The Effect of Pulmonary Hypertension on Tricuspid Valve Coaptation in Normal and Pathologic Valve Geometries: An In Vitro Study

2012 ◽  
Author(s):  
Joseph R. Dolensky ◽  
Lauren D. C. Casa ◽  
Ajit P. Yoganathan
Keyword(s):  
Pulmonary Hypertension ◽  
Tricuspid Valve ◽  
Pathological Condition ◽  
In Vitro Study ◽  
Pulmonary Vasculature ◽  
Papillary Muscles ◽  
Left Heart ◽  
Right Heart ◽  
The Right

Pulmonary hypertension (PHTN) is a pathological condition defined as a mean pulmonary artery pressure (mPAP) greater than 25 mmHg. PHTN can result from a number of lung and heart pathologies, including abnormalities of the pulmonary vasculature, left heart disease, chronic lung disease, and chronic thrombotic disease [1]. Regardless of the cause, the increased afterload on the right heart results in right ventricle (RV) hypertrophy and dilatation and tricuspid regurgitation (TR) [2]. RV dilatation is thought to result in the displacement of the tricuspid valve (TV) papillary muscles (PM) and dilatation of the TV annulus, negatively impacting TV function.

In Vitro Study of Flow Regulation for Pulmonary Insufficiency Using Diode Valves

2007 ◽  
Author(s):  
Tiffany A. Camp ◽  
Stephanie Hequembourg ◽  
Richard S. Figliola ◽  
Tim McQuinn
Keyword(s):  
Pulmonary Valve ◽  
Pulmonary Regurgitation ◽  
Circulatory System ◽  
In Vitro Study ◽  
Pulmonary Insufficiency ◽  
Pressure Gradients ◽  
Right Heart ◽  
Mock Circulatory System ◽  
The Right

The operating pressures in the right heart are significantly lower than those of the left heart and with marked differences in the circulation impedances. The pulmonary circulation shows a tolerance for mild regurgitation and pressure gradient [1]. Pulmonary regurgitation fractions on the order of 20% and transvalvular pressure gradients of less than 25mm Hg are considered mild [4]. Given this tolerance, we examine the concept of using a motionless valve to regulate flow in the pulmonary position. In a previous study, the use of fluid diodes was shown to be a promising concept for use as a pulmonary valve [2]. In this study, we test two different diode designs. For each diode valve, flow performance was documented as a function of pulmonary vascular resistance (PVR) and compliance. Tests were done using a pulmonary mock circulatory system [3] over the normal adult range of PVR and compliance settings.

Pathophysiological Considerations concerning Uni- and Biventricular Mechanical Cardiac Assist

1997 ◽  
Vol 20 (12) ◽  
pp. 684-691 ◽  
Author(s):  
F.R. Waldenberger
Keyword(s):  
Pulmonary Hypertension ◽  
Right Heart Failure ◽  
Assisted Circulation ◽  
Left Heart ◽  
Right Heart ◽  
Early Reperfusion ◽  
Cardiac Assist ◽  
Mechanical Unloading ◽  
The Right ◽  
The Impact

Mechanical assisted circulation by the means of cardiac assist devices is a routine procedure in modern cardiac surgery and cardiology. We investigated the impact of mechanical unloading on regional myocardial “stunning” and the influence of assisted circulation on left heart and right heart failure persevered by an ultimate addition of pulmonary hypertension in experimental set ups. We found that mechanical unloading either during ischemia or in the early reperfusion phase attenuates stunning and enhances the return of synchronous heart performance. In our global dysfunction model we showed that the right heart is dispensable. Sufficient inflow to the left heart is provided unless pulmonary hypertension is present. Also additional left heart support can not overcome the deleterious situation and in select cases only additional right heart support can prevent the “low LVAD output” syndrome. We conclude that mechanical assisted circulation and mechanical unloading are beneficial in case of regional and global dysfunction persevered by pulmonary hypertension, however, the knowledge about interactions of assist systems and the circulation has to be improved in order to optimize clinical assist device performance.

Unguarded tricuspid valvar orifice in the fetus

2004 ◽  
Vol 14 (5) ◽  
pp. 557-559 ◽  
Author(s):  
Kenny K. Wong ◽  
Duncan I. Farquharson ◽  
Walter J. Duncan
Keyword(s):  
Right Ventricle ◽  
Tricuspid Valve ◽  
Normal Karyotype ◽  
Retrograde Flow ◽  
Left Heart ◽  
Colour Doppler ◽  
Right Heart ◽  
Atrioventricular Junction ◽  
The Right

The unguarded tricuspid valve is uncommon. We describe herein a fetus with a grossly dilated right ventricle and atrium, with severe tricuspid and pulmonary valvar regurgitation. The right ventricle was akinetic, and no tricuspid tissue or valvar apparatus was identified. Colour Doppler showed a highly unusual retrograde flow of blood through the right heart. The pregnancy was terminated, and necropsy examination confirmed the gross dilation of the right heart chambers, with severely dysplastic valvar tissue at the right atrioventricular junction effectively giving an unguarded orifice. There was no valvar displacement, and the left heart was normal. The fetus had a normal karyotype, albeit with absent kidneys.

CGRP and somatostatin modulate chronic hypoxic pulmonary hypertension

1992 ◽  
Vol 263 (3) ◽  
pp. H681-H690 ◽  
Author(s):  
S. Tjen-A-Looi ◽  
R. Ekman ◽  
H. Lippton ◽  
J. Cary ◽  
I. Keith
Keyword(s):  
Pulmonary Hypertension ◽  
Main Pulmonary Artery ◽  
Pulmonary Vasculature ◽  
Hypoxic Pulmonary Hypertension ◽  
Calcitonin Gene ◽  
Pulmonary Arterial ◽  
Pentobarbital Sodium Anesthesia ◽  
The Right ◽  
Potential Interactions

Chronic hypoxic pulmonary hypertension (PH), associated with increased pulmonary arterial pressure (PPA) and right ventricular hypertrophy (RVH), correlates significantly with calcitonin gene-related peptide (CGRP) and somatostatin (SOM) levels in lung and blood. CGRP's role in regulation of PPA in chronic hypoxia and its potential interactions with SOM were investigated. CGRP, its antibody (ab) and blocker, CGRP-(8–37), SOM-14, SOM-28, and SOM-ab, respectively, were infused into the pulmonary circulation of hypobaric hypoxia rats for 4, 8, and 16 days. Thereafter, under pentobarbital sodium anesthesia, PPA was measured in the right ventricle and main pulmonary artery. Chronic CGRP infusion prevented PH at all times, whereas immunoneutralization and receptor blocking exacerbated PH. SOM-28 also exacerbated while SOM-14 and SOM-ab decreased PH. RVH generally reflected the PPA. Radioimmunoassay confirmed successful infusion of the peptides with negligible peptide degradation in the pumps throughout 16 days and showed complete immunoneutralization of CGRP with its ab. Peptide levels in lung tissue suggest inhibition of CGRP release by SOM-28 and increased plasma SOM with CGRP infusion. In vitro pharmacological studies suggest that CGRP exerts a receptor-mediated nonadrenergic, nonmuscarinic vasodilatory effect in the lung which is independent of endothelium-derived relaxing factor and does not involve ATP-dependent potassium channels. We conclude that endogenous CGRP plays an important role in pulmonary pressure homeostasis during hypoxia, by directly dilating pulmonary vasculature, thus ameliorating the development of chronic hypoxic pulmonary hypertension in rats.

scholarly journals Intertraffic of Endothelin 1 and Thrombospondin 1 between lungs and myocard via pulmonary circulation can alter cardiac loads, tissue integrity and atrial blood coagulability

F1000Research ◽  
2017 ◽  
Vol 6 ◽  
pp. 1583
Author(s):  
Sven Kurbel
Keyword(s):  
Pulmonary Circulation ◽  
Expression Patterns ◽  
Venous Blood ◽  
Pulmonary Vasculature ◽  
Left Heart ◽  
Right Heart ◽  
Endothelin 1 ◽  
Tissue Integrity ◽  
Thrombospondin 1 ◽  
The Right

Similar expression patterns of mRNA profiles for Endothelin 1 (ET-1) and Thrombospondin 1 (TSP1) from GeneAtlas U133A, gcrma, suggest that these two mediators are dominantly synthesized in the myocard and lungs. This paper proposes that intertraffic of these two mediators between myocard and lungs via pulmonary and coronary vessels optimizes cardiopulmonary functions and maintains their tissue integrity. A controlled delivery of endocrine mediators to the left and to the right heart is done by the coronary sinus (CS) that drains venous blood to the right atrium, and Thebesian veins (TVs) that open in all four heart cavities. Myocard and pulmonary capillaries are connected as a bidirectional portal system. Mediators from lungs can directly influence myocardial cells after entering the coronary circulation, while mediators in the myocardial venous blood that drain into the right heart will initially affect lungs. Strain induced myocardial ET-1 secretion into the right heart and pulmonary circulation increases the right heart afterload by constricting pulmonary vasculature. The same action reduces the left heart preload. Pulmonary ET-1 secretion can protect lungs from overperfusion by increasing the left heart afterload through constriction of peripheral arterioles. Chronic tissue overexposure to ET-1 leads to pulmonary and myocardial fibrosis.  TSP1 availability is important in tissues under mechanical stress, since TSP1 is an adhesive glycoprotein involved in cell-to-cell and cell-to-matrix interactions. Pulmonary and myocardial TSP1 secretion that enter the fibrillating left atrium can mimic actions of the platelet-derived TSP1 in promoting the thrombus formation.

scholarly journals EXPRESS: Chronic thromboembolic pulmonary hypertension following pulmonary embolism with a right ventricular thrombus: A report of two cases

2021 ◽  
pp. 204589402110136
Author(s):  
Tailong Zhang ◽  
Weitao Liang ◽  
Longrong Bian ◽  
Zhong Wu
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Imaging Features ◽  
Pulmonary Endarterectomy ◽  
Right Heart ◽  
Thromboembolic Pulmonary Hypertension ◽  
The Right ◽  
Cardiac Masses

Right heart thrombus (RHT) accompanied by chronic thromboembolic pulmonary hypertension (CTEPH) is a rare entity. RHT may develop in the peripheral veins or in situ within the right heart chambers. The diagnosis of RHT is challenging, since its symptoms are typically non-specific and its imaging features resemble those of cardiac masses. Here, we report two cases of RHT with CTEPH that presented as right ventricular masses initially. Both patients underwent simultaneous pulmonary endarterectomy (PEA) and resection of the ventricular thrombi. Thus, when mass-like features are confirmed by imaging, RHT should be suspected in patients with CTEPH, and simultaneous RHT resection is required along with PEA.

Transient severe isolated right ventricular hypertrophy in neonates

2003 ◽  
Vol 13 (4) ◽  
pp. 384-386 ◽  
Author(s):  
Munesh Tomar ◽  
Sitaraman Radhakrishnan ◽  
Savitri Shrivastava
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Posterior Wall ◽  
Right Ventricular Hypertrophy ◽  
Pulmonary Vasculature ◽  
Normal Thickness ◽  
The Right

We report two instances of transient isolated right-sided myocardial hypertrophy in patients with an intact ventricular septum, normal thickness of the posterior wall of the left ventricle, and normal ventricular function, diagnosed by echocardiography on the third day of life. The two neonates, born at 36 and 38 weeks gestation respectively, had perinatal distress. Both were diagnosed as having isolated right ventricular hypertrophy with mild pulmonary hypertension, which disappeared in both cases within 8 weeks without any specific therapy. Though the cause of the ventricular hypertrophy remains unclear, we believe that it is the consequence of remodeling of pulmonary vasculature secondary to acute perinatal distress, resulting in persistent pulmonary hypertension and producing pressure overload on the right ventricle, and hence right ventricular hypertrophy. The finding of early and transient right ventricular hypertrophy, with normal left-sided structures and normal ventricular function, has thus far failed to gain attention in the paediatric cardiologic literature.

Pulmonary Hypertension Associated With Myocardial Amyloid Degeneration: a Case Report

2021 ◽  
Author(s):  
Lu Yan ◽  
Qixian Zeng ◽  
Changming Xiong ◽  
Zhihui Zhao ◽  
Qing Zhao ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Blood Vessels ◽  
Amyloid Fibrils ◽  
Right Heart Failure ◽  
Pulmonary Artery Hypertension ◽  
Pulmonary Vasculature ◽  
Vascular Involvement ◽  
Right Heart ◽  
Protein Deposits

Abstract Background: There is very little literature on Pulmonary hypertension associated with myocardial amyloid degeneration. At present, only 10 cases pulmonary hypertension cased by amyloid protein deposits in the pulmonary blood vessels have been reported by Eder et al. We reported a case that the patient was pulmonary artery hypertension combined with myocardial amyloid change. It’s aim to claims that pulmonary hypertension is most likely caused by amyloid fibrin deposition in pulmonary blood vessels.Case presentation: We report a case of a 65-year-old male patient with with AL and ATTR combined type amyloidosis who developed right heart failure because of severe pulmonary hypertension. Pulmonary hypertension due to deposition of amyloid in the pulmonary vasculature is an uncommon finding; however, it should be considered in cases of unexplained pulmonary hypertension in patients with amyloidosis.Conclusion: we present a men with amyloidosis who developed dyspnea and right heart failure and was diagnosed with pulmonary hypertension, most probably secondary to pulmonary vascular involvement by amyloid fibrils.

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