Multifactorial analysis of differential diagnostic parameters in patients with moderate bronchial asthma with pulmogenic arterial hypertension and essential arterial hypertension

2020 ◽  
Vol 21 (4) ◽  
pp. 135-139
Author(s):  
O. V. Shevchenko ◽  
◽  
V. F. Ushakov ◽  
E. V. Sadrieva ◽  
T. V. Zuevskaya ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Bronchial Asthma ◽  
Heart Function ◽  
Systolic Pressure ◽  
Cold Test ◽  
Gas Composition ◽  
Asthma Patients ◽  
Essential Arterial Hypertension ◽  
Group 1

Objective: to analyze differential diagnostic parameters in patients with moderate bronchial asthma with pulmogenic arterial hypertension with essential arterial hypertension. Material and Methods: 25 patients with moderate bronchial asthma with pulmogenic arterial hypertension (the 1st group) and 25 patients with moderate bronchial asthma with essential arterial hypertension (the 2nd group) were included in the study. Both groups of patients received step therapy (berodual + inhaled glucocorticosteroids). All patients underwent complex ultrasound examination of intracardiac hemodynamics, examination of blood flow in the right ventricle excretory tract. Systemic arterial pressure was measured according to N. S. Korotkov’s method. ECG was studied (24-hour monitoring). Cold test (at -20 °C-40 °C) was performed in both groups of patients, blood gas composition and pulmonary ventilation function indices were studied. Results: As a result of research established reliable differences in the spirographic indices, blood gas composition in patients with moderate bronchial asthma with pulmogenic arterial hypertension (the 1st group), and reliable differences in partial pressure of oxygen and carbon dioxide (p < 0,05). The 1st group of patients has also higher values of PaCO2 and reliably (p < 0,0,5) and lower values of PaO2, SaO2 in comparison with the comparison group of patients with bronchial asthma of average severity with essential arterial hypertension (the 2nd group). Our data have shown, that in the 1st and 2nd group patients systolic-diastolic cardiac function indexes reliably (p < 0,05; p < 0,001) differed from those ones in healthy subjects. At the same time systolic pressure in the pulmonary artery in the 1st group patients was higher than in the 2nd group patients, and left ventricular ejection fraction was significantly different from that in healthy people and was lower in the 1st group patients than in the 2nd group. We have revealed a reliable correlation between systolic blood pressure and Sа02 (r = 0,52, p < 0,05), studied after cold test, which confirmed the hypothesis of the formation of pulmogenic arterial hypertension against the background of hypoxia. More pronounced changes of FEV1, Sа02, systolic blood pressure in group 1 patients were to some extent due to significant cold hyperresponsiveness in this category of patients. Conclusions: the results of our studies have shown that the decrease of FEV1, FEV50, FEV75, PaO2, SaO2, increased systolic pressure in the pulmonary artery, signs of right heart hypertrophy, disturbances of systolic-diastolic heart function were more pronounced in moderate bronchial asthma patients with pulmogenic arterial hypertension than in moderate bronchial asthma patients with essential arterial hypertension. The proportion of patients (in %) with rhythm disturbances, especially sinus tachycardia, extrasystoles were detected significantly more frequently in group 1 patients than in group 2 patients, which was due to a more pronounced disturbance of systolic-diastolic heart function, higher systolic pressure in the pulmonary artery in persons with moderate bronchial asthma with pulmogenic arterial hypertension.

Beta3-adrenergic stimulation restores endothelial mitochondrial dynamics and prevents pulmonary arterial hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
E Oliver ◽  
S.F Rocha ◽  
M Spaczynska ◽  
D.V Lalama ◽  
M Gomez ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Therapeutic Strategy ◽  
Mitochondrial Dynamics ◽  
Systolic Pressure ◽  
Funding Source ◽  
Pulmonary Arterial

Abstract Background Endothelial dysfunction is one of the most important hallmarks of pulmonary arterial hypertension (PAH). This leads to anomalous production of vasoactive mediators that are responsible for a higher vascular tone and a subsequent increase in pulmonary artery pressure (PAP), and to an increased vascular permeability that favors perivascular inflammation and remodeling, thus worsening the disease. Therefore, preservation of the endothelial barrier could become a relevant therapeutic strategy. Purpose In previous studies, others and we have suggested the pharmacological activation of the β3-adrenergic receptor (AR) as a potential therapeutic strategy for pulmonary hypertension (PH) due to left heart disease. However, its potential use in other forms of PH remain unclear. The aim of the present study was to elucidate whether the β3-AR agonist mirabegron could preserve pulmonary endothelium function and be a potential new therapy in PAH. Methods For this purpose, we have evaluated the effect of mirabegron (2 and 10 mg/kg·day) in different animal models, including the monocrotaline and the hypoxia-induced PAH models in rats and mice, respectively. Additionally, we have used a transgenic mouse model with endothelial overexpression of human β3-AR in a knockout background, and performed in vitro experiments with human pulmonary artery endothelial cells (HPAECs) for mechanistic experiments. Results Our results show a dose dependent effect of mirabegron in reducing mean PAP and Right Ventricular Systolic Pressure in both mice and rats. In addition, the use of transgenic mice has allowed us to determine that pulmonary endothelial cells are key mediators of the beneficial role of β3-AR pathway in ameliorating PAH. Mechanistically, we have shown in vitro that activation of β3-AR with mirabegron protects HPAECs from hypoxia-induced ROS production and mitochondrial fragmentation by restoring mitochondrial fission/fusion dynamics. Conclusions This protective effect of mirabegron would lead to endothelium integrity and preserved pulmonary endothelial function, which are necessary for a correct vasodilation, avoiding increased permeability and remodeling. Altogether, the current study demonstrates a beneficial effect of the β3-AR agonist mirabegron that could open new therapeutic avenues in PAH. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Programa de Atracciόn de Talento, Comunidad de Madrid

Abstract 532: New Agonist of A2a Receptor Reduces Ventricular and Vascular Dysfunction in Monocrotaline-induced Pulmonary Arterial Hypertension in Rats

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Allan K Alencar ◽  
Sharlene L Pereira ◽  
Arthur E Kummerle ◽  
Sharon S Langraf ◽  
Celso Caruso-Neves ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Vascular Reactivity ◽  
Vascular Dysfunction ◽  
Systolic Pressure ◽  
Pulmonary Tissue ◽  
A2a Receptor ◽  
Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is characterized by enhanced pulmonary vascular resistance with subsequent remodeling and right ventricular hypertrophy. Vascular reactivity and ventricular function were investigated in rats with monocrotaline-induced PAH and treated with a new N-acylhydrazone derivative named as LASSBio-1359. METHODS: Protocols were approved by Animal Care and Use Committee at Universidade Federal do Rio de Janeiro. Male Wistar rats received a single i.p. injection of monocrotaline (MCT) (60 mg/kg) for PAH induction and were randomly divided in groups which were treated with: saline, vehicle and LASSBio-1359 (50 mg/kg p.o.). After 14 days of treatment, some parameters were evaluated: pulmonary acceleration time (PAT); right ventricular systolic pressure (RVSP); vascular reactivity to acetylcholine; expression of iNOS in pulmonary tissue; wall thickness of pulmonary artery (PAWT). Results: PAT (ms) was increased from 26.2 ± 2.8 to 41.3 ± 3.9 in PAH group treated with vehicle (n=8, p<0.05) and was reduced to 24.2 ± 1.7 when PAH group was treated with LASSBio-1359. RVSP (mmHg) increased from 26.0 ± 2.0 to 55.2 ± 2.3 in PAH group (p<0.05) but was similar to control after treatment with LASSBio-1359 (31.8 ± 2.3 mm Hg). Ratio of right ventricle and body weight (mg/g) was 0.66 ± 0.02, 1.63 ± 0.16 and 0.87 ± 0.10 for control, vehicle- and LASSBio-1359-treated PAH groups, respectively. PAH promoted ventricular dysfunction which was reduced by LASSBio-1359. The pulmonary artery maximum relaxation (%) was 57.3 ± 5.5, 43.6 ± 1.2 and 61.4 ± 8.4 for control, vehicle and LASSBio-1359-treated groups indicating that PAH promoted endothelium injury which was recovered by LASSBio-1359. iNOS expression in pulmonary tissue was increased from 0.48 ± 1.31 to 0.98 ± 3.14 in PAH group and reduced to 0.53 ± 1.83 in rats treated with LASSBio-1359. The PAWT (%) were increased from 74.1 ± 1.3 to 90.2 ± 2.7 in PAH group (p<0.05) but was 74.4 ± 1.3 when treated with LASSBio-1359. This compound showed an in vitro vasodilatory activity mediated by activation of adenosinergic A2A receptor. Conclusion: LASSBio-1359 reduced ventricular and vascular dysfunction in monocrotaline-induced PAH in rats indicating a possible new alternative to treat PAH.

scholarly journals FEATURES OF CYTOKINE PROFILE IN PATIENTS WITH BRONCHIAL ASTHMA COMBINED WITH OBESITY

2018 ◽  
Vol 20 (6) ◽  
pp. 913-920
Author(s):  
M. V. Antonyuk ◽  
T. A. Gvozdenko ◽  
T. P. Novgorodtseva ◽  
T. I. Vitkina ◽  
B. I. Geltser ◽  
...  
Keyword(s):  
Body Weight ◽  
Bronchial Asthma ◽  
Cytokine Profile ◽  
Control Group ◽  
Observation Group ◽  
Normal Body ◽  
Asthma Patients ◽  
Normal Body Weight ◽  
Anti Inflammatory ◽  
Group 1

Combination of bronchial asthma (BA) and obesity is a difficult-to-control phenotype. Studies of inflammatory process with respect to severity of the disease are important for understanding the potential influence of obesity on the BA clinical course. The objective of this study was to determine cytokine profile in patients with mild BA combined with obesity. The study involved fifty-three patients with partially controlled mild BA. The patients were recruited as volunteers and signed an informed consent. The first observation group consisted of 27 asthma patients with normal body weight, the second observation group consisted of 26 patients with BA combined with obesity. A control group included 25 healthy volunteers. All the patients underwent clinical and laboratory examination in accordance with clinical standards for BA and obesity. The levels of TNFα, IL-2, IL-4, IL-6, IL-10 were evaluated in blood serum by means of flow cytometry. The ratios of proand anti-inflammatory cytokines (TNFα/IL-4, TNFα/IL-10, IL-6/IL-4, IL-6/IL-10) were calculated. Asthma patients with obesity (the 2nd group) had elevated levels of IL-2 over control group and group 1, by 38% and 44% respectively(p < 0.05). The concentration of proinflammatory cytokines TNFα and IL-6 was significanty increased in the both patient groups. Mean TNFα level was increased 2.5 times (p < 0.05), and IL-6 levels were increased by 30% (p < 0.05) in the 1st group as compared to the controls. TNFα and IL-6 concentrations showed a 3-fold increase over control values (p < 0.05) in the 2nd group. The level of antiinflammatory cytokine IL-4 was increased in patients with BA, independently of body mass. It should be noted that the concentration of this cytokine in obese patients was higher by 29% than in patients with normal body weight. IL-10 levels in patients from the 2nd group were reduced more than 2 times than in the 1st group. The patients of the 1st group showed a decrease in the IL-6/IL-10 index, in comparison with control parameters, thus indicative of an imbalance due to the elevation of the anti-inflammatory IL-10 cytokine. Among BA patients with obesity (group 2) the TNFα/IL-10 and IL-6/IL-10 indexes were higher than those of the control group (2.3- and 5.5-fold, respectively) and the group 1 (2.6- and 2.5-fold, respectively). Dynamics of these indexes confirms the systemic nature of inflammation and a predominance of non-atopic  inflammation in asthma patients with obesity. Thus, features of the cytokine profile in BA with obesity consist of a significant increase in pro-inflammatory IL-2, IL-6, TNFα cytokines, and a relative decrease in anti-inflammatory IL- 10 cytokine. The development of BA with obesity, even in mild-severity BA, is accompanied by development of a cytokine disbalance, which is typical for a mixed-type inflammation, with a prevalence of neutrophil inflammation. 

scholarly journals Pulmonary hypertension as a risk assessment factor for unfavorable outcome in patients with COVID-19

2020 ◽  
Vol 25 (12) ◽  
pp. 4136
Author(s):  
E. Z. Golukhova ◽  
Inessa Viktorovna Slivneva ◽  
M. M. Rybka ◽  
M. L. Mamalyga ◽  
M. N. Alekhin ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Pulmonary Artery ◽  
Mortality Risk ◽  
Systolic Pressure ◽  
Unfavorable Outcome ◽  
Diagnostic Methods ◽  
Pulmonary Hemodynamics ◽  
Organ System Failure ◽  
Group 3 ◽  
Group 1

Aim. To determine the predictive role of estimated pulmonary artery systolic pressure (ePASP) in COVID-19 patients.Material and methods. A retrospective study of inpatients with documented COVID-19 infection was carried out. Maximal follow-up period was 63 days. The study included 108 patients (men, 62; women, 46; mean age, 62,9±15,5 years). At admission, mean NEWS score was 6,0, blood oxygen saturation — 92%. Echocardiography was performed according to standard protocol using Vivid E9 ultrasound system (GE Healthcare). Quantitative measurements were performed according to the current ASE and EACVI guidelines. Statistical analysis was performed using the IBM SPSS Statistics v.26 software (developed by IBM Corporation).Results. Using the CHAID technique, a classification tree was developed and the strongest predictor of an unfavorable outcome was determined (ePASP). Threshold ePASP values, associated with an increased mortality risk were established (42 mm Hg and 50 mm Hg). Three groups of patients were selected based on the main predictor (<41,0 mm Hg, 42-49 mm Hg and >50 mm Hg). The increased mortality risk was noted in groups 2 and 3 compared to group 1 of patients and amounted to 31,8% and 70% versus 3,9%, respectively. There was also a correlation between the severity of CT lung parenchymal lesions according to computed tomography and the study groups of patients (36% [30-49%] — group 1, 50% [36-76%] — group 2, and 84% [56-92%] — group 3, p=0,001). In groups 2 and 3, the following complications were significantly more frequent: acute respiratory distress syndrome, acute heart failure, multiple organ system failure, venous thrombosis, disseminated intravascular coagulation. In group 3, acute renal failure and systemic inflammatory response syndrome developed significantly more often than in group 1.Conclusion. A comprehensive echocardiography has proven its availability and safety in assessing the condition of COVID-19 patients, allowing to obtain relevant information on pulmonary hemodynamics. Transthoracic echocardiography reduced the risk of complications from invasive diagnostic methods and allowed to abandon the use of the Swan-Ganz pulmonary artery catheter in the studied group of patients. As a result, a relationship was noted between the increase of ePASP and the severity of clinical performance and lung tissue damage according to computed tomography, changes in laboratory blood tests, the severity of the comorbid profile, an increase in respiratory support need.

scholarly journals Distribution of Polymorphic Marker of Genes of the Renin-angiotensin System RAS (AGT, AGTR1, АСЕ), ITGB3, PPARG) in Pa-tients With Essential Arterial Hypertension Depending on the Nature of the Nocturnal De-crease of BP

2021 ◽  
Vol 15 ◽  
pp. 212-218
Author(s):  
T. Yu. Zotova ◽  
M. M. Azova ◽  
A. A. Lukanina ◽  
A. Ait Aissa ◽  
M. L. Blagonravov
Keyword(s):  
Insulin Resistance ◽  
Arterial Hypertension ◽  
Renin Angiotensin System ◽  
Population Data ◽  
Clinical Genetic ◽  
Autonomic Nervous System Dysfunction ◽  
Genotype Frequencies ◽  
Essential Arterial Hypertension ◽  
Group 2 ◽  
Group 1

A clinical-genetic study using ABPM (24-hour BP monitoring) and Holter’s ECG methods in 49 pa-tients with essential arterial hypertension (group 1: 17 patients without sufficient nocturnal BP de-crease СI≤10%, and group 2: 32 patients with suf-ficient nocturnal BP decrease СI≥10%,) was per-formed for comparative analysis of the genotype frequencies of ACE, AGT, AGTR1, ITGB3, and PPARG. The study was conducted in order to clari-fy the pathogenetic mechanisms of the implementa-tion of different dynamics of nocturnal blood pres-sure in patients with hypertension without metabol-ic syndrome. It was found that in group 1, protec-tive genotype II of the ACE gene was more com-mon (p ≤ 0.025) than in the population data. A sig-nificant increase (p ≤ 0.025) in the frequency of the CC genotype of the AGTR1 gene responsible for the formation of insulin resistance compared to the population data was combined with a significant increase in the frequency of autonomic dysfunction in patients of group 1 - 83.4% vs. 64.5% group 2 respectively. The results obtained indicate the pos-sible pathogenetic links between genetically deter-mined insulin resistance and autonomic nervous system dysfunction and allows us to determine therapeutic approaches for correcting the noctur-nal blood pressure profile.

scholarly journals Platelet glycolytic metabolism correlates with hemodynamic severity in pulmonary arterial hypertension

2020 ◽  
Vol 318 (3) ◽  
pp. L562-L569
Author(s):  
Ruth E. McDowell ◽  
Kulwant S. Aulak ◽  
Allaa Almoushref ◽  
Celia A. Melillo ◽  
Brittany E. Brauer ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Time Window ◽  
Healthy Controls ◽  
Metabolic Shift ◽  
Glycolytic Metabolism ◽  
Pulmonary Arterial ◽  
Group 2 ◽  
Group 1

Group 1 pulmonary hypertension (PH), i.e., pulmonary arterial hypertension (PAH), is associated with a metabolic shift favoring glycolysis in cells comprising the lung vasculature as well as skeletal muscle and right heart. We sought to determine whether this metabolic switch is also detectable in circulating platelets from PAH patients. We used Seahorse Extracellular Flux to measure bioenergetics in platelets isolated from group 1 PH (PAH), group 2 PH, patients with dyspnea and normal pulmonary artery pressures, and healthy controls. We show that platelets from group 1 PH patients exhibit enhanced basal glycolysis and lower glycolytic reserve compared with platelets from healthy controls but do not differ from platelets of group 2 PH or dyspnea patients without PH. Although we were unable to identify a glycolytic phenotype unique to platelets from PAH patients, we found that platelet glycolytic metabolism correlated with hemodynamic severity only in group 1 PH patients, supporting the known link between PAH pathology and altered glycolytic metabolism and extending this association to ex vivo platelets. Pulmonary artery pressure and pulmonary vascular resistance in patients with group 1 PH were directly associated with basal platelet glycolysis and inversely associated with maximal and reserve glycolysis, suggesting that PAH progression reduces the capacity for glycolysis even while demanding an increase in glycolytic metabolism. Therefore, platelets may provide an easy-to-harvest, real-time window into the metabolic shift occurring in the lung vasculature and represent a useful surrogate for interrogating the glycolytic shift central to PAH pathology.

scholarly journals The Effects of Dexmedetomidine Prescription in Paediatric Patients With Pulmonary Hypertension Under Congenital Heart Surgery

2020 ◽  
Author(s):  
Bahram Ghasemzadeh ◽  
Bahador Azizi ◽  
Simin Azemati ◽  
Mostafa Bagherinasab
Keyword(s):  
Blood Pressure ◽  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Pulmonary Artery ◽  
Arterial Hypertension ◽  
Systolic Blood Pressure ◽  
Systolic Pressure ◽  
Pulmonary Artery Systolic Pressure ◽  
Anesthetic Care ◽  
Pulmonary Arterial

Anesthetized patient management for pediatric patients with pulmonary arterial hypertension (PAH) is a major challenge. The aim of this study was to evaluate the ability of dexmedetomidine to reduce pulmonary arterial hypertension in patients with pulmonary arterial hypertension undergoing cardiac surgery. Sixty-six patients with pulmonary arterial hypertension underwent the study. Patients were randomly divided into two groups: group D received a dexmedetomidine injection in a dose of 1 μg/kg in the first hour and then decreased to 0.5 μg/kg/hr, injection continued after surgery until extubation in the post-anesthetic care unit (PACU). Group C received normal saline 0.9% in a similar volume. Pulmonary artery systolic pressure (PASP) and systemic systolic blood pressure (SSBP) were recorded during and after the surgery in the postanesthetic care unit. Needing vasodilators, sedatives, extubation time, and the length of ICU stay were recorded for all patients. Patients in the dexmedetomidine group showed a significant reduction in Pulmonary artery systolic pressure and Pulmonary artery systolic pressure/systemic systolic blood pressure rates during surgery and during the first 24 hours in the post-anesthetic care unit (P<0.001). The dexmedetomidine group, in comparison with the control group, needed a significantly lower dose of a vasodilator (P<0.001) and a lower dose of sedation (P<0.001). It is concluded that the use of dexmedetomidine during the surgery in children with pulmonary hypertension reduces pulmonary artery systolic pressure during and after the surgery.

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