Left atrial remodeling, characterized by enlargement and hypertrophy of the left atrium and increased fibrosis, was accompanied by an increased incidence of atrial fibrillation. While before morphological changes at the early stage of hypertension, how overloaded hypertension influences the transcriptomic profile of the left atrium remains unclear. Therefore, RNA-sequencing was performed to define the RNA expressing profiles of left atrium in spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats as a control group. We also compared the changes in the RNA expression profiles in SHRs treated with an angiotensin receptor blocker (ARB) and angiotensin receptor-neprilysin inhibitor (ARNI) to assess the distinct effects on the left atrium. In total, 1,558 differentially expressed genes were found in the left atrium between WKY rats and SHRs. Bioinformatics analysis showed that these mRNAs could regulate upstream pathways in atrial remodeling through atrial fibrosis, inflammation, electrical remodeling, and cardiac metabolism. The regulated transcripts detected in the left atrial tissue in both the ARB-treated and ARNI-treated groups were related to metabolism. In contrast to the ARB-treated rates, the transcripts in ARNI-treated rats were mapped to the cyclic guanosine monophosphate-protein kinase G signaling pathway.
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http://dx.doi.org/10.3389/fphar.2022.989636 | DOI Listing |
Curr Cardiol Rep
January 2025
Hasselt University, Faculty of Medicine and Life Sciences / Limburg Clinical Research Centre, Agoralaan, Diepenbeek, Belgium.
Purpose Of Review: This review aims to explore the complex interplay between atrial functional mitral regurgitation (AFMR), atrial fibrillation (AF), and heart failure with preserved ejection fraction (HFpEF). The goal is to define these conditions, examine their underlying mechanisms, and discuss treatment perspectives, particularly addressing diagnostic challenges.
Recent Findings: Recent research highlights the rising prevalence of AFMR, now accounting for nearly one-third of significant mitral regurgitation cases.
JACC Clin Electrophysiol
December 2024
Physiology, Amsterdam Cardiovascular Sciences, Heart Failure, and Arrhythmias, Amsterdam University Medical Center, location Vrije Universiteit Amsterdam, Amsterdam, the Netherlands. Electronic address:
Background: Atrial fibrillation (AF) persistence is associated with molecular remodeling that fuels electrical conduction abnormalities in atrial tissue. Previous research revealed DNA damage as a molecular driver of AF.
Objectives: This study sought to explore the diagnostic value of DNA damage in atrial tissue and blood samples as an indicator of the prevalence of electrical conduction abnormalities and stage of AF.
Turk Kardiyol Dern Ars
January 2025
Department of Cardiology, Gülhane Faculty of Medicine, University of Health Sciences, Ankara, Türkiye.
Severe mitral regurgitation (MR) following surgical repair of the mitral valve poses a significant clinical challenge. Patients who have undergone surgery are typically at high risk for a second operation. This report details the case of a 54-year-old male who underwent aortic valve replacement and mitral valve repair using a 34-ring, 14 years prior.
View Article and Find Full Text PDFJ Clin Med
December 2024
Department of Cardiac Surgery, MEDINET Heart Center Ltd., 51-124 Wrocław, Poland.
Cardiac myxomas are benign tumors of the heart. They occur mostly in the left atrium. The preferred treatment is surgical resection, which can be performed via conventional median sternotomy, minimally invasive, or robotic-assisted approaches.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Second Department of Cardiology, Hippokration General Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
Atrial fibrosis is a hallmark of atrial cardiomyopathy and plays a pivotal role in the pathogenesis of atrial fibrillation (AF), contributing to its onset and progression. The mechanisms underlying atrial fibrosis are multifaceted, involving stretch-induced fibroblast activation, oxidative stress, inflammation, and coagulation pathways. Variations in fibrosis types-reactive and replacement fibrosis-are influenced by patient-specific factors such as age, sex, and comorbidities, complicating therapeutic approaches.
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