Three-Dimensional Modeling of the Right Ventricle from Two-Dimensional Transthoracic Echocardiographic Images: Utility of Knowledge-Based Reconstruction in Pulmonary Arterial Hypertension

2013 ◽  
Vol 26 (8) ◽  
pp. 860-867 ◽  
Author(s):  
Nicole M. Bhave ◽  
Amit R. Patel ◽  
Lynn Weinert ◽  
Megan Yamat ◽  
Benjamin H. Freed ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Three Dimensional ◽  
Two Dimensional ◽  
Knowledge Based ◽  
Three Dimensional Modeling ◽  
Dimensional Modeling ◽  
Pulmonary Arterial ◽  
Echocardiographic Images ◽  
The Right

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.

Mechanisms of right ventricular failure

ESC CardioMed ◽  
2018 ◽  
pp. 2493-2495
Author(s):  
Joanne A. Groeneveldt ◽  
Anton Vonk Noordegraaf ◽  
Frances S. de Man
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Right Ventricular Dysfunction ◽  
Right Ventricular Failure ◽  
Ventricular Failure ◽  
Adaptive Mechanisms ◽  
Patient Will ◽  
Pulmonary Arterial ◽  
The Right

In pulmonary arterial hypertension, afterload on the right ventricle is increased. Due to several adaptive mechanisms, the right ventricle is able to cope with a three- to fivefold increase in afterload. However, when adaptive mechanisms are no longer sufficient to compensate for this increase, the patient will develop right ventricular dysfunction and failure. This chapter provides an overview of mechanisms currently considered as having important roles in right ventricular adaptation and right ventricular failure.

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