ArticleCardiovascular research2009
Chronic heart failure and the substrate for atrial fibrillation.
Article in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 75 citations in OpenAlex.
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- Gene Therapies in Atrial Fibrillation.Journal of cardiovascular translational research · 2025Review
- Aging-associated atrial fibrillation: A comprehensive review focusing on the potential mechanisms.Aging cell · 2024Review
- Increased Risk for Atrial Alternans in Rabbit Heart Failure: The Role of CaBiomolecules · 2023Article
- Causal association of calcific aortic valve stenosis and atrial fibrillation: a Mendelian randomization study.Scientific reports · 2023Article
- Diversity of cells and signals in the cardiovascular system.The Journal of physiology · 2023Article
- IiScience · 2022Article
- Ero1α-Dependent ERp44 Dissociation From RyR2 Contributes to Cardiac Arrhythmia.Circulation research · 2022Article
- Slowing down as we age: aging of the cardiac pacemaker's neural control.GeroScience · 2022Review
- Arrhythmogenic Remodeling in the Failing Heart.Cells · 2021Review
- Left Atrial Myopathy in Atrial Fibrillation and Heart Failure: Clinical Implications, Mechanisms, and Therapeutic Targets.Current heart failure reports · 2021Review
- Fetal cardiomyocyte phenotype, ketone body metabolism, and mitochondrial dysfunction in the pathology of atrial fibrillation.Molecular and cellular biochemistry · 2021Review
- Towards the Development of AgoKirs: New Pharmacological Activators to Study KInternational journal of molecular sciences · 2020Review
- Heart failure-induced atrial remodelling promotes electrical and conduction alternans.PLoS computational biology · 2020Article
- Role of Oxidative Stress in the Genesis of Ventricular Arrhythmias.International journal of molecular sciences · 2020Review
- Ischemic Heart Disease and Heart Failure: Role of Coronary Ion Channels.International journal of molecular sciences · 2020Review
- Chronic heart failure increases negative chronotropic effects of adenosine in canine sinoatrial cells via A1R stimulation and GIRK-mediated ILife sciences · 2020Article
- The imminent epidemic of atrial fibrillation and its concomitant diseases - Myocardial infarction and heart failure - A cause for concern.International journal of cardiology · 2019Review
- Heart Failure Differentially Modulates Natural (Sinoatrial Node) and Ectopic (Pulmonary Veins) Pacemakers: Mechanism and Therapeutic Implication for Atrial Fibrillation.International journal of molecular sciences · 2019Review
- Profibrotic, Electrical, and Calcium-Handling Remodeling of the Atria in Heart Failure Patients With and Without Atrial Fibrillation.Frontiers in physiology · 2018Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
aimsWe sought to define the underlying mechanisms for atrial fibrillation (AF) during chronic heart failure (HF). METHODS AND
resultsPreliminary studies showed that 4 months of HF resulted in irreversible systolic dysfunction (n = 9) and a substrate for sustained inducible AF (>3 months, n = 3). We used a chronic (4-month) canine model of tachypacing-induced HF (n = 10) to assess atrial electrophysiological remodelling, relative to controls (n = 5). Left ventricular fractional shortening was reduced from 37.2 +/- 0.83 to 13.44 +/- 2.63% (P < 0.05). Left atrial (LA) contractility (fractional area change) was reduced from 34.9 +/- 7.9 to 27.9 +/- 4.23% (P < 0.05). Action potential durations (APDs) at 50 and 90% repolarization were shortened by approximately 60 and 40%, respectively, during HF (P < 0.05). HF-induced atrial remodelling included increased fibrosis, increased I(to), and decreased I(K1), I(Kur), and I(Ks) (P < 0.05). HF induced increases in LA Kv channel interacting protein 2 (P < 0.05), no change in Kv4.3, Kv1.5, or Kir2.3, and reduced Kir2.1 (P < 0.05). When I(Ca-L) was elicited by action potential (AP) clamp, HF APs reduced the integral of I(Ca) in control myocytes, with a larger reduction in HF myocytes (P < 0.05). I(CaL) measured with standard voltage clamp was unchanged by HF. Incubation of myocytes with N-acetylcysteine (a glutathione precursor) attenuated HF-induced electrophysiological alterations. LA angiotensin-1 receptor expression was increased in HF.
conclusionChronic HF causes alterations in ion channel expression and ion currents, resulting in attenuation of the APD and atrial contractility and a substrate for persistent AF.
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Registered trials
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