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.

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

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 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.

scholarly journals Right heart failure in pulmonary hypertension: Diagnosis and new perspectives on vascular and direct right ventricular treatment

2019 ◽  
Vol 178 (1) ◽  
pp. 90-107 ◽  
Author(s):  
Khodr Tello ◽  
Werner Seeger ◽  
Robert Naeije ◽  
Rebecca Vanderpool ◽  
Hossein Ardeschir Ghofrani ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Right Heart Failure ◽  
Right Heart ◽  
Hypertension Diagnosis

Persistent pulmonary hypertension results in reduced tetralinoleoyl-cardiolipin and mitochondrial complex II + III during the development of right ventricular hypertrophy in the neonatal pig heart

2011 ◽  
Vol 301 (4) ◽  
pp. H1415-H1424 ◽  
Author(s):  
Harjot K. Saini-Chohan ◽  
Shyamala Dakshinamurti ◽  
William A. Taylor ◽  
Garry X. Shen ◽  
Robert Murphy ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Weight Ratio ◽  
Right Heart Failure ◽  
Persistent Pulmonary Hypertension ◽  
Mitochondrial Complex ◽  
Right Heart ◽  
Complex Ii ◽  
Mitochondrial Respiratory

Persistent pulmonary hypertension of the newborn (PPHN) results in right ventricular (RV) hypertrophy followed by right heart failure and an associated mitochondrial dysfunction. The phospholipid cardiolipin plays a key role in maintaining mitochondrial respiratory and cardiac function via modulation of the activities of enzymes involved in oxidative phosphorylation. In this study, changes in cardiolipin and cardiolipin metabolism were investigated during the development of right heart failure. Newborn piglets (<24 h old) were exposed to a hypoxic (10% O2) environment for 3 days, resulting in the induction of PPHN. Two sets of control piglets were used: 1) newborn or 2) exposed to a normoxic (21% O2) environment for 3 days. Cardiolipin biosynthetic and remodeling enzymes, mitochondrial complex II + III activity, incorporation of [1-14C]linoleoyl-CoA into cardiolipin precursors, and the tetralinoleoyl-cardiolipin pool size were determined in both the RV and left ventricle (LV). PPHN resulted in an increased heart-to-body weight ratio, RV-to-LV plus septum weight ratio, and expression of brain naturetic peptide in RV. In addition, PPHN reduced cardiolipin biosynthesis and remodeling in the RV and LV, which resulted in decreased tetralinoleoyl-cardiolipin levels and reduced complex II + III activity and protein levels of mitochondrial complexes II, III, and IV in the RV. This is the first study to examine the pattern of cardiolipin metabolism during the early development of both the RV and LV of the newborn piglet and to demonstrate that PPHN-induced alterations in cardiolipin biosynthetic and remodeling enzymes contribute to reduced tetralinoleoyl-cardiolipin and mitochondrial respiratory chain function during the development of RV hypertrophy. These defects in cardiolipin may play an important role in the rapid development of RV dysfunction and right heart failure in PPHN.

Myocyte cytoskeletal disorganization and right heart failure in hypoxia-induced neonatal pulmonary hypertension

2000 ◽  
Vol 279 (3) ◽  
pp. H1365-H1376 ◽  
Author(s):  
Matthew S. Lemler ◽  
Roger D. Bies ◽  
Maria G. Frid ◽  
Amornrate Sastravaha ◽  
Lawrence S. Zisman ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Total Content ◽  
Immunohistochemical Analysis ◽  
Right Heart Failure ◽  
Barometric Pressure ◽  
Ventricular Myocardium ◽  
Cytoskeletal Proteins ◽  
Right Heart

Previous studies have demonstrated that environmentally or genetically induced changes in the intracellular proteins that compose the cytoskeleton can contribute to heart failure. Because neonatal right ventricular myocytes are immature and are in the process of significant cytoskeletal change, we hypothesized that they may be particularly susceptible to pressure stress. Newborn calves exposed to hypobaric hypoxia (barometric pressure = 430 mmHg) for 14 days developed severe pulmonary hypertension (pulmonary arterial pressure = 101 ± 6 vs. 27 ± 1 mmHg) and right heart failure compared with age-matched controls. Light microscopy showed partial loss of myocardial striations in the failing neonatal right but not left ventricles and in neither ventricle of adolescent cattle dying of altitude-induced right heart failure. In neonatal calves, immunohistochemical analysis of the cytoskeletal proteins (vinculin, metavinculin, desmin, vimentin, and cadherin) showed selectively, within the failing right ventricles, patchy areas characterized by loss and disorganization of costameres and intercalated discs. Within myocytes from the failing ventricles, vinculin and desmin were observed to redistribute diffusely within the cytosol, metavinculin appeared in disorganized clumps, and vimentin immunoreactivity was markedly decreased. Western blot analysis of the failing right ventricular myocardium showed, compared with control, vinculin and desmin to be little changed in total content but redistributed from insoluble (structural) to soluble (cytosolic) fractions; metavinculin total content was markedly decreased, tubulin content increased, particularly in the structural fraction, and cadherin total content and distribution were unchanged. We conclude that hypoxic pulmonary hypertensive-induced neonatal right ventricular failure is associated with disorganization of the cytoskeletal architecture.

Circulatory responses to high altitude in the cat and rabbit

1963 ◽  
Vol 18 (3) ◽  
pp. 575-579 ◽  
Author(s):  
John T. Reeves ◽  
Estelle B. Grover ◽  
Robert F. Grover
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
High Altitude ◽  
Oxygen Transport ◽  
Right Heart Failure ◽  
Blood Oxygenation ◽  
Right Heart ◽  
Arterial Blood ◽  
Mixed Venous

Cats were taken from Denver (5,200 ft.) to Mt. Evans (14,150 ft.) anticipating that this degree of hypoxia would induce pulmonary hypertension. Rabbits were included for comparison with the cat. All cats died without developing pulmonary hypertension or right heart failure, and in spite of arterial and mixed venous O2 tensions maintained well above those of the rabbit. Presumably the cat's failure to survive was not a failure of oxygen transport to the arterial blood, or to the systemic capillaries. Paradoxically, five of eight rabbits survived despite poor arterial blood oxygenation. The rabbits developed marked polycythemia associated with modest right ventricular hypertension and dilatation. Submitted on June 6, 1962

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