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.

scholarly journals Early detection of left ventricular failure in right ventricular congenital heart diseases

2019 ◽  
Vol 11 (4) ◽  
pp. e388
Author(s):  
Angèle Boët ◽  
Julien Guihaire ◽  
Emmanuel Le Bret ◽  
Sébastien Hascoet ◽  
Gilles Jourdain ◽  
...  
Keyword(s):  
Early Detection ◽  
Right Ventricular ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Left Ventricular ◽  
Left Ventricular Failure ◽  
Congenital Heart Diseases ◽  
Ventricular Failure

Electrocardiographic recognition of benign and malignant right ventricular arrhythmias

EP Europace ◽  
2021 ◽  
Author(s):  
John Lee ◽  
Oluwaseun Adeola ◽  
Hasan Garan ◽  
William G Stevenson ◽  
Hirad Yarmohammadi
Keyword(s):  
Right Ventricle ◽  
Right Ventricular ◽  
Ventricular Arrhythmias ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Congenital Heart Diseases ◽  
Structural Heart Diseases ◽  
Procedural Planning ◽  
The Right

Abstract Ventricular arrhythmias (VAs) can originate from different anatomical locations of the right ventricle. Ventricular arrhythmias originating from right ventricle have unique electrocardiographic (ECG) characteristics that can be utilized to localize the origin of the arrhythmia. This is crucial in pre-procedural planning particularly for ablation treatments. Moreover, non-ischaemic structural heart diseases, such as infiltrative and congenital heart diseases, are associated with the VAs that exhibit particular ECG findings. This article comprehensively reviews discriminatory ECG characteristics of VAs in the right ventricle with and without structural right ventricular diseases.

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.

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