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1.
Rational Pharmacotherapy in Cardiology ; 19(1):65-70, 2023.
Artigo em Russo | EMBASE | ID: covidwho-20235021

RESUMO

The experience of managing patients with COVID-19 around the world has shown that, although respiratory symptoms predominate during the manifestation of infection, then many patients can develop serious damage to the cardiovascular system. However, coronary artery disease (CHD) remains the leading cause of death worldwide. The purpose of the review is to clarify the possible pathogenetic links between COVID-19 and acute coronary syndrome (ACS), taking into account which will help to optimize the management of patients with comorbid pathology. Among the body's responses to SARS-CoV-2 infection, which increase the likelihood of developing ACS, the role of systemic inflammation, the quintessence of which is a "cytokine storm" that can destabilize an atherosclerotic plaque is discussed. Coagulopathy, typical for patients with Covid-19, is based on immunothrombosis, caused by a complex interaction between neutrophilic extracellular traps and von Willebrandt factor in conditions of systemic inflammation. The implementation of a modern strategy for managing patients with ACS, focused on the priority of percutaneous interventions (PCI), during a pandemic is experiencing great difficulties due to the formation of time delays before the start of invasive procedures due to the epidemiological situation. Despite this, the current European, American and Russian recommendations for the management of infected patients with ACS confirm the inviolability of the position of PCI as the first choice for treating patients with ACS and the undesirability of replacing invasive treatment with thrombolysis.Copyright © 2023 Stolichnaya Izdatelskaya Kompaniya. All rights reserved.

2.
Pulmonologiya ; 33(1):17-26, 2023.
Artigo em Russo | EMBASE | ID: covidwho-20233602

RESUMO

The new coronavirus infection COVID-19 (Coronavirus Disease 2019) caused by SARS-CoV-2, has posed scientific and public health challenges. The problem of treating COVID-19 still remains, and the pathogenesis of COVID-19 needs to be studied in detail, including the involvement of mast cells (MCs) and their specific proteases. The aim of this study was to characterize the role of mast cell proteases chymase, tryptase, and carboxypeptidase A3 (CPA3) in the lung damage associated with COVID-19. Methods. The study included postmortem lung biopsies from 30 patients who died of severe COVID-19, and biopsies from 9 control group patients. Histological preparations were made and protease profile and degranulation activity of MCs were analyzed. In addition, some demographic, clinical, and laboratory parameters were analyzed. Results. The average number of tryptase-positive MCs without evidence of degranulation and the total number of CPA3-positive MCs were statistically significantly higher in patients with COVID-19, and the number of tryptase-positive and CPA3-positive MCs fragments was lower compared with controls. Negative correlations were established between the numbers of tryptase-positive MCs and red blood cell count. Negative correlations were found between non-granulating tryptase-positive MCs and hemoglobin levels. Positive correlations were noted between tryptase-positive MCs and the leukocytes and eosinophils counts, and negative correlations were noted between the number of CPA3-positive cells and the platelet count. A positive correlation was found between the number of adjoining MCs, as well as fragments of tryptase-positive MCs, and the erythrocyte sedimentation rate (ESR). A negative correlation was also observed between the number of non-degranulated CPA3-positive MCs and the blood level of C-reactive protein. In patients with COVID-19, reduced degranulation activity of tryptase-positive MCs was found along with increased representation of CPA3-positive MCs. Several trends and associations with laboratory test results were noted. The potential involvement of MCs in the development of anemia and thrombocytopenia is considered. Associations were established between tryptase-positive MCs and the peripheral blood counts of leukocytes and eosinophils, as well as ESR. Conclusion. The results obtained are highly contradictory. Since many aspects of the involvement of MCs and their proteases in COVID-19 pathogenesis are still unknown, studies with larger cohorts of patients are needed.Copyright © Budnevsky A.V. et al., 2023.

3.
Rational Pharmacotherapy in Cardiology ; 19(1):65-70, 2023.
Artigo em Inglês | Web of Science | ID: covidwho-20230621

RESUMO

The experience of managing patients with COVID-19 around the world has shown that, although respiratory symptoms predominate during the man-ifestation of infection, then many patients can develop serious damage to the cardiovascular system. However, coronary artery disease (CHD) remains the leading cause of death worldwide. The purpose of the review is to clarify the possible pathogenetic links between COVID-19 and acute coronary syndrome (ACS), taking into account which will help to optimize the management of patients with comorbid pathology. Among the body's responses to SARS-CoV-2 infection, which increase the likelihood of developing ACS, the role of systemic inflammation, the quintessence of which is a "cytokine storm" that can destabilize an atherosclerotic plaque is discussed. Coagulopathy, typical for patients with Covid-19, is based on immunothrombosis, caused by a complex interaction between neutrophilic extracellular traps and von Willebrandt factor in conditions of systemic inflammation. The im-plementation of a modern strategy for managing patients with ACS, focused on the priority of percutaneous interventions (PCI), during a pandemic is experiencing great difficulties due to the formation of time delays before the start of invasive procedures due to the epidemiological situation. Despite this, the current European, American and Russian recommendations for the management of infected patients with ACS confirm the inviolability of the position of PCI as the first choice for treating patients with ACS and the undesirability of replacing invasive treatment with thrombolysis.

4.
Rational Pharmacotherapy in Cardiology ; 19(1):65-70, 2023.
Artigo em Russo | EMBASE | ID: covidwho-2314208

RESUMO

The experience of managing patients with COVID-19 around the world has shown that, although respiratory symptoms predominate during the manifestation of infection, then many patients can develop serious damage to the cardiovascular system. However, coronary artery disease (CHD) remains the leading cause of death worldwide. The purpose of the review is to clarify the possible pathogenetic links between COVID-19 and acute coronary syndrome (ACS), taking into account which will help to optimize the management of patients with comorbid pathology. Among the body's responses to SARS-CoV-2 infection, which increase the likelihood of developing ACS, the role of systemic inflammation, the quintessence of which is a "cytokine storm" that can destabilize an atherosclerotic plaque is discussed. Coagulopathy, typical for patients with Covid-19, is based on immunothrombosis, caused by a complex interaction between neutrophilic extracellular traps and von Willebrandt factor in conditions of systemic inflammation. The implementation of a modern strategy for managing patients with ACS, focused on the priority of percutaneous interventions (PCI), during a pandemic is experiencing great difficulties due to the formation of time delays before the start of invasive procedures due to the epidemiological situation. Despite this, the current European, American and Russian recommendations for the management of infected patients with ACS confirm the inviolability of the position of PCI as the first choice for treating patients with ACS and the undesirability of replacing invasive treatment with thrombolysis.Copyright © 2023 Stolichnaya Izdatelskaya Kompaniya. All rights reserved.

5.
Pulmonologiya ; 33(1):17-26, 2023.
Artigo em Russo | EMBASE | ID: covidwho-2313269

RESUMO

The new coronavirus infection COVID-19 (Coronavirus Disease 2019) caused by SARS-CoV-2, has posed scientific and public health challenges. The problem of treating COVID-19 still remains, and the pathogenesis of COVID-19 needs to be studied in detail, including the involvement of mast cells (MCs) and their specific proteases. The aim of this study was to characterize the role of mast cell proteases chymase, tryptase, and carboxypeptidase A3 (CPA3) in the lung damage associated with COVID-19. Methods. The study included postmortem lung biopsies from 30 patients who died of severe COVID-19, and biopsies from 9 control group patients. Histological preparations were made and protease profile and degranulation activity of MCs were analyzed. In addition, some demographic, clinical, and laboratory parameters were analyzed. Results. The average number of tryptase-positive MCs without evidence of degranulation and the total number of CPA3-positive MCs were statistically significantly higher in patients with COVID-19, and the number of tryptase-positive and CPA3-positive MCs fragments was lower compared with controls. Negative correlations were established between the numbers of tryptase-positive MCs and red blood cell count. Negative correlations were found between non-granulating tryptase-positive MCs and hemoglobin levels. Positive correlations were noted between tryptase-positive MCs and the leukocytes and eosinophils counts, and negative correlations were noted between the number of CPA3-positive cells and the platelet count. A positive correlation was found between the number of adjoining MCs, as well as fragments of tryptase-positive MCs, and the erythrocyte sedimentation rate (ESR). A negative correlation was also observed between the number of non-degranulated CPA3-positive MCs and the blood level of C-reactive protein. In patients with COVID-19, reduced degranulation activity of tryptase-positive MCs was found along with increased representation of CPA3-positive MCs. Several trends and associations with laboratory test results were noted. The potential involvement of MCs in the development of anemia and thrombocytopenia is considered. Associations were established between tryptase-positive MCs and the peripheral blood counts of leukocytes and eosinophils, as well as ESR. Conclusion. The results obtained are highly contradictory. Since many aspects of the involvement of MCs and their proteases in COVID-19 pathogenesis are still unknown, studies with larger cohorts of patients are needed.Copyright © Budnevsky A.V. et al., 2023.

6.
Pulmonologiya ; 32(6):834-841, 2022.
Artigo em Russo | EMBASE | ID: covidwho-2253226

RESUMO

Cough is a frequent manifestation of COVID-19 (COronaVIrus Disease 2019), therefore, it has an important diagnostic value. There is little information about the characteristics of cough of COVID-19 patients in the literature. To perform a spectral analysis of cough sounds in COVID-19 patients in comparison with induced cough of healthy individuals. Methods. The main group consisted of 218 COVID-19 patients (48.56% - men, 51.44% - women, average age 40.2 (32.4;50.1) years). The comparison group consisted of 60 healthy individuals (50.0% men, 50.0% women, average age 41.7 (31.2;53.0) years) who were induced to cough. Each subject had a cough sound recorded, followed by digital processing using a fast Fourier transform algorithm. The temporal-frequency parameters of cough sounds were evaluated: duration (ms), the ratio of the energy of low and medium frequencies (60 - 600 Hz) to the energy of high frequencies (600 - 6 000 Hz), the frequency of the maximum sound energy (Hz). These parameters were determined in relation to both the entire cough and individual phases of the cough sound. Results. Significant differences were found between some cough parameters in the main group and in the comparison group. The total duration of the coughing act was significantly shorter in patients with COVID-19, in contrast to the induced cough of healthy individuals (T = 342.5 (277.0;394.0) - in the main group;T (c) = 400.5 (359.0;457.0) - in the comparison group;p = 0.0000). In addition, it was found that the cough sounds of COVID-19 patients are dominated by the energy of higher frequencies as compared to the healthy controls (Q = 0.3095 (0.223;0.454) - in the main group;Q (c) = 0.4535 (0.3725;0.619) - in the comparison group;p = 0.0000). The maximum frequency of cough sound energy in the main group was significantly higher than in the comparison group (Fmax = 463.0 (274.0;761.0) - in the main group;Fmax = 347 (253.0;488.0) - in the comparison group;p = 0.0013). At the same time, there were no differences between the frequencies of the maximum energy of cough sound of the individual phases of cough act and the duration of the first phase. Conclusion. The cough of patients with COVID-19 is characterized by a shorter duration and a predominance of high-frequency energy compared to the induced cough of healthy individuals.Copyright © 2022 Budnevsky A.V. et al.

7.
Pulmonologiya ; 32(6):834-841, 2022.
Artigo em Russo | EMBASE | ID: covidwho-2239415

RESUMO

Cough is a frequent manifestation of COVID-19 (COronaVIrus Disease 2019), therefore, it has an important diagnostic value. There is little information about the characteristics of cough of COVID-19 patients in the literature. To perform a spectral analysis of cough sounds in COVID-19 patients in comparison with induced cough of healthy individuals. Methods. The main group consisted of 218 COVID-19 patients (48.56% - men, 51.44% - women, average age 40.2 (32.4;50.1) years). The comparison group consisted of 60 healthy individuals (50.0% men, 50.0% women, average age 41.7 (31.2;53.0) years) who were induced to cough. Each subject had a cough sound recorded, followed by digital processing using a fast Fourier transform algorithm. The temporal-frequency parameters of cough sounds were evaluated: duration (ms), the ratio of the energy of low and medium frequencies (60 - 600 Hz) to the energy of high frequencies (600 - 6 000 Hz), the frequency of the maximum sound energy (Hz). These parameters were determined in relation to both the entire cough and individual phases of the cough sound. Results. Significant differences were found between some cough parameters in the main group and in the comparison group. The total duration of the coughing act was significantly shorter in patients with COVID-19, in contrast to the induced cough of healthy individuals (T = 342.5 (277.0;394.0) - in the main group;T (c) = 400.5 (359.0;457.0) - in the comparison group;p = 0.0000). In addition, it was found that the cough sounds of COVID-19 patients are dominated by the energy of higher frequencies as compared to the healthy controls (Q = 0.3095 (0.223;0.454) - in the main group;Q (c) = 0.4535 (0.3725;0.619) - in the comparison group;p = 0.0000). The maximum frequency of cough sound energy in the main group was significantly higher than in the comparison group (Fmax = 463.0 (274.0;761.0) - in the main group;Fmax = 347 (253.0;488.0) - in the comparison group;p = 0.0013). At the same time, there were no differences between the frequencies of the maximum energy of cough sound of the individual phases of cough act and the duration of the first phase. Conclusion. The cough of patients with COVID-19 is characterized by a shorter duration and a predominance of high-frequency energy compared to the induced cough of healthy individuals.

8.
Pakistan Journal of Medical and Health Sciences ; 16(6):422-424, 2022.
Artigo em Inglês | EMBASE | ID: covidwho-1939798

RESUMO

Background: The Coronavirus Disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) was first reported in December 2019 in Wuhan. The problem of COVID-19 treatment is still relevant, and it is necessary to study in details the pathogenesis of COVID-19, including the role of mast cells (MCs). Aim: The aim of the review is to reveal the role of MCs, their receptors and mediators in the pathogenesis of the COVID-19. Results: This review demonstrates a possible role of MCs in the pathogenesis of COVID-19. Conclusion: MCs may be key elements of inflammation caused by COVID-19. MCs express various receptors on their surface that ensure the interaction of SARS-CoV-2 and MCs. Activated MCs release inflammatory cytokines, chemokines and proteases, which are involved in both the protective function and hyperinflammation in COVID-19.

9.
INTERNATIONAL JOURNAL OF BIOMEDICINE ; 12(2):179-182, 2022.
Artigo em Inglês | Web of Science | ID: covidwho-1912498

RESUMO

Background: Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). First reported in 2019, it has already caused more than 500 million cases worldwide. The problem of COVID-19 treatment is still relevant, and it is necessary to study in detail the pathogenesis of COVID-19, including the involvement of different immune cells and their mediators. There is increasing evidence of the important role of mast cells (MCs) and their specific protease carooxypeptidase A3 (CPA3) in the pathogenesis of COVID-19. MCs chymase and tryptase are already well studied, while CPA3 is of growing interest. The aim of this review is to study the CPA3 features and mechanisms of its participation in the pathogenesis of COVID-19 and some other infectious and non-infectious diseases. Methods and Results: A literature search was carried out using Scopus, Web of Science, PubMed, Medlin, and E-Library databases. Of the158 articles analyzed, 33 were included in the review. CPA3, expressed by MCs in various organs, including human lungs, plays a role in the pathogenesis of COVID-19 by indirectly causing pulmonary fibrosis, associating with levels of inflammatory cytokines and chemokines, and severity of COVID-19.

10.
Profilakticheskaya Meditsina ; 24(9):110-115, 2021.
Artigo em Russo | Scopus | ID: covidwho-1524695

RESUMO

The COVID-19 pandemic is associated with a high mortality rate. The SARS-CoV-2 virus has multisystemic effect and also affects the respiratory system. Melatonin is a strong antioxidant with immunomodulatory and anti-inflammatory effects. This article re-views the literature data on the effects of melatonin in COVID-19. Melatonin is an inhibitor of NLRP3 inflammasome, TLR2, TLR4, TLR9 Toll-like receptors and can be classified as an indirect inhibitor of SARS-CoV-2 and angiotensin-converting enzyme 2 binding. Exogenous melatonin restores aerobic glycolysis by inhibiting hypoxia-inducible factor HIF-1 and mTOR serine-threonine protein kinase, thus reactivating the pyruvate dehydrogenase complex and stimulating the synthesis of acetyl coenzyme A, which in turn contributes to local melatonin production. The drug doses required to alter the intracellular level of melatonin are significantly higher than those used for chronobiotic. The efficacy and tolerability of high-dose melatonin (36-72 mg/day) in addition to standard and/or empirical therapy for COVID-19 pneumonia was determined. Melatonin can be used as an effective therapy for cognitive impairment associated with COVID-19. Clearly, melatonin is a promising adjuvant for therapy of COVID-19 and its complications. © 2021, Media Sphera Publishing Group. All rights reserved.

11.
Tuberculosis and Lung Diseases ; 99(9):6-14, 2021.
Artigo em Russo | Scopus | ID: covidwho-1481270

RESUMO

This literature review presents findings on various aspects of concurrent bronchial asthma and COVID-19. In particular, it discusses issues of bronchial asthma incidence among patients with confirmed COVID-19, the influence of bronchial asthma on the risk of the new coronavirus infection, and the specific course of bronchial asthma in COVID-19 patients. It considers the use of individual components of basic asthma therapy during the pandemic, in particular, inhaled and systemic corticosteroids, antileukotriene drugs, and targeted therapy. The article pays attention to recommendations for the choice of inhalation devices in light of prevention of the new coronavirus infection spread. © 2021 New Terra Publishing House. All rights reserved.

12.
International Journal of Biomedicine ; 11(2):177-180, 2021.
Artigo em Inglês | Scopus | ID: covidwho-1289930

RESUMO

The COVID-19 pandemic has presented challenges to finding effective treatment for lung damage. Medical researchers from different countries recognize the deficiency of pulmonary surfactant (PS) as a significant cause of the alveolar collapse, followed by microatelectasis and severe disturbances in the ventilation-perfusion relationship. Due to the pathophysiological rationale, experimental confirmations, and accumulated clinical experience, the PS preparations can be used to treat patients with severe COVID-19. The article provides a description of a case when surfactant therapy was successfully used in a patient with severe COVID-19 pneumonia.(International Journal of Biomedicine. 2021;11(2):177-180.). © 2021, International Medical Research and Development Corporation. All rights reserved.

13.
Tuberculosis and Lung Diseases ; 99(2):6-15, 2021.
Artigo em Russo | Scopus | ID: covidwho-1184110

RESUMO

The article reviews 60 publications and addresses key aspects of concurrent COVID-19 and chronic obstructive pulmonary disease (COPD). It presents data stating that COPD patients have higher expression of the receptor of angiotensin-converting enzyme 2 in the lungs and this may contribute to a greater susceptibility to COVID-19. In COPD, signs of endothelial cell dysfunction and tendency to thrombus formation have been identified which can present the risk of unfavorable outcomes of COVID-19. Cohort study data do not confirm that COPD patients are more susceptible to SARS-CoV-2 infection, but their clinical outcomes of COVID-19 appear to be worse including the need for mechanical ventilation and lethality. There is no clinical evidence about the role of inhaled glucocorticosteroids used to manage COPD in the development and course of COVID-19. © 2021 New Terra Publishing House. All rights reserved.

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