scholarly journals Stage IV Sarcoidosis with Cor pulmonale: A Case Report

2016 ◽  
Vol 30 (1) ◽  
pp. 37-42
Author(s):  
Mostashirul Haque ◽  
Tunaggina Afrin Khan ◽  
Md Rasul Amin ◽  
Montasin Rezwan ◽  
Md Rashidul Hasan ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Systolic Pressure ◽  
Stage Iv ◽  
Pulmonary Involvement ◽  
Cor Pulmonale ◽  
Right Ventricular Hypertrophy ◽  
Pulmonary Artery Systolic Pressure ◽  
Strain Pattern

Sarcoidosis is a well known systemic disorder that invariably involves lungs. However, pulmonary hypertension and cor-pulmanle are not common due to pulmonary involvement of sarcoidosis. We report a case of pulmonary hypertension leading to corpulmonale due to sarcoidosis. An elderly female suffering from hypertension & sarcoidosis developed complications and arrived at the diagnosis by correlating various investigations. X-ray chest (P/A) showed cardiomegaly (right ventricular type), reticulo-nodular shadow involving both mid and lower zone; characteristic high resolution CT (HRCT) scan appearances include reticulonodular opacities; pulmonary function test showed restrictive type of defect; ECG showed right ventricular hypertrophy with strain pattern; in echocardiogram there were right ventricular hypertrophy (RVH) with pulmonary artery systolic pressure (PASP) of 63 mmHg indicating severe pulmonary arterial hypertension (PH); along with significantly elevated B-type natriuretic peptide(BNP) level.Bangladesh Heart Journal 2015; 30(1) : 37-42

Cystamine Treatment Fails to Prevent the Development of Pulmonary Hypertension in Chronic Hypoxic Rats

2021 ◽  
pp. 1-15
Author(s):  
Lars K. Markvardsen ◽  
Lene D. Sønderskov ◽  
Christine Wandall-Frostholm ◽  
Estéfano Pinilla ◽  
Judit Prat-Duran ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Lung Tissue ◽  
Ventricular Hypertrophy ◽  
Systolic Pressure ◽  
Right Ventricular Hypertrophy ◽  
Ventricular Systolic Pressure ◽  
Pulmonary Arterial ◽  
The Right

<b><i>Introduction:</i></b> Pulmonary hypertension is characterized by vasoconstriction and remodeling of pulmonary arteries, leading to right ventricular hypertrophy and failure. We have previously found upregulation of transglutaminase 2 (TG2) in the right ventricle of chronic hypoxic rats. The hypothesis of the present study was that treatment with the transglutaminase inhibitor, cystamine, would inhibit the development of pulmonary arterial remodeling, pulmonary hypertension, and right ventricular hypertrophy. <b><i>Methods:</i></b> Effect of cystamine on transamidase activity was investigated in tissue homogenates. Wistar rats were exposed to chronic hypoxia and treated with vehicle, cystamine (40 mg/kg/day in mini-osmotic pumps), sildenafil (25 mg/kg/day), or the combination for 2 weeks. <b><i>Results:</i></b> Cystamine concentration-dependently inhibited TG2 transamidase activity in liver and lung homogenates. In contrast to cystamine, sildenafil reduced right ventricular systolic pressure and hypertrophy and decreased pulmonary vascular resistance and muscularization in chronic hypoxic rats. Fibrosis in the lung tissue decreased in chronic hypoxic rats treated with cystamine. TG2 expression was similar in the right ventricle and lung tissue of drug and vehicle-treated hypoxic rats. <b><i>Discussion/Conclusions:</i></b> Cystamine inhibited TG2 transamidase activity, but cystamine failed to prevent pulmonary hypertension, right ventricular hypertrophy, and pulmonary arterial muscularization in the chronic hypoxic rat.

Lung vascular smooth muscle as a determinant of pulmonary hypertension at high altitude

1975 ◽  
Vol 228 (3) ◽  
pp. 762-767 ◽  
Author(s):  
A Tucker ◽  
IF McMurtry ◽  
JT Reeves ◽  
AF Alexander ◽  
DH Will ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Right Ventricular ◽  
High Altitude ◽  
Ventricular Hypertrophy ◽  
Mammalian Species ◽  
Systolic Pressure ◽  
Right Ventricular Hypertrophy ◽  
Ventricular Systolic Pressure

The pulmonary hypertensive response to chronic hypoxia varies markedly among mammalian species. An explanation for this variability was sought by exposing seven species to hypobaric hypoxia (PB equal to 435 mmHg) for 19-48 days. Control animals were studied at 1,600 m (PB equal to 630 mmHg). The pulmonary hypertension that developed varied in the following order of decreasing severity: calf and pig (severe); rat and rabbit (moderate); sheep, guinea pig, and dog (mild). Right ventricular hypertrophy developed in proportion to the elevation in right ventricular systolic pressure. These interspecies variations in response were not correlated with the degree of arterial hypoxemia, degree of polycythemia, elevation in heart rate, or postnatal age. However, the medial thickness of the small pulmonary arteries in control animals was highly correlated with the development of pulmonary hypertension and right ventricular hypertrophy in hypoxic animals. Thus, the amount of lung vascular smooth muscle inherent within each species is a major determinant of the pulmonary hypertensive response to high altitude and contributes to the interspecies variability in this response.

scholarly journals Magnesium Sulfate Mitigates the Progression of Monocrotaline Pulmonary Hypertension in Rats

2019 ◽  
Vol 20 (18) ◽  
pp. 4622 ◽  
Author(s):  
Chao-Yuan Chang ◽  
Hung-Jen Shih ◽  
I-Tao Huang ◽  
Pei-Shan Tsai ◽  
Kung-Yen Chen ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Magnesium Sulfate ◽  
Ventricular Hypertrophy ◽  
Systolic Pressure ◽  
Right Ventricular Hypertrophy ◽  
Male Rats ◽  
Wall Thickening ◽  
Artery Wall

We investigated whether magnesium sulfate (MgSO4) mitigated pulmonary hypertension progression in rats. Pulmonary hypertension was induced by a single intraperitoneal injection of monocrotaline (60 mg/kg). MgSO4 (100 mg/kg) was intraperitoneally administered daily for 3 weeks, from the seventh day after monocrotaline injection. Adult male rats were randomized into monocrotaline (MCT) or monocrotaline plus MgSO4 (MM) groups (n = 15 per group); control groups were maintained simultaneously. For analysis, surviving rats were euthanized on the 28th day after receiving monocrotaline. The survival rate was higher in the MM group than in the MCT group (100% versus 73.3%, p = 0.043). Levels of pulmonary artery wall thickening, α-smooth muscle actin upregulation, right ventricular systolic pressure increase, and right ventricular hypertrophy were lower in the MM group than in the MCT group (all p < 0.05). Levels of lipid peroxidation, mitochondrial injury, inflammasomes and cytokine upregulation, and apoptosis in the lungs and right ventricle were lower in the MM group than in the MCT group (all p < 0.05). Notably, the mitigation effects of MgSO4 on pulmonary artery wall thickening and right ventricular hypertrophy were counteracted by exogenous calcium chloride. In conclusion, MgSO4 mitigates pulmonary hypertension progression, possibly by antagonizing calcium.

scholarly journals The protective of baicalin on pulmonary hypertension vascular remodeling through regulation of TNF-α signaling pathway

2020 ◽  
Author(s):  
Xia Xue ◽  
Wen Jiang ◽  
Chao Sun ◽  
Jue Wang ◽  
Qian Xin ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Signaling Pathway ◽  
Vascular Remodeling ◽  
Ventricular Hypertrophy ◽  
Systolic Pressure ◽  
Right Ventricular Hypertrophy ◽  
Intragastric Administration ◽  
Tnf Α

Abstract Background: Pulmonary hypertension (PH) is a life-threatening disease, so far no effective method for it. Baicalin can attenuate pulmonary artery pressure and reduce right ventricular hypertrophy in PH, however, the potential mechanism remains unexplored. Therefore, the main aim of the present study was to investigate the protective effect and of baicalin on experimental PH vascular remodeling, and reveal the underlying mechanism.Methods: Monocrotaline (MCT)-induced PH rats models was established, and baicalin was given by intragastric administration. Six weeks later, right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) were recorded, lung tissue hematoxylin-eosin (H&E) staining was analysis to reveal the effect of baicalin on MCT-induced PH. In Vitro, we established TNF-α induced pulmonary artery smooth muscle cells (PASMCs) to detect the inhibition of baicalin on vascular remodeling. Furthermore, quantitative real-time polymerase chain reaction (qRT-PCR), western blot and immunofluorescence were used to detect the mRNA and protein expressions.Results: Our results indicated that baicalin could significantly attenuate MCT induced the RVSP and the right ventricular hypertrophy index (RVHI); inhibit pulmonary vascular remodeling and lung fibrosis. Moreover, our results showed baicalin could significantly decrease the expression of inflammatory cytokines, but increase the protein expression of bone morphogenetic protein type II receptor (BMPR2), ID1 and Smad1//5/8.Conclusion:Taken together, our present study confirmed the mechanism of baicalin against PH was associated with inhibition of TNF-α signaling pathway.

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.

scholarly journals Bosentan attenuates right ventricular hypertrophy and fibrosis in normobaric hypoxia model of pulmonary hypertension

2011 ◽  
Vol 30 (7) ◽  
pp. 827-833 ◽  
Author(s):  
Gaurav Choudhary ◽  
Frederick Troncales ◽  
Douglas Martin ◽  
Elizabeth O. Harrington ◽  
James R. Klinger
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Normobaric Hypoxia
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