scholarly journals PATHOPHYSIOLOGY IN PULMONARY HEART DISEASES, WITH SPECIAL REFERENCE TO ROLE OF PULMONARY HYPERTENSION, HYPOXEMIA AND RIGHT VENTRICULAR HYPERTROPHY ON RIGHT HEART FAILURE

1974 ◽  
Vol 38 (1) ◽  
pp. 23-31
Author(s):  
TATSUO SATAKE ◽  
KAZUO RYUGE ◽  
TAKEO IIDA
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Special Reference ◽  
Ventricular Hypertrophy ◽  
Heart Diseases ◽  
Right Heart Failure ◽  
Right Ventricular Hypertrophy ◽  
Right Heart

Production and reversibility of right ventricular hypertrophy and right heart failure in dogs

1992 ◽  
Vol 54 (1) ◽  
pp. 104-110 ◽  
Author(s):  
Chia-Ming Hsieh ◽  
Gregory J. Mishkel ◽  
Paulo F.G. Cardoso ◽  
Harry Rakowski ◽  
Stephen C. Dunn ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Right Heart Failure ◽  
Right Ventricular Hypertrophy ◽  
Right Heart

scholarly journals Oxidative Stress, Kinase Activity and Inflammatory Implications in Right Ventricular Hypertrophy and Heart Failure under Hypobaric Hypoxia

2020 ◽  
Vol 21 (17) ◽  
pp. 6421
Author(s):  
Eduardo Pena ◽  
Julio Brito ◽  
Samia El Alam ◽  
Patricia Siques
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Right Ventricular ◽  
Hypobaric Hypoxia ◽  
Ventricular Hypertrophy ◽  
Current Knowledge ◽  
Right Heart Failure ◽  
Right Ventricular Hypertrophy ◽  
Therapeutic Approaches ◽  
Inflammatory Molecules

High altitude (hypobaric hypoxia) triggers several mechanisms to compensate for the decrease in oxygen bioavailability. One of them is pulmonary artery vasoconstriction and its subsequent pulmonary arterial remodeling. These changes can lead to pulmonary hypertension and the development of right ventricular hypertrophy (RVH), right heart failure (RHF) and, ultimately to death. The aim of this review is to describe the most recent molecular pathways involved in the above conditions under this type of hypobaric hypoxia, including oxidative stress, inflammation, protein kinases activation and fibrosis, and the current therapeutic approaches for these conditions. This review also includes the current knowledge of long-term chronic intermittent hypobaric hypoxia. Furthermore, this review highlights the signaling pathways related to oxidative stress (Nox-derived O2.- and H2O2), protein kinase (ERK5, p38α and PKCα) activation, inflammatory molecules (IL-1β, IL-6, TNF-α and NF-kB) and hypoxia condition (HIF-1α). On the other hand, recent therapeutic approaches have focused on abolishing hypoxia-induced RVH and RHF via attenuation of oxidative stress and inflammatory (IL-1β, MCP-1, SDF-1 and CXCR-4) pathways through phytotherapy and pharmacological trials. Nevertheless, further studies are necessary.

P5370Pulmonary pressure overload stimulates cardiac stem or progenitor cell-derived cardiac regeneration in the right ventricular area

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
M Kanda ◽  
T Nagai ◽  
N Kondou ◽  
K Tateno ◽  
M Hirose ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Progenitor Cell ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Free Wall ◽  
Right Heart ◽  
The Right

Abstract Introduction and purpose The number of patients with right heart failure due to pulmonary hypertension has been increasing. Although several drugs have reportedly improved pulmonary hypertension, no treatments have been established for decompensated right heart failure. The heart has an innate ability to regenerate, and cardiac stem or progenitor cells (e.g., side population [SP] cells) have been reported to contribute to the regeneration process. However, their contribution to right ventricular pressure overload has not been clarified. Here, this regeneration process was evaluated using a genetic fate-mapping model. Methods and results We used Cre-LacZ mice, in which more than 99.9% of the cardiomyocytes in the left ventricular field were positive for 5-bromo-4-chloro-3-indolyl-β-D-galactoside (X-gal) staining immediately after tamoxifen injection. Then, we performed either a pulmonary binding (PAB) or sham operation on the main pulmonary tract. In the PAB-treated mice, the right ventricular cavity was significantly enlarged (right-to-left ventricular [RV/LV] ratio, 0.24±0.04 in the sham group and 0.68±0.04 in the PAB group). Increased peak flow velocity in the PAB group (1021±80 vs 1351±62 mm/sec) was confirmed by echocardiography. One month after the PAB, the PAB-treated mice had more X-gal-negative (newly generated) cells than the sham mice (94.8±34.2 cells/mm2 vs 23.1±10.5 cells/mm2; p<0.01). The regeneration was biased in the RV free wall (RV free wall, 225.5±198.7 cells/mm2; septal area, 88.9±56.5/mm2; LV lateral area, 46.8±22.0/mm2; p<0.05). To examine the direct effects of PAB on the cardiac progenitor cells, bromodeoxyuridine was administered to the mice daily until 1 week after the PAB operation. Then, the hearts were isolated and SP cells were harvested. The SP cell population increased from 0.65±0.23% in the sham mice to 1.87% ± 1.18% in the PAB-treated mice. Immunostaining analysis revealed a significant increase in the number of BrdU-positive SP cells, from 11.6±2.0% to 44.0±18%, therefore showing SP cell proliferation. Conclusions Pulmonary pressure overload stimulated cardiac stem or progenitor cell-derived regeneration with a RV bias, and SP cell proliferation may partially contribute to this process. Acknowledgement/Funding JSPS KAKENHI Grant Number JP 17K17636, GSK Japan Research Grant 2016

Effects of chronic treprostinil treatment on experimental right heart hypertrophy and failure

2016 ◽  
Vol 27 (1) ◽  
pp. 90-100 ◽  
Author(s):  
Sofie Axelgaard ◽  
Sarah Holmboe ◽  
Steffen Ringgaard ◽  
Thomas K. Hillgaard ◽  
Stine Andersen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Right Ventricular Function ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Pulmonary Trunk ◽  
Right Ventricular Hypertrophy ◽  
High Dose ◽  
Right Heart

AbstractBackgroundRight heart function is an important predictor of morbidity and mortality in pulmonary arterial hypertension and many CHD. We investigated whether treatment with the prostacyclin analogue treprostinil could prevent pressure overload-induced right ventricular hypertrophy and failure.MethodsMale Wistar rats were randomised to severe pulmonary trunk banding with a 0.5-mm banding clip (n=41), moderate pulmonary trunk banding with a 0.6-mm banding clip (n=36), or sham procedure (n=10). The banded rats were randomised to 6 weeks of treatment with a moderate dose of treprostinil (300 ng/kg/minute), a high dose of treprostinil (900 ng/kg/minute), or vehicle.ResultsPulmonary trunk banding effectively induced hypertrophy, dilatation, and decreased right ventricular function. The severely banded animals presented with decompensated heart failure with extracardial manifestations. Treatment with treprostinil neither reduced right ventricular hypertrophy nor improved right ventricular function.ConclusionsIn the pulmonary trunk banding model of pressure overload-induced right ventricular hypertrophy and failure, moderate- and high-dose treatment with treprostinil did not improve right ventricular function neither in compensated nor in decompensated right heart failure.

scholarly journals Right ventricular dysfunction and pulmonary hypertension: a neglected presentation of thyrotoxicosis

2018 ◽  
Vol 2018 ◽  
Author(s):  
Carolina Shalini Singarayar ◽  
Foo Siew Hui ◽  
Nicholas Cheong ◽  
Goay Swee En
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Newly Diagnosed ◽  
Right Heart

Summary Thyrotoxicosis is associated with cardiac dysfunction; more commonly, left ventricular dysfunction. However, in recent years, there have been more cases reported on right ventricular dysfunction, often associated with pulmonary hypertension in patients with thyrotoxicosis. Three cases of thyrotoxicosis associated with right ventricular dysfunction were presented. A total of 25 other cases of thyrotoxicosis associated with right ventricular dysfunction published from 1994 to 2017 were reviewed along with the present 3 cases. The mean age was 45 years. Most (82%) of the cases were newly diagnosed thyrotoxicosis. There was a preponderance of female gender (71%) and Graves’ disease (86%) as the underlying aetiology. Common presenting features included dyspnoea, fatigue and ankle oedema. Atrial fibrillation was reported in 50% of the cases. The echocardiography for almost all cases revealed dilated right atrial and or ventricular chambers with elevated pulmonary artery pressure. The abnormal echocardiographic parameters were resolved in most cases after rendering the patients euthyroid. Right ventricular dysfunction and pulmonary hypertension are not well-recognized complications of thyrotoxicosis. They are life-threatening conditions that can be reversed with early recognition and treatment of thyrotoxicosis. Signs and symptoms of right ventricular dysfunction should be sought in all patients with newly diagnosed thyrotoxicosis, and prompt restoration of euthyroidism is warranted in affected patients before the development of overt right heart failure. Learning points: Thyrotoxicosis is associated with right ventricular dysfunction and pulmonary hypertension apart from left ventricular dysfunction described in typical thyrotoxic cardiomyopathy. Symptoms and signs of right ventricular dysfunction and pulmonary hypertension should be sought in all patients with newly diagnosed thyrotoxicosis. Thyrotoxicosis should be considered in all cases of right ventricular dysfunction or pulmonary hypertension not readily explained by other causes. Prompt restoration of euthyroidism is warranted in patients with thyrotoxicosis complicated by right ventricular dysfunction with or without pulmonary hypertension to allow timely resolution of the abnormal cardiac parameters before development of overt right heart failure.

scholarly journals Acute decompensated pulmonary hypertension

2017 ◽  
Vol 26 (146) ◽  
pp. 170092 ◽  
Author(s):  
Laurent Savale ◽  
Jason Weatherald ◽  
Xavier Jaïs ◽  
Constance Vuillard ◽  
Athénaïs Boucly ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Life Support ◽  
Extracorporeal Life Support ◽  
Right Heart Failure ◽  
Right Heart ◽  
Adaptation Capacity ◽  
Ventricular Afterload ◽  
Time Specific

Acute right heart failure in chronic precapillary pulmonary hypertension is characterised by a rapidly progressive syndrome with systemic congestion resulting from impaired right ventricular filling and/or reduced right ventricular flow output. This clinical picture results from an imbalance between the afterload imposed on the right ventricle and its adaptation capacity. Acute decompensated pulmonary hypertension is associated with a very poor prognosis in the short term. Despite its major impact on survival, its optimal management remains very challenging for specialised centres, without specific recommendations. Identification of trigger factors, optimisation of fluid volume and pharmacological support to improve right ventricular function and perfusion pressure are the main therapeutic areas to consider in order to improve clinical condition. At the same time, specific management of pulmonary hypertension according to the aetiology is mandatory to reduce right ventricular afterload. Over the past decade, the development of extracorporeal life support in refractory right heart failure combined with urgent transplantation has probably contributed to a significant improvement in survival for selected patients. However, there remains a considerable need for further research in this field.

scholarly journals Levosimendan in pulmonary hypertension and right heart failure

2018 ◽  
Vol 8 (3) ◽  
pp. 204589401879090 ◽  
Author(s):  
Mona Sahlholdt Hansen ◽  
Asger Andersen ◽  
Jens Erik Nielsen-Kudsk
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Current Knowledge ◽  
Right Heart Failure ◽  
Morbidity And Mortality ◽  
High Morbidity ◽  
Ventricular Failure ◽  
Right Heart ◽  
Pharmacodynamic Profile

Pulmonary hypertension is a multifactorial disease with a high morbidity and mortality. Right ventricular function is the most important predictor of morbidity and mortality in patients suffering from pulmonary hypertension, but currently there are no approved treatments directly supporting the failing right ventricle. Levosimendan is a calcium sensitizing agent with inotropic, pulmonary vasodilatory, and cardioprotective properties. Given its pharmacodynamic profile, levosimendan could be a potential novel agent for the treatment of right ventricular failure caused by pulmonary hypertension. The aim of this review is to provide an overview of the current knowledge on the effects of levosimendan in pulmonary hypertension and right heart failure.

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