scholarly journals Histological Justification for the Need of Radiofrequency Ablation of Pulmonary Arteries in Patients with High-Grade Secondary Pulmonary Hypertension

2021 ◽  
Vol 13 (6) ◽  
pp. 56
Author(s):  
N.A. Trofimov ◽  
A.L. Rodionov ◽  
D.V. Egorov ◽  
T.V. Surkova ◽  
A.V. Nikolsky
Keyword(s):  
Pulmonary Hypertension ◽  
Radiofrequency Ablation ◽  
Pulmonary Arteries ◽  
High Grade ◽  
Secondary Pulmonary Hypertension

PRIMARY PULMONARY HYPERTENSION

PEDIATRICS ◽  
1957 ◽  
Vol 20 (3) ◽  
pp. 408-415
Author(s):  
Harvey S. Rosenberg ◽  
Dan G. McNamara
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Primary Pulmonary Hypertension ◽  
Pulmonary Arteries ◽  
Right Ventricular Hypertrophy ◽  
Vascular Change ◽  
Progressive Dyspnea ◽  
Peripheral Lung ◽  
Secondary Pulmonary Hypertension

A case is reported of a 4-month-old infant in which the outstanding clinical features were failure to gain weight, cough, and progressive dyspnea. There was marked accentuation of the second pulmonic sound and no significant murmur. The electrocardiogram was interpreted as showing right ventricular hypertrophy and roentgenographically, there was unusual clarity of peripheral lung fields and prominence of hilar vessels. Cardiac catheterization demonstrated pulmonary hypertension and revealed no left to right intracardiac shunt. Anatomically, there was right ventricular hypertrophy and prominence of the medial layer of the small pulmonary arteries. This vascular change is indistinguishable from that seen in the normal newborn and certain varieties of secondary pulmonary hypertension. Although the clinical diagnosis can be suspected, the definitive anomaly can be determined only at post-mortem examination.

Development of antioxidant peptides that target the pulmonary arteries for the treatment of pulmonary hypertension

Planta Medica ◽  
2015 ◽  
Vol 81 (11) ◽  
Author(s):  
LR Villegas ◽  
L Kirkbride-Romeo ◽  
JM Martinez ◽  
MPT Le
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Arteries ◽  
Antioxidant Peptides

Pulmonary Endarterectomy: Assessment of Operability, Surgical Description, and Post-op Care

2014 ◽  
Vol 12 (4) ◽  
pp. 186-192 ◽  
Author(s):  
David Poch ◽  
Victor Pretorius
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Arteries ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Artery Wedge Pressure ◽  
Pulmonary Endarterectomy ◽  
Pulmonary Thromboendarterectomy ◽  
Thromboembolic Pulmonary Hypertension ◽  
Wedge Pressure

Chronic thromboembolic pulmonary hypertension (CTEPH) is defined as a mean pulmonary artery pressure ≥25 mm Hg and pulmonary artery wedge pressure ≤15 mm Hg in the presence of occlusive thrombi within the pulmonary arteries. Surgical pulmonary thromboendarterectomy (PTE) is considered the best treatment option for CTEPH.

scholarly journals Oxygen-Sensitivity and Pulmonary Selectivity of Vasodilators as Potential Drugs for Pulmonary Hypertension

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 155
Author(s):  
Daniel Morales-Cano ◽  
Bianca Barreira ◽  
Beatriz De Olaiz Navarro ◽  
María Callejo ◽  
Gema Mondejar-Parreño ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Gas Exchange ◽  
Pulmonary Circulation ◽  
Pulmonary Arteries ◽  
Blood Perfusion ◽  
Mesenteric Arteries ◽  
Oxygen Sensitivity ◽  
Low Oxygen ◽  
Oxygen Selectivity

Current approved therapies for pulmonary hypertension (PH) aim to restore the balance between endothelial mediators in the pulmonary circulation. These drugs may exert vasodilator effects on poorly oxygenated vessels. This may lead to the derivation of blood perfusion towards low ventilated alveoli, i.e., producing ventilation-perfusion mismatch, with detrimental effects on gas exchange. The aim of this study is to analyze the oxygen-sensitivity in vitro of 25 drugs currently used or potentially useful for PH. Additionally, the study analyses the effectiveness of these vasodilators in the pulmonary vs. the systemic vessels. Vasodilator responses were recorded in pulmonary arteries (PA) and mesenteric arteries (MA) from rats and in human PA in a wire myograph under different oxygen concentrations. None of the studied drugs showed oxygen selectivity, being equally or more effective as vasodilators under conditions of low oxygen as compared to high oxygen levels. The drugs studied showed low pulmonary selectivity, being equally or more effective as vasodilators in systemic than in PA. A similar behavior was observed for the members within each drug family. In conclusion, none of the drugs showed optimal vasodilator profile, which may limit their therapeutic efficacy in PH.

scholarly journals The mechanism of ions in pulmonary hypertension

2021 ◽  
Vol 11 (1) ◽  
pp. 204589402098794
Author(s):  
Guogu Liu ◽  
Daiyan Fu ◽  
Heshen Tian ◽  
Aiguo Dai
Keyword(s):  
Pulmonary Hypertension ◽  
Calcium Ion ◽  
Pulmonary Arteries ◽  
Chloride Ion ◽  
Vasoactive Substances ◽  
Pulmonary Vasoconstriction ◽  
Concentration Of Ions ◽  
Inducing Factors ◽  
Effective Drugs ◽  
Pathological Manifestation

Pulmonary hypertension（PH）is a kind of hemodynamic and pathophysiological state, in which the pulmonary artery pressure (PAP) rises above a certain threshold. The main pathological manifestation is pulmonary vasoconstriction and remodelling progressively. More and more studies have found that ions play a major role in the pathogenesis of PH. Many vasoactive substances, inflammatory mediators, transcription-inducing factors, apoptosis mediators, redox substances and translation modifiers can control the concentration of ions inside and outside the cell by regulating the activity of ion channels, which can regulate vascular contraction, cell proliferation, migration, apoptosis, inflammation and other functions. We all know that there are no effective drugs to treat PH. Ions are involved in the occurrence and development of PH, so it is necessary to clarify the mechanism of ions in PH as a therapeutic target for PH. The main ions involved in PH are calcium ion (Ca2+), potassium ion (K+), sodium ion (Na+) and chloride ion (Cl–). Here, we mainly discuss the distribution of these ions and their channels in pulmonary arteries and their role in the pathogenesis of PH.

scholarly journals The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension

2021 ◽  
Vol 22 (9) ◽  
pp. 4980
Author(s):  
Inés Roger ◽  
Javier Milara ◽  
Paula Montero ◽  
Julio Cortijo
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Vascular Remodeling ◽  
Pulmonary Arteries ◽  
Clinical Manifestations ◽  
Different Types ◽  
Artery Remodeling ◽  
Stat Pathway ◽  
Pulmonary Artery Remodeling

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular, and cellular processes involved in PH. Chronic inflammation contributes to pulmonary artery remodeling and PH, among other vascular disorders, and many inflammatory mediators signal through the JAK/STAT pathway. Recent evidence indicates that the JAK/STAT pathway is overactivated in the pulmonary arteries of patients with PH of different types. In addition, different profibrotic cytokines such as IL-6, IL-13, and IL-11 and growth factors such as PDGF, VEGF, and TGFβ1 are activators of the JAK/STAT pathway and inducers of pulmonary remodeling, thus participating in the development of PH. The understanding of the participation and modulation of the JAK/STAT pathway in PH could be an attractive strategy for developing future treatments. There have been no studies to date focused on the JAK/STAT pathway and PH. In this review, we focus on the analysis of the expression and distribution of different JAK/STAT isoforms in the pulmonary arteries of patients with different types of PH. Furthermore, molecular canonical and noncanonical JAK/STAT pathway transactivation will be discussed in the context of vascular remodeling and PH. The consequences of JAK/STAT activation for endothelial cells and pulmonary artery smooth muscle cells’ proliferation, migration, senescence, and transformation into mesenchymal/myofibroblast cells will be described and discussed, together with different promising drugs targeting the JAK/STAT pathway in vitro and in vivo.

Effect of Intentional Hemodilution on Platelet Survival in Secondary Pulmonary Hypertension

CHEST Journal ◽  
1989 ◽  
Vol 95 (6) ◽  
pp. 1207-1210 ◽  
Author(s):  
Antonio A.B. Lopes ◽  
Nair Y. Maeda ◽  
Munir Ebaid ◽  
Daltom F. Chamone ◽  
Fulvio Pileggi
Keyword(s):  
Pulmonary Hypertension ◽  
Platelet Survival ◽  
Secondary Pulmonary Hypertension
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