scholarly journals Echocardiographic-Derived Strain-Area Loop of the Right Ventricle is Related to Pulmonary Vascular Resistance in Pulmonary Arterial Hypertension

2017 ◽  
Vol 10 (10) ◽  
pp. 1286-1288 ◽  
Author(s):  
Hugo G. Hulshof ◽  
Arie P. van Dijk ◽  
Keith P. George ◽  
Daphne Merkus ◽  
Kelly Stam ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial ◽  
The Right

scholarly journals Purinergic Dysfunction in Pulmonary Arterial Hypertension

2020 ◽  
Vol 9 (18) ◽  
Author(s):  
Zongye Cai ◽  
Ly Tu ◽  
Christophe Guignabert ◽  
Daphne Merkus ◽  
Zhichao Zhou
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Remodeling ◽  
Purinergic Signaling ◽  
Receptor Activation ◽  
Pulmonary Vascular Remodeling ◽  
Pulmonary Arterial

Abstract Pulmonary arterial hypertension (PAH) is a life‐threatening disease characterized by increased pulmonary arterial pressure and pulmonary vascular resistance, which result in an increase in afterload imposed onto the right ventricle, leading to right heart failure. Current therapies are incapable of reversing the disease progression. Thus, the identification of novel and potential therapeutic targets is urgently needed. An alteration of nucleotide‐ and nucleoside‐activated purinergic signaling has been proposed as a potential contributor in the pathogenesis of PAH. Adenosine‐mediated purinergic 1 receptor activation, particularly A 2A R activation, reduces pulmonary vascular resistance and attenuates pulmonary vascular remodeling and right ventricle hypertrophy, thereby exerting a protective effect. Conversely, A 2B R activation induces pulmonary vascular remodeling, and is therefore deleterious. ATP‐mediated P2X 7 R activation and ADP‐mediated activation of P2Y 1 R and P2Y 12 R play a role in pulmonary vascular tone, vascular remodeling, and inflammation in PAH. Recent studies have revealed a role of ectonucleotidase nucleoside triphosphate diphosphohydrolase, that degrades ATP/ADP, in regulation of pulmonary vascular remodeling. Interestingly, existing evidence that adenosine activates erythrocyte A 2B R signaling, counteracting hypoxia‐induced pulmonary injury, and that ATP release is impaired in erythrocyte in PAH implies erythrocyte dysfunction as an important trigger to affect purinergic signaling for pathogenesis of PAH. The present review focuses on current knowledge on alteration of nucleot(s)ide‐mediated purinergic signaling as a potential disease mechanism underlying the development of PAH.

scholarly journals RETROSPECTIVE EFFICACY ANALYSIS OF ACUTE VASOREACTIVE TEST AS A CRITERIA FOR SURGERY IN CHILDREN WITH INBORN LEFT-TO-RIGHT BLOOD SHUNTING AND PULMONARY ARTERIAL HYPERTENSION

2018 ◽  
pp. 41-46
Author(s):  
A. Mullen ◽  
G. Butrous ◽  
K. Abzaliev
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Retrospective Analysis ◽  
Vascular Resistance ◽  
Systolic Pressure ◽  
Pulmonary Arterial ◽  
Group 2 ◽  
The Right ◽  
Group 1

Aim. Retrospective analysis of efficacy of the acute vasoreactive test (AVRT) as a criteria for operability of children with inborn left-to-right blood shunting complicated by pulmonary arterial hypertension (IRLBS-PAH), by an experience of one center.Material and methods. Retrospective analysis of the data of right heart chambers catheterization and echocardiographic study from 29 case histories of BS-PAH patients during 2012-2016. Results of AVRT are interpreted by modified Barst criteria (decline of pulmonary vascular resistance index, PVRI, and relation of PVRI to the index of systemic vascular resistance, SVR more than 20%, and the and PVRI <6 Wood units/m2 in PVR/SVR <0,3). In accordance with the results of AVRT, patients were selected to two main groups: group 1 — children with positive response, group 2 — children with negative response. After correction of the inborn defect in bith groups, following assessment of cardiovascular system condition was done by echocardiographical study in one week and one month. Metrics of echocardiography data was indexed. For the defect of interventricular septum (DIVS), indexation of the size was done via the relation to aortic root diameter, that was measured in parasternal position, longitudinal axis. Systolic pressure in the right ventricle was measured by the velocity of tricuspid regurgitation, measured in apical four-chamber position. Mean values with the standard deviation and p-values were calculated in R studio 2017 software, v.1.0.153.Results. Among 29 patients, girls to boys relation was 4,8:1. Mean age 6,0±4,9 y. o. For group 1: median of DIVS 1,4 with the value of additional shunting 9,93±9,39 mm, baseline systolic pressure in the right ventricle (SPRV) 57,96±20,16 mmHg, in one month after surgery 38,96±14,16 mmHg. No complications registered. In the second group, median DIVS 0,4 with additional shunting 3,3±0 mm. Baseline SPRV 66,05±17,27 mmHg, with the decline in one month after transcatheter closure to 57,4±17,35 mmHg. During the early post-surgery period, in 2 patients of group 2 there was pulmonary crisis, treated with inhalatory iloprost. Conclusion. Acute vasoreactive test is effective criteria of operability assessment of inborn left-to-right blood shunting, complicated by pulmonary arterial hypertension, in pediatrics.

scholarly journals Sex Dimorphism in Pulmonary Hypertension: The Role of the Sex Chromosomes

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 779
Author(s):  
Daria S. Kostyunina ◽  
Paul McLoughlin
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Sex Chromosomes ◽  
Bone Morphogenetic Protein 2 ◽  
Sex Dimorphism ◽  
Pulmonary Arterial ◽  
The Impact

Pulmonary hypertension (PH) is a condition characterised by an abnormal elevation of pulmonary artery pressure caused by an increased pulmonary vascular resistance, frequently leading to right ventricular failure and reduced survival. Marked sexual dimorphism is observed in patients with pulmonary arterial hypertension, a form of pulmonary hypertension with a particularly severe clinical course. The incidence in females is 2–4 times greater than in males, although the disease is less severe in females. We review the contribution of the sex chromosomes to this sex dimorphism highlighting the impact of proteins, microRNAs and long non-coding RNAs encoded on the X and Y chromosomes. These genes are centrally involved in the cellular pathways that cause increased pulmonary vascular resistance including the production of reactive oxygen species, altered metabolism, apoptosis, inflammation, vasoconstriction and vascular remodelling. The interaction with genetic mutations on autosomal genes that cause heritable pulmonary arterial hypertension such as bone morphogenetic protein 2 (BMPR2) are examined. The mechanisms that can lead to differences in the expression of genes located on the X chromosomes between females and males are also reviewed. A better understanding of the mechanisms of sex dimorphism in this disease will contribute to the development of more effective therapies for both women and men.

scholarly journals Effects of ovariectomy on antioxidant defence systems in the right ventricle of female rats with pulmonary arterial hypertension induced by monocrotaline

2018 ◽  
Vol 96 (3) ◽  
pp. 295-303 ◽  
Author(s):  
Rafaela Siqueira ◽  
Rafael Colombo ◽  
Adriana Conzatti ◽  
Alexandre Luz de Castro ◽  
Cristina Campos Carraro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Protein Expression ◽  
Arterial Hypertension ◽  
Female Rats ◽  
Antioxidant Defenses ◽  
Thioredoxin 1 ◽  
Pulmonary Arterial ◽  
The Right

The aim of this study was to evaluate the impact of ovariectomy on oxidative stress in the right ventricle (RV) of female rats with pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT). Rats were divided into 4 groups (n = 6 per group): sham (S), sham + MCT (SM), ovariectomized (O), and ovariectomized + MCT (OM). MCT (60 mg·kg−1 i.p.) was injected 1 week after ovariectomy or sham surgery. Three weeks later, echocardiographic analysis and RV catheterisation were performed. RV morphometric, biochemical, and protein expression analysis through Western blotting were done. MCT promoted a slight increase in pulmonary artery pressure, without differences between the SM and OM groups, but did not induce RV hypertrophy. RV hydrogen peroxide increased in the MCT groups, but SOD, CAT, and GPx activities were also enhanced. Non-classical antioxidant defenses diminished in ovariectomized groups, probably due to a decrease in the nuclear factor Nrf2. Hemoxygenase-1 and thioredoxin-1 protein expression was increased in the OM group compared with SM, being accompanied by an elevation in the estrogen receptor β (ER-β). Hemoxygenase-1 and thioredoxin-1 may be involved in the modulation of oxidative stress in the OM group, and this could be responsible for attenuation of PAH and RV remodeling.

scholarly journals The striated muscles in pulmonary arterial hypertension: adaptations beyond the right ventricle

2015 ◽  
Vol 46 (3) ◽  
pp. 832-842 ◽  
Author(s):  
Emmy Manders ◽  
Silvia Rain ◽  
Harm-Jan Bogaard ◽  
M. Louis Handoko ◽  
Ger J.M. Stienen ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Right Heart Failure ◽  
Exercise Intolerance ◽  
Muscle Dysfunction ◽  
Striated Muscles ◽  
Pulmonary Arterial ◽  
The Right ◽  
The Impact

Pulmonary arterial hypertension (PAH) is a fatal lung disease characterised by progressive remodelling of the small pulmonary vessels. The daily-life activities of patients with PAH are severely limited by exertional fatigue and dyspnoea. Typically, these symptoms have been explained by right heart failure. However, an increasing number of studies reveal that the impact of the PAH reaches further than the pulmonary circulation. Striated muscles other than the right ventricle are affected in PAH, such as the left ventricle, the diaphragm and peripheral skeletal muscles. Alterations in these striated muscles are associated with exercise intolerance and reduced quality of life. In this Back to Basics article on striated muscle function in PAH, we provide insight into the pathophysiological mechanisms causing muscle dysfunction in PAH and discuss potential new therapeutic strategies to restore muscle dysfunction.

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