scholarly journals Mechanisms of right heart disease in pulmonary hypertension (2017 Grover Conference Series)

2017 ◽  
Vol 8 (1) ◽  
pp. 204589321775312 ◽  
Author(s):  
Kewal Asosingh ◽  
Serpil Erzurum
Keyword(s):  
Heart Disease ◽  
Right Ventricle ◽  
Vascular Remodeling ◽  
Cardiac Tissue ◽  
Direct Consequence ◽  
Right Heart Failure ◽  
Right Heart ◽  
Pulmonary Vascular Remodeling ◽  
Right Ventricle Dysfunction ◽  
The Right

Current dogma is that pathological hypertrophy of the right ventricle is a direct consequence of pulmonary vascular remodeling. However, progression of right ventricle dysfunction is not always lung-dependent. Increased afterload caused by pulmonary vascular remodeling initiates the right ventricle hypertrophy, but determinants leading to adaptive or maladaptive hypertrophy and failure remain unknown. Ischemia in a hypertrophic right ventricle may directly contribute to right heart failure. Rapidly enlarging cardiomyocytes switch from aerobic to anaerobic energy generation resulting in cell growth under relatively hypoxic conditions. Cardiac muscle reacts to an increased afterload by over-activation of the sympathetic system and uncoupling and downregulation of β-adrenergic receptors. Recent studies suggest that β blocker therapy in PH is safe, well tolerated, and preserves right ventricle function and cardiac output by reducing right ventricular glycolysis. Fibrosis, an evolutionary conserved process in host defense and wound healing, is dysregulated in maladaptive cardiac tissue contributing directly to right ventricle failure. Despite several mechanisms having been suggested in right heart disease, the causes of maladaptive cardiac remodeling remain unknown and require further research.

Early Predictive Biochemical, Electrocardiographic and Echocardiographic Markers for Cardiac Damage in Patients with Pulmonic Silicosis

2019 ◽  
Vol 70 (1) ◽  
pp. 63-68 ◽  
Author(s):  
Venera Cristina Dinescu ◽  
Ileana Puiu ◽  
Sorin Nicolae Dinescu ◽  
Diana Rodica Tudorascu ◽  
Elena Catalina Bica ◽  
...  
Keyword(s):  
Heart Disease ◽  
Right Ventricle ◽  
Control Group ◽  
Cardiac Damage ◽  
Right Heart ◽  
Pulmonary Heart Disease ◽  
Upper Limit ◽  
Echocardiographic Parameters ◽  
The Right ◽  
Chronic Pulmonary Heart Disease

The aim of this study was to identify correlations between electrocardiographic and echocardiographic changes in patients with silicosis prior to the occurrence of chronic pulmonary heart disease. We conducted a prospective, descriptive, analytical study, in which we included a group of 67 patients consecutively admitted to the Health Promotion and Occupational Medicine Clinic between December 2016 and January 2018, aged 47 to 78 years.There was a biochemical and electrocardiographic evaluation for each patient as well as a right ventricle echocardiographic evaluation (diameters, volumes, function). A control group, including 25 patients with benign minor diseases that required a cardiologist consultation, was also used. From the electrocardiographic point of view, slight changes were observed regarding the waves of electrical activity of the right ventricle. Taking into account the degree of ventilatory dysfunction (depending on FEV1), changes in right heart echocardiographic parameters were identified. Thus, in what the most important right ventricular parameters, including the tricuspid annular plane systolic excursion (TAPSE) or the RV index of myocardial performance (RVMPI) were concerned, values at the upper limit of normality were recorded in most patients with moderate and severe ventilatory dysfunction. Values of echocardiographic parameters of the right heart at the upper limit of normality, correlated with the degree of ventilatory dysfunction, are early markers for cardiovascular damage in patients with pulmonary silicosis prior to the occurrence of chronic pulmonary heart disease also known ascor pulmonale.

scholarly journals Metastatic adenocarcinoma involving the right ventricle and pulmonary artery leading to right heart failure: case report

2017 ◽  
Vol 136 (3) ◽  
pp. 262-265 ◽  
Author(s):  
Turgut Karabag ◽  
Caner Arslan ◽  
Turab Yakisan ◽  
Aziz Vatan ◽  
Duygu Sak
Keyword(s):  
Heart Failure ◽  
Case Report ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Right Ventricular Outflow Tract ◽  
Right Heart Failure ◽  
Ventricular Outflow Tract ◽  
Right Heart ◽  
The Right

ABSTRACT CONTEXT: Obstruction of the right ventricular outflow tract due to metastatic disease is rare. Clinical recognition of cardiac metastatic tumors is rare and continues to present a diagnostic and therapeutic challenge. CASE REPORT: We present the case of a patient who had severe respiratory insufficiency and whose clinical examinations revealed a giant tumor mass extending from the right ventricle to the pulmonary artery. We discuss the diagnostic and therapeutic options. CONCLUSION: In patients presenting with acute right heart failure, right ventricular masses should be kept in mind. Transthoracic echocardiography appears to be the most easily available, noninvasive, cost-effective and useful technique in making the differential diagnosis.

The Hemodynamic Characteristics of Right Ventricle After Gradient Pulmonary Artery Banding in Rats

2020 ◽  
Author(s):  
Song Jiyang ◽  
Wan Nan ◽  
Shen Shutong ◽  
Wei Ying ◽  
Cao Yunshan
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Right Heart Failure ◽  
Therapeutic Strategies ◽  
Pulmonary Artery Banding ◽  
Right Heart ◽  
Pulmonary Arterial ◽  
The Right

Abstract Background: Right ventricular (RV) failure induced by sustained pressure overload is a major contributor to morbidity and mortality in several cardiopulmonary disorders. Reliable and reproducible animal models of RV failure are important in order to investigate disease mechanisms and effects of potential therapeutic strategies. To establish a rat model of RV failure perfectly, we observed the right ventricle and carotid artery hemodynamics characteristics in different degrees of pulmonary artery banding of rats of different body weights. Methods: Rats were subjected to 6 groups：control(0%, n=5)(pulmonary arterial banding 0%), PAB(1-30%, n=4)(pulmonary arterial banding1-30%), PAB(31-60%, n=6)(pulmonary arterial banding31-60%),PAB(61-70%, n=5)(pulmonary arterial bandin61-70%), PAB(71-80%,n=4)(pulmonary arterial banding71-80%), PAB(100%, n=3)(pulmonary arterial banding 100%). We measured the right ventricular pressure(RVP) by right heart catheterization when the pulmonary arterial was ligated. Results: The RVP gradually increased with increasing degree of banding, but when occlusion level exceeding 70%, high pressure state can be only maintained for a few minutes or seconds, and then the RVP drops rapidly until it falls below the normal pressure, which in Group F particularly evident.Conclusions: RVP have different reactions when the occlusion level is not the same, and the extent of more than 70% ligation is a successful model of acute right heart failure. These results may have important consequences for therapeutic strategies to prevent acute right heart failure.

scholarly journals Cellular Pathways Promoting Pulmonary Vascular Remodeling by Hypoxia

Physiology ◽  
2020 ◽  
Vol 35 (4) ◽  
pp. 222-233
Author(s):  
Larissa A. Shimoda
Keyword(s):  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Remodeling ◽  
Pulmonary Arterial Pressure ◽  
Right Heart Failure ◽  
Right Heart ◽  
Pulmonary Vascular Remodeling ◽  
Vascular Stiffening ◽  
Pulmonary Arterial ◽  
Cellular Pathways

Exposure to hypoxia increases pulmonary vascular resistance, leading to elevated pulmonary arterial pressure and, potentially, right heart failure. Vascular remodeling is an important contributor to the increased pulmonary vascular resistance. Hyperproliferation of smooth muscle, endothelial cells, and fibroblasts, and deposition of extracellular matrix lead to increased wall thickness, extension of muscle into normally non-muscular arterioles, and vascular stiffening. This review highlights intrinsic and extrinsic modulators contributing to the remodeling process.

scholarly journals Pathophysiology of the right ventricle and of the pulmonary circulation in pulmonary hypertension: an update

2019 ◽  
Vol 53 (1) ◽  
pp. 1801900 ◽  
Author(s):  
Anton Vonk Noordegraaf ◽  
Kelly Marie Chin ◽  
François Haddad ◽  
Paul M. Hassoun ◽  
Anna R. Hemnes ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Vascular System ◽  
Right Heart Failure ◽  
Imaging Data ◽  
Right Heart ◽  
Future Directions ◽  
Right Heart Catheterisation ◽  
The Right ◽  
Key Pathways

The function of the right ventricle determines the fate of patients with pulmonary hypertension. Since right heart failure is the consequence of increased afterload, a full physiological description of the cardiopulmonary unit consisting of both the right ventricle and pulmonary vascular system is required to interpret clinical data correctly. Here, we provide such a description of the unit and its components, including the functional interactions between the right ventricle and its load. This physiological description is used to provide a framework for the interpretation of right heart catheterisation data as well as imaging data of the right ventricle obtained by echocardiography or magnetic resonance imaging. Finally, an update is provided on the latest insights in the pathobiology of right ventricular failure, including key pathways of molecular adaptation of the pressure overloaded right ventricle. Based on these outcomes, future directions for research are proposed.

Tricuspid valve relocation with endomyocardial fibrosis removal for Löeffler’s endocarditis

2019 ◽  
Vol 56 (3) ◽  
pp. 622-624
Author(s):  
Tohru Asai ◽  
Fumihiro Miyashita ◽  
Hiromitsu Nota ◽  
Piers N Vigers
Keyword(s):  
Heart Failure ◽  
Right Ventricle ◽  
Right Atrium ◽  
Hypereosinophilic Syndrome ◽  
Right Heart Failure ◽  
Right Atrial ◽  
Endomyocardial Fibrosis ◽  
Right Heart ◽  
Atrial Enlargement ◽  
The Right

Abstract Löffler endocarditis with hypereosinophilic syndrome is rare but can cause critical ventricular obliteration by endomyocardial fibrosis. A 52-year-old woman experienced severe right heart failure with extreme shrinkage of her right ventricle, severe tricuspid regurgitation and marked right atrial enlargement. Preoperative tests showed identical pressures in the right atrium and pulmonary artery. Endocardial stripping was done, and to enlarge the right ventricle, we relocated the anterior and posterior tricuspid leaflets cephalad, up the right atrium wall, to ‘ventricularize’ a portion of the right atrium, with autologous pericardial augmentation of the tricuspid leaflets. An annuloplasty ring was added to reinforce the relocated tricuspid attachment. Right heart pressures normalized postoperatively. The patient recovered uneventfully. She has received corticosteroid therapy continuously and has shown no recurrence of heart failure in the 5 years since surgery.

scholarly journals Hypoxia-induced mitogenic factor (FIZZ1/RELMα) induces endothelial cell apoptosis and subsequent interleukin-4-dependent pulmonary hypertension

2014 ◽  
Vol 306 (12) ◽  
pp. L1090-L1103 ◽  
Author(s):  
Kazuyo Yamaji-Kegan ◽  
Eiki Takimoto ◽  
Ailan Zhang ◽  
Noah C. Weiner ◽  
Lucas W. Meuchel ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Endothelial Cell ◽  
Vascular Remodeling ◽  
Lung Inflammation ◽  
Critical Role ◽  
Right Heart Failure ◽  
Right Heart ◽  
Pulmonary Vascular Remodeling ◽  
Mitogenic Factor

Pulmonary hypertension (PH) is characterized by elevated pulmonary artery pressure that leads to progressive right heart failure and ultimately death. Injury to endothelium and consequent wound repair cascades have been suggested to trigger pulmonary vascular remodeling, such as that observed during PH. The relationship between injury to endothelium and disease pathogenesis in this disorder remains poorly understood. We and others have shown that, in mice, hypoxia-induced mitogenic factor (HIMF, also known as FIZZ1 or RELMα) plays a critical role in the pathogenesis of lung inflammation and the development of PH. In this study, we dissected the mechanism by which HIMF and its human homolog resistin (hRETN) induce pulmonary endothelial cell (EC) apoptosis and subsequent lung inflammation-mediated PH, which exhibits many of the hallmarks of the human disease. Systemic administration of HIMF caused increases in EC apoptosis and interleukin (IL)-4-dependent vascular inflammatory marker expression in mouse lung during the early inflammation phase. In vitro, HIMF, hRETN, and IL-4 activated pulmonary microvascular ECs (PMVECs) by increasing angiopoietin-2 expression and induced PMVEC apoptosis. In addition, the conditioned medium from hRETN-treated ECs had elevated levels of endothelin-1 and caused significant increases in pulmonary vascular smooth muscle cell proliferation. Last, HIMF treatment caused development of PH that was characterized by pulmonary vascular remodeling and right heart failure in wild-type mice but not in IL-4 knockout mice. These data suggest that HIMF contributes to activation of vascular inflammation at least in part by inducing EC apoptosis in the lung. These events lead to subsequent PH.

scholarly journals Pulmonary Embolism and Intracardiac Type A Thrombus with an Unexpected Outcome

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
João Português ◽  
Lucy Calvo ◽  
Margarida Oliveira ◽  
Vítor Hugo Pereira ◽  
Joana Guardado ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Type A ◽  
Complete Recovery ◽  
Right Atrial ◽  
Individual Risk ◽  
Right Heart ◽  
Right Ventricle Dysfunction ◽  
The Right ◽  
Unexpected Outcome ◽  
Risk Of Hemorrhage

Detection of right heart thrombi (RHT) in the context of pulmonary thromboembolism (PE) is uncommon (4–18%) and increases the risk of mortality beyond the presence of PE alone. Type A thrombi are serpiginous and highly mobile and are thought to be originated from large veins and captured in-transit within the right heart. Optimal management of RHT is still uncertain. A 79-year-old woman, with a history of recent total hysterectomy with adnexectomy and a Wells procedure, presented to the emergency department following an episode of syncope. Computed tomography revealed bilateral PE and the presence of a right atrial thrombus. Transthoracic echocardiography demonstrated a free-floating type A thrombus in the right atrium, protruding into the right ventricle, and signs of pulmonary hypertension and right ventricle dysfunction. Considering the recent surgery and clinical stability, treatment with heparin alone was decided. Subsequent clinical improvement was observed and echocardiographic follow-up revealed complete thrombus dissolution and complete recovery of right ventricle function. Most authors recommend treatment of PE with RHT with thrombolysis or embolectomy followed by anticoagulation, although evidence is scarce. Individual risk of hemorrhage and operatory-related mortality should be taken into account when defining the treatment strategy especially when benefit is not firmly established.

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