Letter by Legchenko et al Regarding Article, “Transcriptomic Analysis of Right Ventricular Remodeling in Two Rat Models of Pulmonary Hypertension: Identification and Validation of Epithelial-to-Mesenchymal Transition in Human Right Ventricular Failure”

2021 ◽  
Author(s):  
Ekaterina Legchenko ◽  
Philippe Chouvarine ◽  
Georg Hansmann
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Epithelial To Mesenchymal Transition ◽  
Ventricular Remodeling ◽  
Right Ventricular Failure ◽  
Ventricular Failure ◽  
Human Right ◽  
Mesenchymal Transition ◽  
Rat Models ◽  
Right Ventricular Remodeling

scholarly journals Current Knowledge and Recent Advances of Right Ventricular Molecular Biology and Metabolism from Congenital Heart Disease to Chronic Pulmonary Hypertension

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Samantha Guimaron ◽  
Julien Guihaire ◽  
Myriam Amsallem ◽  
François Haddad ◽  
Elie Fadel ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Congenital Heart ◽  
Ventricular Remodeling ◽  
Heart Diseases ◽  
Right Ventricular Failure ◽  
Congenital Heart Diseases ◽  
Ventricular Failure ◽  
Right Ventricular Remodeling

Studies about pulmonary hypertension and congenital heart diseases have introduced the concept of right ventricular remodeling leading these pathologies to a similar outcome: right ventricular failure. However right ventricular remodeling is also a physiological process that enables the normal fetal right ventricle to adapt at birth and gain its adult phenotype. The healthy mature right ventricle is exposed to low pulmonary vascular resistances and is compliant. However, in the setting of chronic pressure overload, as in pulmonary hypertension, or volume overload, as in congenital heart diseases, the right ventricle reverts back to a fetal phenotype to sustain its function. Mechanisms include angiogenic changes and concomitant increased metabolic activity to maintain energy production. Eventually, the remodeled right ventricle cannot resist the increased afterload, leading to right ventricular failure. After comparing the fetal and adult healthy right ventricles, we sought to review the main metabolic and cellular changes occurring in the setting of PH and CHD. Their association with RV function and potential impact on clinical practice will also be discussed.

Abstract P150: Estrogen Protects Against and Reverses Adverse Ventricular Remodeling in Pulmonary Hypertension-Induced Right Ventricular Failure

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Rangarajan D Nadadur ◽  
Soban Umar ◽  
Andrea Iorga ◽  
Humann Matori ◽  
Rod Partow-Navid ◽  
...  
Keyword(s):  
Gender Differences ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Remodeling ◽  
Right Ventricular Failure ◽  
Female Rats ◽  
Male Rats ◽  
Protective Effects ◽  
Ventricular Failure ◽  
Male And Female Rats

Pulmonary hypertension (PH) leads to right-ventricular failure (RVF). RVF is characterized by adverse RV remodeling including hypertrophy and changes in the cardiac Extracellular Matrix (ECM) such as fibrosis and re-expression of cardiac fetal genes. Among the potentially re-expressed genes are the novel ECM interacting proteins Osteopontin (OPN) and Osteocalcin (OCN). Gender differences found in experimental PH are attributed to protective effects of Estrogen (E2). We hypothesize that gender differences observed in experimental PH are partially due to the effects of E2 on the cardiac ECM, and that exogenous E2 may be able to reverse adverse RV remodeling. Male and female rats received single monocrotaline (MCT, 60mg/kg) injection. Some rats were given E2 (42.5μg/kg/day) from day 21–30. Saline treated rats were controls. Cardiopulmonary hemodynamics were serially monitored and RV pressures (RVP) were recorded terminally. RV fibrosis was assessed by trichrome staining. Gene expression was determined by RT PCR and plasma OPN by ELISA. All rats developed PH by day 21 and RVF by day 30. Male rats developed more severe PH-induced RVF than females (RVP=70 vs. 41.5±5 mmHg; RV/(LV+IVS)= 0.69±0.07 vs. 0.47±0.04; RVEF = 30.4±1.8 vs. 42.8±2% resp., all p<0.05). Males also revealed more severe RV fibrosis and greater re-expression of OPN (4.5 fold vs. females, p<0.05) and OCN (2-fold vs. females, p<0.05). Plasma OPN was also elevated in RVF males (1.00±0.11 in control to 1.47±0.18 pg/ml, p<0.05) but not RVF females (0.848±0.18 in control to 0.859±0.294 pg/ml, p=ns). Since females experienced less severe RV remodeling than males, MCT injected males were treated with exogenous E2 from day 21–30. Some E2 treated male rats were sacrificed at day 30, and some were kept an additional 12 days after E2-withdrawal (E2-W group). E2 reversed PH-induced RVF (RVP=38mmHg; RV/(LV+IVS) = 0.28±0.03; RVEF=61.5±0.8%, all p<0.05 vs. male RVF) and fibrosis. OPN and OCN were fully restored following E2 withdrawal by day 42. E2 therapy also restored circulating OPN levels (p<0.05 vs. RVF) showing that OPN has potential value as a plasma marker for PH-induced RV failure. These results suggest that E2 protects against adverse RV remodeling in females, and reverses adverse RV remodeling in males.

scholarly journals Supra-systemic pulmonary hypertension after complicated percutaneous mitral balloon valvuloplasty: a case report and review of literature

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jose R. Navas-Blanco ◽  
Justin Miranda ◽  
Victor Gonzalez ◽  
Asif Mohammed ◽  
Oscar D. Aljure
Keyword(s):  
Pulmonary Hypertension ◽  
Case Report ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Tissue Perfusion ◽  
Venous Hypertension ◽  
Right Ventricular Failure ◽  
Balloon Valvuloplasty ◽  
Ventricular Failure ◽  
The Moment

Abstract Background The World Symposium of Pulmonary Hypertension in 2018, updated the definition of pulmonary hypertension (PH) as mean pulmonary artery pressures (PAP) > 20 mmHg. Pulmonary venous hypertension secondary to left-heart disease, constitutes the most common cause of PH, and the determination of a co-existent pre-capillary (primary) PH becomes paramount, particularly at the moment of evaluating and managing patients with heart failure. Pulmonary artery pressures above the systemic pressures define supra-systemic PH and generally leads to frank right ventricular failure and high mortality. Case presentation We present the perioperative management of a patient with rheumatic mitral valve disease, initially found to have severe PH due to pulmonary venous hypertension, who underwent percutaneous mitral balloon valvuloplasty complicated with mitral chordae rupture, severe mitral regurgitation and supra-systemic PH. Multiple medical therapies and an intra-aortic balloon pump were used as means of non-surgical management of this complication. Conclusions This case report illustrates the perioperative implications of combined pre- and post-capillary PH and supra-systemic PH, as this has not been widely discussed in previous literature. A thorough literature review of the clinical characteristics of PH, methods to determine co-existent pre- and post-capillary PH components, as well as concomitant right ventricular failure is presented. Severe PH has known detrimental effects on the hemodynamic status of patients, which can ultimately lead to a decrease in effective cardiac output and poor tissue perfusion.

scholarly journals Pulmonary Hypertension in Pregnancy: Critical Care Management

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Adel M. Bassily-Marcus ◽  
Carol Yuan ◽  
John Oropello ◽  
Anthony Manasia ◽  
Roopa Kohli-Seth ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Critical Care ◽  
Right Ventricular ◽  
Pregnant Women ◽  
Signs And Symptoms ◽  
Right Ventricular Failure ◽  
Team Approach ◽  
Ventricular Failure ◽  
Critical Care Management ◽  
New Treatments

Pulmonary hypertension is common in critical care settings and in presence of right ventricular failure is challenging to manage. Pulmonary hypertension in pregnant patients carries a high mortality rates between 30–56%. In the past decade, new treatments for pulmonary hypertension have emerged. Their application in pregnant women with pulmonary hypertension may hold promise in reducing morbidity and mortality. Signs and symptoms of pulmonary hypertension are nonspecific in pregnant women. Imaging workup may have undesirable radiation exposure. Pulmonary artery catheter remains the gold standard for diagnosing pulmonary hypertension, although its use in the intensive care unit for other conditions has slowly fallen out of favor. Goal-directed bedside echocardiogram and lung ultrasonography provide attractive alternatives. Basic principles of managing pulmonary hypertension with right ventricular failure are maintaining right ventricular function and reducing pulmonary vascular resistance. Fluid resuscitation and various vasopressors are used with caution. Pulmonary-hypertension-targeted therapies have been utilized in pregnant women with understanding of their safety profile. Mainstay therapy for pulmonary embolism is anticoagulation, and the treatment for amniotic fluid embolism remains supportive care. Multidisciplinary team approach is crucial to achieving successful outcomes in these difficult cases.

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