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Patients with heart failure who have a prolonged PR interval are at a greater risk of adverse clinical outcomes than those with a normal PR interval. Potential mechanisms of harm relating to prolonged PR intervals include reduced ventricular filling and also the potential progression to a higher degree heart block. There has, however, been relatively little work specifically focusing on isolated PR prolongation as a therapeutic target. Secondary analyses of trials of biventricular pacing in heart failure have suggested that PR prolongation is both a prognostic marker and a promising treatment target. However, while biventricular pacing offers an improved activation pattern, it is nonetheless less physiological than native conduction in patients with a narrow QRS duration, and thus, may not be the ideal option for achieving therapeutic shortening of atrioventricular delay. Conduction system pacing aims to preserve physiological ventricular activation and may therefore be the ideal method for ventricular pacing in patients with isolated PR prolongation. Acute haemodynamic experiments and the recently reported His-optimized pacing evaluated for heart failure (HOPE HF) Randomised Controlled Trial demonstrates the potential benefits of physiological ventricular pacing on patient symptoms and left ventricular function in patients with heart failure.
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http://dx.doi.org/10.1093/eurheartjsupp/suad116 | DOI Listing |
Am J Respir Crit Care Med
September 2025
Temple University Hospital, Pulm & Crit Care Medicine, Philadelphia, Pennsylvania, United States.
Rationale: AIRFLOW-3 was a 1:1 randomized, double blind, sham controlled trial of the d'Nerva Targeted Lung Denervation (TLD) System in patients with COPD.
Objective: Evaluate the impact of TLD on COPD exacerbations compared to optimal medical treatment.
Methods: AIRFLOW-3 patients were symptomatic (CAT ≥10) with moderate to very severe airflow obstruction (25% ≤ FEV ≤ 80% predicted) and GOLD E status (≥2 moderate or ≥1 severe exacerbation over prior 12 months).
PLoS One
September 2025
Department of Cardiology Ullevaal, Oslo University Hospital, Oslo, Norway.
Background: The gut microbiota produces numerous metabolites that can enter the circulation and exert effects outside the gut. Several studies have reported altered gut microbiota composition and circulating metabolites in patients with chronic heart failure (HF) compared to healthy controls. Limited data is available on the interplay between dysbiotic features of the gut microbiota and altered circulating metabolites in HF patients.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
September 2025
Institute of Pharmacology and Toxicology, Goethe University Frankfurt, Frankfurt, Germany.
The A20 binding inhibitor of nuclear factor-kappa B (NF-κB)-1 (ABIN-1) serves as a ubiquitin sensor and autophagy receptor, crucial for modulating inflammation and cell death. Our previous in vitro investigation identified the LC3-interacting region (LIR) motifs 1 and 2 of ABIN-1 as key mitophagy regulators. This study aimed to explore the in vivo biological significance of ABIN1-LIR domains using a novel CRISPR-engineered ABIN1-ΔLIR1/2 mouse model, which lacks both LIR motifs.
View Article and Find Full Text PDFJ Vis Exp
August 2025
Physiology Unit, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases.
Resistance arteries, which include small arteries and arterioles, play essential roles in regulating blood pressure and tissue perfusion. Dysfunction in these arteries can lead to various cardiovascular conditions such as hypertension, atherosclerosis, and heart failure, as well as neurovascular conditions. The examination of human resistance arteries is crucial for understanding cardiovascular disease mechanisms and developing targeted therapeutic strategies.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
September 2025
Department of Kinesiology, University of Virginia, Charlottesville, VA, USA.
Nitric oxide (NO) is essential for cardiovascular health and is purported as an ergogenic aid. Endothelial dysfunction and reduced endogenous NO production are hallmarks of heart failure (HF), which may contribute to impaired exercise capacity. Oral inorganic nitrate supplementation offers an exogenous route to increase bioavailable NO via reduction of nitrate by oral commensal bacteria.
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