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Tricuspid regurgitation (TR) is a well-recognized factor contributing to adverse outcomes and mortality. Recent developments in transcatheter valve repair techniques, with the emergence of tricuspid transcatheter edge-to-edge repair (TEER) devices, have altered the treatment algorithm of TR and now offer a safe and feasible alternative for the effective management of the disease and an improvement in patient symptoms. Evidence from large studies and registries showcases the benefit of tricuspid interventions in terms of heart failure hospitalization and quality of life; however, most studies do not report a significant benefit in terms of hard outcomes. Even though longer-term follow-up may be needed to identify such differences, it is important to also identify distinct patient phenotypes that would benefit the most from such interventions, moving from pure anatomical criteria to an overall assessment of the patient's clinical status. Therefore, the aim of this review is to provide updates on potential moderators of the effect of tricuspid TEER, focusing on novel anatomical criteria, right cardiac function, and renal physiology, in order to guide patient selection and provide an insightful discussion on the optimal patient phenotype for future trial design.
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http://dx.doi.org/10.3390/jcdd12080293 | DOI Listing |
JCI Insight
September 2025
Edinburgh Medical School: Biomedical Sciences & Euan MacDonald Centre for M, University of Edinburgh, Edinburgh, United Kingdom.
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by low levels of SMN protein. Several therapeutic approaches boosting SMN are approved for human patients, delivering remarkable improvements in lifespan and symptoms. However, emerging phenotypes, including neurodevelopmental comorbidities, are being reported in some treated SMA patients, indicative of alterations in brain development.
View Article and Find Full Text PDFJ Clin Invest
September 2025
Department of Cellular and Molecular Medicine, UCSD, La Jolla, United States of America.
3-O-sulfation of heparan sulfate (HS) is the key determinant for binding and activation of Antithrombin III (AT). This interaction is the basis of heparin treatment to prevent thrombotic events and excess coagulation. Antithrombin-binding HS (HSAT) is expressed in human tissues, but is thought to be expressed in the subendothelial space, mast cells, and follicular fluid.
View Article and Find Full Text PDFJAMA Netw Open
September 2025
Perelman School of Medicine, University of Pennsylvania, Philadelphia.
Importance: As obesity rates rise in the US, managing associated metabolic comorbidities presents a growing burden to the health care system. While bariatric surgery has shown promise in mitigating established metabolic conditions, no large studies have quantified the risk of developing major obesity-related comorbidities after bariatric surgery.
Objective: To identify common metabolic phenotypes for patients eligible for bariatric surgery and to estimate crude and adjusted incidence rates of additional metabolic comorbidities associated with bariatric surgery compared with weight management program (WMP) alone.
J Neurooncol
September 2025
Department of Neurological Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Purpose: NOTCH3 is increasingly implicated for its oncogenic role in many malignancies, including meningiomas. While prior work has linked NOTCH3 expression to higher-grade meningiomas and treatment resistance, the metabolic phenotype of NOTCH3 activation remains unexplored in meningioma.
Methods: We performed single-cell RNA sequencing on NOTCH3 + human meningioma cell lines.
Clin Res Cardiol
September 2025
AGEL Hospital Trinec-Podlesi, Konska 453, Trinec, 739 61, Czech Republic.
Background: Pulmonary hypertension (PH) often coexists in patients undergoing transcatheter edge-to-edge mitral valve repair procedure (M-TEER). Its pre-procedural severity is considered a negative prognostic marker. Whether the post-procedural PH resulting from M-TEER can also serve as a long-term prognostic marker is unknown.
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