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Life
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Pulmonary Hypertension: From Bench to Bedside: 2nd Edition
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Pulmonary Hypertension: From Bench to Bedside: 2nd Edition

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: 1 July 2024 | Viewed by 4596

Special Issue Editor

Dr. Satoshi Akagi

E-Mail Website
Guest Editor
Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8530, Japan
Interests: pulmonary hypertension; right ventricular dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Pulmonary arterial hypertension is life-threatening diseases caused by constriction and remodeling of pulmonary arteries. Prostacyclin, endothelin receptor antagonist, phosphodiesterase 5 inhibitor and soluble guanylate cyclase stimulator is an available for treatment of pulmonary arterial hypertension, which improve hemodynamics and exercise capacity. However, sufficient improvement of long-term prognosis is not achieved in all patients with pulmonary arterial hypertension. New findings from basic research contribute to therapeutic advances of pulmonary arterial hypertension. In this special issue, we focus on basic research in pulmonary arterial hypertension.

Volume I: https://www.mdpi.com/journal/life/special_issues/pulmonary_hypertension_2022

Dr. Satoshi Akagi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pulmonary arterial hypertension
  • chronic thromboembolic pulmonary hypertension
  • imaging
  • physiological tests
  • genetics
  • inflamation
  • metabolic dysfunction
  • proriferative signaling

Published Papers (3 papers)

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Research

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15 pages, 2626 KiB  
Article
Potential Prognostic Value of Native T1 in Pulmonary Hypertension Patients
by John W. Cerne, Christina Shehata, Ann Ragin, Ashitha Pathrose, Manik Veer, Kamal Subedi, Bradley D. Allen, Ryan J. Avery, Michael Markl and James C. Carr
Life 2023, 13(3), 775; https://doi.org/10.3390/life13030775 - 13 Mar 2023
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Abstract
Native T1, extracellular volume fraction (ECV), and late gadolinium enhancement (LGE) characterize myocardial tissue and relate to patient prognosis in a variety of diseases, including pulmonary hypertension. The purpose of this study was to evaluate if left ventricle (LV) fibrosis measurements have prognostic [...] Read more.
Native T1, extracellular volume fraction (ECV), and late gadolinium enhancement (LGE) characterize myocardial tissue and relate to patient prognosis in a variety of diseases, including pulmonary hypertension. The purpose of this study was to evaluate if left ventricle (LV) fibrosis measurements have prognostic value for cardiac outcomes in pulmonary hypertension subgroups. 54 patients with suspected pulmonary hypertension underwent right-heart catheterization and were classified into pulmonary hypertension subgroups: pre-capillary component (PreCompPH) and isolated post-capillary (IpcPH). Cardiac magnetic resonance imaging (MRI) scans were performed with the acquisition of balanced cine steady-state free precession, native T1, and LGE pulse sequences to measure cardiac volumes and myocardial fibrosis. Associations between cardiac events and cardiac MRI measurements were analyzed within PreCompPH and IpcPH patients. IpcPH: LV native T1 was higher in patients who experienced a cardiac event within two years vs. those who did not. In patients with LV native T1 > 1050 ms, the rate of cardiac events was higher. ECV and quantitative LGE did not differ between groups. PreCompPH: native T1, ECV, and quantitative/qualitative LGE did not differ between patients who experienced a cardiac event within two years vs. those who did not. LV native T1 may have potential value for forecasting cardiac events in IpcPH, but not in PreCompPH, patients. Full article
(This article belongs to the Special Issue Pulmonary Hypertension: From Bench to Bedside: 2nd Edition)
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Review

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13 pages, 1125 KiB  
Review
Primary Role of the Kidney in Pathogenesis of Hypertension
by Gheun-Ho Kim
Life 2024, 14(1), 119; https://doi.org/10.3390/life14010119 - 14 Jan 2024
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Abstract
Previous transplantation studies and the concept of ‘nephron underdosing’ support the idea that the kidney plays a crucial role in the development of essential hypertension. This suggests that there are genetic factors in the kidney that can either elevate or decrease blood pressure. [...] Read more.
Previous transplantation studies and the concept of ‘nephron underdosing’ support the idea that the kidney plays a crucial role in the development of essential hypertension. This suggests that there are genetic factors in the kidney that can either elevate or decrease blood pressure. The kidney normally maintains arterial pressure within a narrow range by employing the mechanism of pressure-natriuresis. Hypertension is induced when the pressure-natriuresis mechanism fails due to both subtle and overt kidney abnormalities. The inheritance of hypertension is believed to be polygenic, and essential hypertension may result from a combination of genetic variants that code for renal tubular sodium transporters or proteins involved in regulatory pathways. The renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system (SNS) are the major regulators of renal sodium reabsorption. Hyperactivity of either the RAAS or SNS leads to a rightward shift in the pressure-natriuresis curve. In other words, hypertension is induced when the activity of RAAS and SNS is not suppressed despite increased salt intake. Sodium overload, caused by increased intake and/or reduced renal excretion, not only leads to an expansion of plasma volume but also to an increase in systemic vascular resistance. Endothelial dysfunction is caused by an increased intracellular Na+ concentration, which inhibits endothelial nitric oxide (NO) synthase and reduces NO production. The stiffness of vascular smooth muscle cells is increased by the accumulation of intracellular Na+ and subsequent elevation of cytoplasmic Ca++ concentration. In contrast to the hemodynamic effects of osmotically active Na+, osmotically inactive Na+ stimulates immune cells and produces proinflammatory cytokines, which contribute to hypertension. When this occurs in the gut, the microbiota may become imbalanced, leading to intestinal inflammation and systemic hypertension. In conclusion, the primary cause of hypertension is sodium overload resulting from kidney dysregulation. Full article
(This article belongs to the Special Issue Pulmonary Hypertension: From Bench to Bedside: 2nd Edition)
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14 pages, 578 KiB  
Review
Pulmonary Hypertension in Left Ventricular Valvular Diseases: A Comprehensive Review on Pathophysiology and Prognostic Value
by Nikolaos Velidakis, Elina Khattab, Evangelia Gkougkoudi and Nikolaos P. E. Kadoglou
Life 2023, 13(9), 1793; https://doi.org/10.3390/life13091793 - 22 Aug 2023
Viewed by 1118
Abstract
Left ventricular (LV) valvular diseases, make up one of the most common etiologies for pulmonary hypertension (PH), and it is not well understood how and at which degree it affects prognosis. The aim of the present study was a comprehensive review of the [...] Read more.
Left ventricular (LV) valvular diseases, make up one of the most common etiologies for pulmonary hypertension (PH), and it is not well understood how and at which degree it affects prognosis. The aim of the present study was a comprehensive review of the pathophysiologic mechanism of PH in patients with LV valvular diseases and the prognostic value of baseline and post-intervention PH in patients undergoing interventional treatment. The pathophysiology of PH in patients with LV valvular diseases involves gradual elevation of left ventricular filling pressure and left atrial pressure, which are passively transmitted to the pulmonary circulation and raise pulmonary artery systolic pressure (PASP). A long-lasting exposure to elevated PASP progressively leads to initially functional and thereafter irreversible structural changes in the pulmonary vasculature, leading up to high pulmonary vascular resistance. Surgical treatment of severe LV valvular diseases is highly effective in patients without resting PH or those with exercise-induced PH (EIPH) before intervention. In the case of pre-operative PH, successful interventional therapy decreases PASP, but the post-operative cardiac and all-cause mortality remain higher compared to patients without pre-operative PH. Hence, it is of paramount importance to detect patients with severe LV valvulopathies before the development of PH, since they will get greater benefits from early intervention. Full article
(This article belongs to the Special Issue Pulmonary Hypertension: From Bench to Bedside: 2nd Edition)
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