEMI patients the increase revealed of residual lung volumes. Mostly the level of residual volumes is high in STEMI and COPD patients. There are associations of NT­proBNP and CRP with structural and functional parameters of the lungs regardless of COPD.


2014 ◽  
pp. 48-56
Author(s):  
Van Thi Tran ◽  
Van Bang Le ◽  
Thị Thu Huong Hoang

Aim: Some studies have linked the present of chronic obstructive oulmonary disease (COPD) to coronary artery disease (CAD). Low grade systemic inflammation occurs in patients with COPD as well as patients with CAD. This study was designed to find out the concentration differences of hs-CRP and TNF-a in patients having both chronic obstructive pulmonary and coronary artery diseases with those having either. Methods: A cross - sectional descriptive study was conducted in 200 patients undergoing a coronary artery angiography in the Heart Institute, Thong Nhat Hospital and 115 People Hospital. COPD was diagnosed using GOLD classification. Result: Our study had shown that the levels of hs-CRP and TNF-a were statistically increased in patients with COPD, CAD as well as in patients who had COPD with CAD (p<0,05). The levels of hs-CRP were higher in CAD than in COPD nad the levels of TNF-a were higher in COPD than in CAD. In patients with COPD and CAD, there were increased the levels of both hs-CRP and TNF-a in serum. Conclusion: Systemic inflammation presents in both COPD and CAD. Key words: hs-CRP, TNF-a, coronary artery disease (CAD).


2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Jie Yang ◽  
Chuanmei Liu ◽  
Lingling Li ◽  
Xiongwen Tu ◽  
Zhiwei Lu

Purpose. This study aims at investigating the predictive value of red blood cell distribution width (RDW) in pulmonary hypertension (PH) secondary to chronic obstructive pulmonary disease (COPD). Methods. 213 eligible in-hospital COPD patients were reviewed between May 2016 and May 2018, including 39 cases with PH and 174 without PH. Clinical data including demographic characteristics, comorbidities, and results of ultrasound scans, imaging examinations, and laboratory tests were recorded. Results. Increased RDW level was observed in COPD patients with PH compared with COPD patients without PH, with 15.10 ± 1.72% versus 13.70 ± 1.03%, respectively (p<0.001). RDW shared positive relationships with brain natriuretic peptide (BNP) (p=0.001, r = 0.513), pulmonary artery (PA) systolic pressure (p=0.014, r = 0.390), and PA-to-ascending aorta (A) ratio (PA : A) (p=0.001, r = 0.502). Multivariate analysis indicated that RDW, BNP, and PA : A > 1 were the independent risk factors of PH secondary to COPD (p<0.05). The AUC of the RDW in patients with PH was 0.749 ± 0.054 (p<0.001). The optimal cutoff value of RDW for predicting PH was 14.65, with a sensitivity and a specificity value of 69.2% and 82.8%, respectively. Conclusion. RDW is significantly increased in COPD patients with PH and thus may be a useful biomarker for PH secondary to COPD.


2015 ◽  
Vol 46 (2) ◽  
pp. 431-443 ◽  
Author(s):  
Rozenn Quarck ◽  
Marijke Wynants ◽  
Erik Verbeken ◽  
Bart Meyns ◽  
Marion Delcroix

Deficient angiogenesis and systemic inflammation could be involved in the pathophysiology of chronic thromboembolic pulmonary hypertension (CTEPH). We aimed to characterise the histopathology of pulmonary vascular lesions from 52 CTEPH patients who underwent a pulmonary endarterectomy (PEA) and investigate a potential link between clinical, biological and morphometric parameters.Collagen, elastin, fibrin, lipid, endothelial, smooth muscle and inflammatory cell content was investigated using immunohistochemistry. Qualitative changes were evaluated using severity scores. Circulating levels of inflammatory mediators were measured using ELISA.Neointima, thrombotic, recanalised and atherosclerotic lesions were found. Accumulation of macrophages, T-lymphocytes and neutrophils was found mainly in atherosclerotic and thrombotic lesions. Angiogenesis was observed in all kinds of lesions; low-scored angiogenesis predicted adverse outcome, including persistent pulmonary hypertension post-PEA, start of medical therapy and poor survival. C-reactive protein (CRP), interleukin-10, monocyte chemotactic protein-1, macrophage inflammatory protein-1α and matrix metalloproteinase (MMP)-9 were significantly elevated in CTEPH patients. Plasma CRP and MMP-9 levels correlated with neutrophil and macrophage accumulation, respectively.Enhanced systemic inflammation parallels local inflammatory cell infiltration in major pulmonary arteries at advanced stages of CTEPH. Impaired neovascularisation is associated with poor survival, start of medical treatment and persistent pulmonary hypertension post-PEA. These findings suggest that inflammation and impaired angiogenesis could contribute to the progression of the disease.


2020 ◽  
Author(s):  
Tzu-Tao Chen ◽  
Sheng-Ming Wu ◽  
Kuan-Yuan Chen ◽  
Chien-Hua Tseng ◽  
Shu-Chuan Ho ◽  
...  

Abstract BACKGROUND: Systemic manifestations and comorbidities are characteristics of chronic obstructive pulmonary disease (COPD) and are probably due to systemic inflammation. The histone methyltransferase SUV39H1 controls the Th1/Th2 balance. We previously reported that reduced SUV39H1 expression contributed to abnormal inflammation in COPD.METHODS: To assess whether impaired SUV39H1 expression in COPD patients leads to neutrophilic inflammation, downstream responses to IL-8 and suppression of Th2 responses, the SUV39H1 levels in peripheral blood mononuclear cells (PBMCs) from 13 healthy subjects and 30 COPD patients were measured by immunoblotting. Clinical outcomes associated with SUV39H1-related inflammation were also studied. The relationships between SUV39H1 and neutrophil or eosinophil (Th2 response) counts and clinical outcomes were evaluated. In an extended COPD cohort (213 patients), association analyses of blood cell counts with comorbidities and exacerbations were performed.RESULTS: Low SUV39H1 expression was associated with high neutrophil counts and a trend towards low eosinophil counts. In the extended cohort, the high comorbidity group had higher neutrophil counts than the low comorbidity group but similar whole white blood cell counts. The eosinophil percentage and eosinophil/neutrophil ratio displayed contrasting results. The proportion of neutrophils was correlated with COPD comorbidities. Patients with 0-1 moderate to severe exacerbations in the past year had numbers of neutrophils and eosinophils similar to those of patients who experienced more than an exacerbation. Finally, patients with high comorbidities had lower SUV39H1 levels in their PBMCs than did those with low comorbidities.CONCLUSION: Blood neutrophil counts are associated with comorbidities in COPD patients. Impaired SUV39H1 expression in PBMCs from COPD patients are correlated with neutrophilic inflammation and comorbidities.


2021 ◽  
Vol 11 ◽  
Author(s):  
Chung-Yu Chen ◽  
Wen-Ting Wu ◽  
Ya-Ling Wang ◽  
Kuang-Ming Liao

Background: Patients with chronic obstructive pulmonary disease (COPD) are at risk for pulmonary hypertension (PH). The aim of our study was to investigate the benefit of statins for PH in patients with COPD.Methods: The study enrolled 23 million individuals from Taiwan’s population database from January 1, 2002, to December 31, 2017. COPD patients who met the inclusion criteria were enrolled, and patients with lung cancer, less than one year of observation, specific drug therapy for PH and lung transplantation were excluded.Results: A total of 643,131 COPD patients were included in the study, and only 12,308 patients developed PH during follow-up. Based on the inclusion and exclusion criteria, 8,577 PH patients were included in the cohort of patients with PH related to COPD for analysis. According to the definition of statin exposure, the final study population had 1,487 statin users and 7,090 statin non-users. The statin user group had a lower mortality related to PH than the non-user group (3.87 vs. 5.55 per 100 person-years, p &lt; 0.001). The mortality rate for PH in the multivariate analysis (aHR = 0.78, 95% CI = 0.62–0.98, p = 0.046) was significantly lower for statin users than for non-users.Conclusion: Statins seem to benefit patients with PH and COPD.


2016 ◽  
Vol 110 ◽  
pp. 46-52 ◽  
Author(s):  
Hendrik J. Prins ◽  
Johannes M.A. Daniels ◽  
Jan H. Lindeman ◽  
René Lutter ◽  
Wim G. Boersma

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