Evaluation of Myocardium Contractile Function and Systemic Inflammatory Response Indices in Hypertensive Disease in Combination with Chronic Obstructive Pulmonary Disease in the Process of Treatment

2017 ◽  
Vol 2 (6) ◽  
pp. 120-124
Author(s):  
O. Yatsenko ◽  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Pulmonary Disease ◽  
Contractile Function ◽  
Systemic Inflammatory Response ◽  
Chronic Obstructive ◽  
Hypertensive Disease ◽  
Obstructive Pulmonary Disease

scholarly journals Pneumonic versus Nonpneumonic Exacerbations of Chronic Obstructive Pulmonary Disease

2020 ◽  
Vol 41 (06) ◽  
pp. 817-829
Author(s):  
Ernesto Crisafulli ◽  
Alessandra Manco ◽  
Miquel Ferrer ◽  
Arturo Huerta ◽  
Claudio Micheletto ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Pulmonary Disease ◽  
Defense Mechanisms ◽  
Community Acquired Pneumonia ◽  
Systemic Inflammatory Response ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Reactive Protein ◽  
The Impact

AbstractPatients with chronic obstructive pulmonary disease (COPD) often suffer acute exacerbations (AECOPD) and community-acquired pneumonia (CAP), named nonpneumonic and pneumonic exacerbations of COPD, respectively. Abnormal host defense mechanisms may play a role in the specificity of the systemic inflammatory response. Given the association of this aspect to some biomarkers at admission (e.g., C-reactive protein), it can be used to help to discriminate AECOPD and CAP, especially in cases with doubtful infiltrates and advanced lung impairment. Fever, sputum purulence, chills, and pleuritic pain are typical clinical features of CAP in a patient with COPD, whereas isolated dyspnea at admission has been reported to predict AECOPD. Although CAP may have a worse outcome in terms of mortality (in hospital and short term), length of hospitalization, and early readmission rates, this has only been confirmed in a few prospective studies. There is a lack of methodologically sound research confirming the impact of severe AECOPD and COPD + CAP. Here, we review studies reporting head-to-head comparisons between AECOPD and CAP + COPD in hospitalized patients. We focus on the epidemiology, risk factors, systemic inflammatory response, clinical and microbiological characteristics, outcomes, and treatment approaches. Finally, we briefly discuss some proposals on how we should orient research in the future.

The effect of a systemic inflammatory response on adaptive mechanisms and the state of homeostasis in patients with respiratory tuberculosis in combination with chronic obstructive pulmonary disease

2020 ◽  
Vol 22 (4) ◽  
pp. 23-27
Author(s):  
A. V. Кaticheva ◽  
N. A. Brazhenko ◽  
O. N. Brazhenko ◽  
A. G. Chuikova ◽  
A. V. Nikolay ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Endothelial Dysfunction ◽  
Inflammatory Response ◽  
Pulmonary Disease ◽  
Systemic Inflammatory Response ◽  
The State ◽  
The Body ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Adaptive Mechanisms

The influence of the systemic inflammatory response on the adaptive mechanisms and the state of homeostasis of the body in patients with respiratory tuberculosis against the background of chronic obstructive pulmonary disease is considered. It has been established that respiratory tuberculosis and chronic obstructive pulmonary disease are widespread among the population and are important causes of bronchopulmonary morbidity and mortality. Chronic obstructive pulmonary disease is determined in one third of newly diagnosed patients with respiratory tuberculosis. The combined course of respiratory tuberculosis and chronic obstructive pulmonary disease is a mutually aggravating condition. Comorbid pathology is much more difficult, accompanied by severe intoxication, disintegration of lung tissue and bacterial excretion. Biomarkers and the severity of the systemic inflammatory response are of great clinical and diagnostic value in chronic obstructive pulmonary disease. It was determined that the systemic inflammatory response in chronic obstructive pulmonary disease is characterized by endothelial dysfunction of the vascular wall, significant changes in white blood cells, changes in the protein spectrum of the blood, and lipid metabolism disorders. The manifestations of systemic inflammation and endothelial dysfunction, characteristic of chronic obstructive pulmonary disease, in patients with respiratory tuberculosis, aggravate the course of both diseases. The comorbid state is also characterized by a change in the lipid profile of patients, an increase in the content of total cholesterol and atherogenic fractions. These changes are interrelated with the state of adaptive mechanisms, homeostasis and reactivity of the organism. The state of homeostasis largely determines the development, course and outcome of pathological processes characteristic of tuberculous inflammation and inflammation in chronic obstructive pulmonary disease, and the increase in the effectiveness of the treatment is closely related to the restoration of homeostatic balance and reactivity of the body. The availability of methods for determining the homeostatic balance of the body in clinical practice, with their high information content, allows a personalized approach to the management of patients with comorbidity.

CONDITION OF HEMODYNAMICS IN THE PULMONARY CIRCULATION OF PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) CONCURRENT WITH METABOLIC SYNDROME WITH HYPERTROPHY AND ATROPHY OF THE MYOCARDIUM

2019 ◽  
Vol 72 (8) ◽  
pp. 1491-1493
Author(s):  
Viktor P. Boriak ◽  
Svitlana V. Shut’ ◽  
Tetiana A. Trybrat ◽  
Olena V. Filatova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Metabolic Syndrome ◽  
Right Ventricular ◽  
Pulmonary Disease ◽  
Pulmonary Circulation ◽  
Contractile Function ◽  
Ventricular Myocardium ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
The Right

Introduction: In recent years, COPD is observed as not an isolated, but an associated pathology, in particular, concurrent with metabolic syndrome. The aim of the research is to identify the differences in changes of the rheopulmonography parameters (RPG) depending on the presence of hypertrophy or atrophy of the right ventricular myocardium in patients with COPD concurrent with metabolic syndrome.. Materials and methods: We studied changes in rheopulmonography (RPG) in 145 patients with chronic obstructive pulmonary disease (COPD) concurrent with metabolic syndrome. Results: We detected precapillary hypertension of the pulmonary circulation in patients with right ventricular myocardial hypertrophy: anacrotism serration; flattened peak of the systolic wave; decreased Vcp; high placement of incisura; horizontal course of catacrotism; decreased amplitude of the systolic wave (in this case, due to a greater increase in the resistance of the blood flow in the pulmonary vessels than the decreased impact volume of the right ventricle); prolonged Q-a (in this group of patients, it depends more on hypertension of the pulmonary circulation than on the reduction of contractile function of the myocardium). In atrophy of the right ventricular myocardium, the following changes in the RPG were revealed: decreased systolic wave at its dramatic rise; prolonged Q-a (in this case, due to the weakened heart contraction); Vmax reduction (it reflects the reduction of myocardial contractility); in hypertrophy of the myocardium, Vcp., unlike RPG, does not decrease, which is explained by the decrease in the pressure of the pulmonary circulation. Conclusions: We believe that these changes in RPG allow differentiating hypertrophy and right ventricular myocardial atrophy along with established diagnostic criteria, and can be used as markers for the diagnosis and treatment of COPD concurrent with metabolic syndrome.

The role of gene polymorphisms in the pathogenesis of chronic obstructive pulmonary disease

Biologia ◽  
2008 ◽  
Vol 63 (1) ◽  
Author(s):  
Eva Slabá ◽  
Pavol Joppa ◽  
Ján Šalagovič ◽  
Ružena Tkáčová
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Candidate Genes ◽  
Pulmonary Disease ◽  
Gene Polymorphisms ◽  
Association Studies ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Positional Candidate ◽  
Linkage Analyses

AbstractChronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Irreversible airflow limitation, both progressive and associated with an inflammatory response of the lungs to noxious particles or gases, is a hallmark of the disease. Cigarette smoking is the most important environmental risk factor for COPD, nevertheless, only approximately 20–30% of smokers develop symptomatic disease. Epidemiological studies, case-control studies in relatives of patients with COPD, and twin studies suggest that COPD is a genetically complex disease with environmental factors and many involved genes interacting together. Two major strategies have been employed to identify the genes and the polymorphisms that likely contribute to the development of complex diseases: association studies and linkage analyses. Biologically plausible pathogenetic mechanisms are prerequisites to focus the search for genes of known function in association studies. Protease-antiprotease imbalance, generation of oxidative stress, and chronic inflammation are recognized as the principal mechanisms leading to irreversible airflow obstruction and parenchymal destruction in the lung. Therefore, genes which have been implicated in the pathogenesis of COPD are involved in antiproteolysis, antioxidant barrier and metabolism of xenobiotic substances, inflammatory response to cigarette smoke, airway hyperresponsiveness, and pulmonary vascular remodelling. Significant associations with COPD-related phenotypes have been reported for polymorphisms in genes coding for matrix metalloproteinases, microsomal epoxide hydrolase, glutathione-S-transferases, heme oxygenase, tumor necrosis factor, interleukines 1, 8, and 13, vitamin D-binding protein and β-2-adrenergic receptor (ADRB2), whereas adequately powered replication studies failed to confirm most of the previously observed associations. Genome-wide linkage analyses provide us with a novel tool to identify the general locations of COPD susceptibility genes, and should be followed by association analyses of positional candidate genes from COPD pathophysiology, positional candidate genes selected from gene expression studies, or dense single nucleotide polymorphism panels across regions of linkage. Haplotype analyses of genes with multiple polymorphic sites in linkage disequilibrium, such as the ADRB2 gene, provide another promising field that has yet to be explored in patients with COPD. In the present article we review the current knowledge about gene polymorphisms that have been recently linked to the risk of developing COPD and/or may account for variations in the disease course.

scholarly journals Characterization of the inflammatory response to inhaled lipopolysaccharide in mild to moderate chronic obstructive pulmonary disease

2015 ◽  
Vol 79 (5) ◽  
pp. 767-776 ◽  
Author(s):  
Vandana Gupta ◽  
Antonia Banyard ◽  
Aoibheann Mullan ◽  
Srividya Sriskantharajah ◽  
Thomas Southworth ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Pulmonary Disease ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease
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