scholarly journals Impaired Spontaneous Baroreceptor Reflex Sensitivity in Patients With COPD Compared to Healthy Controls: The Role of Lung Hyperinflation

2022 ◽  
Vol 8 ◽  
Author(s):  
Anna Katharina Mayr ◽  
Victoria Wieser ◽  
Georg-Christian Funk ◽  
Sherwin Asadi ◽  
Irene Sperk ◽  
...  

Background and Objectives: Patients with chronic obstructive pulmonary disease (COPD) are at increased risk for cardiovascular disease. This study aimed to investigate the relationship between pulmonary hyperinflation and baroreceptor reflex sensitivity (BRS), a surrogate for cardiovascular risk.Methods: 33 patients with COPD, free from clinical cardiovascular disease, and 12 healthy controls were studied. Participants underwent pulmonary function and non-invasive hemodynamic measurements. BRS was evaluated using the sequence method during resting conditions and mental arithmetic stress testing.Results: Patients with COPD had evidence of airflow obstruction [forced expiratory volume in 1 s predicted (FEV1%) 26.5 (23.3–29.1) vs. 91.5 (82.8–100.8); P < 0.001; geometric means (GM) with 95% confidence interval (CI)] and lung hyperinflation [residual volume/total lung capacity (RV/TLC) 67.7 (64.3–71.3) vs. 41.0 (38.8–44.3); P < 0.001; GM with 95% CI] compared to controls. Spontaneous mean BRS (BRSmean) was significantly lower in COPD, both during rest [5.6 (4.2–6.9) vs. 12.0 (9.1–17.6); P = 0.003; GM with 95% CI] and stress testing [4.4 (3.7–5.3) vs. 9.6 (7.7–12.2); P < 0.001; GM with 95% CI]. Stroke volume (SV) was significantly lower in the patient group [−21.0 ml (−29.4 to −12.6); P < 0.001; difference of the means with 95% CI]. RV/TLC was found to be a predictor of BRS and SV (P < 0.05 for both), independent of resting heart rate.Conclusion: We herewith provide evidence of impaired BRS in patients with COPD. Hyperinflation may influence BRS through alteration of mechanosensitive vagal nerve activity.

2018 ◽  
Vol 2 (4) ◽  
Author(s):  
Swarga Jyoti Das

Periodontal disease is an inflammatory disease caused predominantly by Gram-negative, anaerobic, and microaerophilic bacteria that colonise the subgingival area though modified by environment, physical, social and host stresses. It results in progressive destruction of the periodontal ligament and alveolar bone with increased probing depth, recession, or both [1]. Throughout the history of mankind, it has been believed that oral diseases and maladies including periodontal disease may have an effect on the rest of the body. Over the centuries, writings from the ancient Egyptians, Hebrews, Assyrians, Greeks and Romans, have all noted the importance of the mouth in overall health and well-being. Thus, the concept of linking periodontitis and systemic diseases could be traced back to the beginning of recorded history and medicine [2]. Periodontal disease has been linked to an increased risk of various systemic diseases, including the respiratory diseases e.g. pneumonia and chronic obstructive pulmonary disease (COPD) [3]. COPD is a generic term defined by the presence of airflow obstruction with excess production of sputum resulting from chronic bronchitis and/or emphysema. It has been recognized as one of the major causes of death and disability globally and is the fourth leading cause of death in United States [4]. The aetiology of COPD is complex and multifactorial, involving multiple genetic and environmental factors [5]. An enhanced or abnormal inflammatory response to inhaled particles or gases, beyond the normal protective inflammatory response in the lungs, is a characteristic feature of COPD and is potential to produce lung injury


2021 ◽  
Vol 12 ◽  
Author(s):  
Nathalie Acevedo ◽  
Jose Miguel Escamilla-Gil ◽  
Héctor Espinoza ◽  
Ronald Regino ◽  
Jonathan Ramírez ◽  
...  

BackgroundChronic obstructive pulmonary disease (COPD) is associated with increased risk of severe COVID-19, but the mechanisms are unclear. Besides, patients with severe COVID-19 have been reported to have increased levels of several immune mediators.MethodsNinety-two proteins were quantified in 315 plasma samples from 118 asthmatics, 99 COPD patients and 98 healthy controls (age 40-90 years), who were recruited in Colombia before the COVID-19 pandemic. Protein levels were compared between each disease group and healthy controls. Significant proteins were compared to the gene signatures of SARS-CoV-2 infection reported in the “COVID-19 Drug and Gene Set Library” and with experimentally tested protein biomarkers of severe COVID-19.ResultsForty-one plasma proteins showed differences between patients and controls. Asthmatic patients have increased levels in IL-6 while COPD patients have a broader systemic inflammatory dysregulation driven by HGF, OPG, and several chemokines (CXCL9, CXCL10, CXCL11, CX3CL1, CXCL1, MCP-3, MCP-4, CCL3, CCL4 and CCL11). These proteins are involved in chemokine signaling pathways related with response to viral infections and some, were found up-regulated upon SARS-CoV-2 experimental infection of Calu-3 cells as reported in the COVID-19 Related Gene Sets database. An increase of HPG, CXCL9, CXCL10, IL-6, MCP-3, TNF and EN-RAGE has also been experimentally detected in patients with severe COVID-19.ConclusionsCOPD patients have altered levels of plasma proteins that have been reported increased in patients with severe COVID-19. Our study suggests that COPD patients have a systemic dysregulation in chemokine networks (including HGF and CXCL9) that could make them more susceptible to severe COVID-19. Also, that IL-6 levels are increased in some asthmatic patients (especially in females) and this may influence their response to COVID-19. The findings in this study depict a novel panel of inflammatory plasma proteins in COPD patients that may potentially associate with increased susceptibility to severe COVID-19 and might be useful as a biomarker signature after future experimental validation.


2018 ◽  
Vol 16 ◽  
pp. 147997311881569 ◽  
Author(s):  
Preyanate Wilairat ◽  
Kirati Kengkla ◽  
Chaiyawat Thayawiwat ◽  
Phongsathorn Phlaisaithong ◽  
Supakorn Somboonmee ◽  
...  

To examine clinical outcomes of theophylline use in patients with chronic obstructive pulmonary disease (COPD) receiving inhaled corticosteroids (ICS) and long-acting beta-2 agonists (LABA). Electronic data from five hospitals located in Northern Thailand between January 2011 and December 2015 were retrospectively collected. Propensity score (PS) matching (2:1 ratio) technique was used to minimize confounding factors. The primary outcome was overall exacerbations. Secondary outcomes were exacerbation not leading to hospital admission, hospitalization for exacerbation, hospitalization for pneumonia, and all-cause hospitalizations. Cox’s proportional hazards models were used to estimate adjusted hazard ratio (aHR) and 95% confidence interval (CI). After PS matching, of 711 patients with COPD (mean age: 70.1 years; 74.4% male; 60.8% severe airflow obstruction), 474 theophylline users and 237 non-theophylline users were included. Mean follow-up time was 2.26 years. Theophylline significantly increased the risk of overall exacerbation (aHR: 1.48, 95% CI: 1.11–1.96; p = 0.008) and exacerbation not leading to hospital admission (aHR: 1.47, 95% CI: 1.06–2.03; p = 0.020). Theophylline use did not significantly increase the risk of hospitalization for exacerbation (aHR: 1.11, 95% CI: 0.79–1.58; p = 0.548), hospitalization for pneumonia (aHR: 1.28, 95% CI: 0.89–1.84; p = 0.185), and all-cause hospitalizations (aHR: 1.03, 95% CI: 0.80–1.33; p = 0.795). Theophylline use as add-on therapy to ICS and LABA might be associated with an increased risk for overall exacerbation in patients with COPD. A large-scale prospective study of theophylline use investigating both safety and efficacy is warranted.


2019 ◽  
Vol 29 (2) ◽  
pp. 244-251
Author(s):  
Emilie C Risom ◽  
Katrine B Buggeskov ◽  
Ulla B Mogensen ◽  
Martin Sundskard ◽  
Jann Mortensen ◽  
...  

Abstract OBJECTIVES Although reduced lung function and chronic obstructive pulmonary disease (COPD) is associated with higher risk of death following cardiac surgery, preoperative spirometry is not performed routinely. The aim of this study was to investigate the relationship between preoperative lung function and postoperative complications in all comers for cardiac surgery irrespective of smoking or COPD history. METHODS Preoperative spirometry was performed in elective adult cardiac surgery patients. Airflow obstruction was defined as the ratio of forced expiratory volume in 1 s (FEV1)/forced vital capacity ratio below the lower limit of normal (LLN) and reduced forced ventilatory capacity defined as FEV1 <LLN. RESULTS A history of COPD was reported by 132 (19%) patients; however, only 74 (56%) had spirometry-verified airflow obstruction. Conversely, 64 (12%) of the 551 patients not reporting a history of COPD had spirometry-verified airflow obstruction. The probability of death was significantly higher in patients with airflow obstruction (8.8% vs 4.5%, P = 0.04) and in patients with a FEV1 <LLN (8.7% vs 3.7%, P = 0.007). In the multivariate analysis were age [hazard ratio (HR) 1.6, 95% confidence interval (CI) 1.0–2.5; P = 0.04], prolonged cardiopulmonary bypass time (HR 1.2, 95% CI 1.02–1.3; P = 0.03), reduced kidney function (HR 2.5, 95% CI 1.2–5.6; P = 0.02) and FEV1 <LLN (HR 2.4, 95% CI 1.1–5.2; P = 0.03) all independently associated with an increased risk of death. CONCLUSIONS Preoperative spirometry reclassified 18% of the patients. A reduced FEV1 independently doubled the risk of death. Inclusion of preoperative spirometry in routine screening of cardiac surgical patients may improve risk prediction and identify high-risk patients. Clinical trial registration number NCT01614951 (ClinicalTrials.gov).


BMJ Open ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. e024330 ◽  
Author(s):  
Ravi Lokwani ◽  
Peter A B Wark ◽  
Katherine J Baines ◽  
Daniel Barker ◽  
Jodie L Simpson

ObjectivesThe significance of neutrophilic inflammation in obstructive airway disease remains controversial. Recent studies have demonstrated presence of an active neutrophil population in systemic circulation, featuring hypersegmented morphology, with high oxidative burst and functional plasticity in inflammatory conditions. The aim of this study was to characterise neutrophil subsets in bronchial lavage (BL) of obstructive airway disease participants (asthma, chronic obstructive pulmonary disease (COPD) and bronchiectasis) and healthy controls on the basis of nuclear morphology and to assess the association between neutrophil subsets and the clinical parameters of the obstructive airway disease participants.DesignA cross-sectional exploratory study.SettingJohn Hunter Hospital and Hunter Medical Research Institute, Australia.ParticipantsSeventy-eight adults with obstructive airway disease comprised those with stable asthma (n=39), COPD (n=20) and bronchiectasis (n=19) and 20 healthy controls.Materials and methodsCytospins were prepared and neutrophil subsets were classified based on nuclear morphology into hypersegmented (>4 lobes), normal (2–4 lobes) and banded (1 lobe) neutrophils and enumerated.ResultsNeutrophils from each subset were identified in all participants. Numbers of hypersegmented neutrophils were elevated in participants with airway disease compared with healthy controls (p<0.001). Both the number and the proportion of hypersegmented neutrophils were highest in COPD participants (median (Q1–Q3) of 1073.6 (258.8–2742) × 102/mL and 24.5 (14.0–46.5)%, respectively). An increased proportion of hypersegmented neutrophils in airway disease participants was significantly associated with lower forced expiratory volume in 1 s/forced vital capacity per cent (Spearman’s r=−0.322, p=0.004).ConclusionNeutrophil heterogeneity is common in BL and is associated with more severe airflow obstruction in adults with airway disease. Further work is required to elucidate the functional consequences of hypersegmented neutrophils in the pathogenesis of disease.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Robert K. McNamara ◽  
Ronald Jandacek ◽  
Therese Rider ◽  
Patrick Tso ◽  
Yogesh Dwivedi ◽  
...  

Deficiency in long-chain omega-3 (LCn − 3) fatty acids, eicosapentaenoic acid (EPA, 20:5n − 3) and docosahexaenoic acid (DHA, 22:6n − 3), has been implicated in the pathoetiology of cardiovascular disease, a primary cause of excess premature mortality in patients with schizophrenia (SZ). In the present study, we determined erythrocyte EPA + DHA levels in adult medication-free patients SZ (n=20) and age-matched healthy controls (n=24). Erythrocyte EPA + DHA composition exhibited by SZ patients (3.5%) was significantly lower than healthy controls (4.5%, −22%, P=0.007). The majority of SZ patients (72%) exhibited EPA+DHA levels ≤4.0% compared with 37% of controls (Chi-square, P=0.001). In contrast, the omega-6 fatty acid arachidonic acid (AA, 20:4n−6) (+9%, P=0.02) and the AA:EPA + DHA ratio (+28%, P=0.0004) were significantly greater in SZ patients. Linoleic acid (18:2n−6) was significantly lower (−12%, P=0.009) and the erythrocyte 20:3/18:2 ratio (an index of delta6-desaturase activity) was significantly elevated in SZ patients. Compared with same-gender controls, EPA + DHA composition was significantly lower in male (−19%, P=0.04) but not female (−13%, P=0.33) SZ patients, whereas the 20:3/18:2 ratio was significantly elevated in both male (+22%, P=0.008) and female (+22%, P=0.04) SZ patients. These results suggest that the majority of SZ patients exhibit low LCn − 3 fatty acid levels which may place them at increased risk for cardiovascular morbidity and mortality.


2016 ◽  
Vol 47 (5) ◽  
pp. 1365-1373 ◽  
Author(s):  
Roberto A. Rabinovich ◽  
Bruce E. Miller ◽  
Karolina Wrobel ◽  
Kareshma Ranjit ◽  
Michelle C. Williams ◽  
...  

Elastin degradation is a key feature of emphysema and may have a role in the pathogenesis of atherosclerosis associated with chronic obstructive pulmonary disease (COPD). Circulating desmosine is a specific biomarker of elastin degradation. We investigated the association between plasma desmosine (pDES) and emphysema severity/progression, coronary artery calcium score (CACS) and mortality.pDES was measured in 1177 COPD patients and 110 healthy control subjects from two independent cohorts. Emphysema was assessed on chest computed tomography scans. Aortic arterial stiffness was measured as the aortic–femoral pulse wave velocity.pDES was elevated in patients with cardiovascular disease (p<0.005) and correlated with age (rho=0.39, p<0.0005), CACS (rho=0.19, p<0.0005) modified Medical Research Council dyspnoea score (rho=0.15, p<0.0005), 6-min walking distance (rho=−0.17, p<0.0005) and body mass index, airflow obstruction, dyspnoea, exercise capacity index (rho=0.10, p<0.01), but not with emphysema, emphysema progression or forced expiratory volume in 1 s decline. pDES predicted all-cause mortality independently of several confounding factors (p<0.005). In an independent cohort of 186 patients with COPD and 110 control subjects, pDES levels were higher in COPD patients with cardiovascular disease and correlated with arterial stiffness (p<0.05).In COPD, excess elastin degradation relates to cardiovascular comorbidities, atherosclerosis, arterial stiffness, systemic inflammation and mortality, but not to emphysema or emphysema progression. pDES is a good biomarker of cardiovascular risk and mortality in COPD.


2015 ◽  
Vol 30 (2) ◽  
pp. 228-232 ◽  
Author(s):  
A. Voggt ◽  
M. Berger ◽  
M. Obermeier ◽  
A. Löw ◽  
F. Seemueller ◽  
...  

AbstractBackground:Affective disorders are associated with an increased risk of cardiovascular disease, which, at least partly, appears to be independent of psychopharmacological treatments used to manage these disorders. Reduced heart rate variability (SDNN) and a low Omega-3 Index have been shown to be associated with increased risk for death after myocardial infarction. Therefore, we set out to investigate heart rate variability and the Omega-3 Index in euthymic patients with bipolar disorders.Methods:We assessed heart rate variability (SDNN) and the Omega-3 Index in 90 euthymic, mostly medicated patients with bipolar disorders (Bipolar-I, Bipolar-II) on stable psychotropic medication, free of significant medical comorbidity and in 62 healthy controls. Heart rate variability was measured from electrocardiography under a standardized 30 minutes resting state condition. Age, sex, BMI, smoking, alcohol consumption and caffeine consumption as potential confounders were also assessed.Results:Heart rate variability (SDNN) was significantly lower in patients with bipolar disorders compared to healthy controls (35.4 msec versus 60.7 msec; P < 0.0001), whereas the Omega-3 Index did not differ significantly between the groups (5.2% versus 5.3%). In a linear regression model, only group membership (patients with bipolar disorders versus healthy controls) and age significantly predicted heart rate variability (SDNN).Conclusion:Heart rate variability (SDNN) may provide a useful tool to study the impact of interventions aimed at reducing the increased risk of cardiovascular disease in euthymic patients with bipolar disorders. The difference in SDNN between cases and controls cannot be explained by a difference in the Omega-3 Index.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
K. Egervall ◽  
A. Rosso ◽  
S. Elmståhl

Abstract Background Cardiovascular disease (CVD) is a common comorbidity in chronic obstructive pulmonary disease (COPD) and reduced lung function is an important risk factor for CVD and CVD-related death. However, the mechanisms behind the increased risk for CVD in COPD patients are not fully understood. Methods We examined the association between CVD- and inflammation-related serum biomarkers, and pulmonary function in a geriatric population. 266 biomarkers related to CVD and inflammation were analyzed in blood samples from 611 subjects aged 66–86 years who participated in the Good Aging in Skåne study. Serum levels were assessed by a proximity extension assay. Pulmonary function was measured using the lower limit of normality (LLN) spirometry criteria, i.e., forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC)  <  LLN. Logistic regression models were implemented and multiple comparisons were accounted for. Results 10.3% of the study participants fulfilled pulmonary function decline criteria according to LLN. Out of the 266 biomarkers, only plasminogen activator, urokinase receptor (PLAUR) was statistically significantly associated with decreased pulmonary function. We could not find a statistically significant association between pulmonary function decline and other biomarkers previously linked to COPD, such as interleukin 6, tumor necrosis factor and surfactant protein D. Conclusion We found that serum levels of PLAUR are associated with pulmonary function decline in older adults. PLAUR is activated following inflammation and promotes matrix metallopeptidase (MMP) activation and extracellular matrix (ECM) degradation. This implies that PLAUR could play a role in the early phase of COPD pathogenesis.


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