| Electrophysiologic remodeling of the left ventricle in pressure overload-induced right ventricular failure. | |
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MedLine Citation:
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PMID: 22676940 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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OBJECTIVES: The purpose of this study was to analyze the electrophysiologic remodeling of the atrophic left ventricle (LV) in right ventricular (RV) failure (RVF) after RV pressure overload. BACKGROUND: The LV in pressure-induced RVF develops dysfunction, reduction in mass, and altered gene expression, due to atrophic remodeling. LV atrophy is associated with electrophysiologic remodeling. METHODS: We conducted epicardial mapping in Langendorff-perfused hearts, patch-clamp studies, gene expression studies, and protein level studies of the LV in rats with pressure-induced RVF (monocrotaline [MCT] injection, n = 25; controls with saline injection, n = 18). We also performed epicardial mapping of the LV in patients with RVF after chronic thromboembolic pulmonary hypertension (CTEPH) (RVF, n = 10; no RVF, n = 16). RESULTS: The LV of rats with MCT-induced RVF exhibited electrophysiologic remodeling: longer action potentials (APs) at 90% repolarization and effective refractory periods (ERPs) (60 ± 1 ms vs. 44 ± 1 ms; p < 0.001), and slower longitudinal conduction velocity (62 ± 2 cm/s vs. 70 ± 1 cm/s; p = 0.003). AP/ERP prolongation agreed with reduced Kcnip2 expression, which encodes the repolarizing potassium channel subunit KChIP2 (0.07 ± 0.01 vs. 0.11 ± 0.02; p < 0.05). Conduction slowing was not explained by impaired impulse formation, as AP maximum upstroke velocity, whole-cell sodium current magnitude/properties, and mRNA levels of Scn5a were unaltered. Instead, impulse transmission in RVF was hampered by reduction in cell length (111.6 ± 0.7 μm vs. 122.0 ± 0.4 μm; p = 0.02) and width (21.9 ± 0.2 μm vs. 25.3 ± 0.3 μm; p = 0.002), and impaired cell-to-cell impulse transmission (24% reduction in Connexin-43 levels). The LV of patients with CTEPH with RVF also exhibited ERP prolongation (306 ± 8 ms vs. 268 ± 5 ms; p = 0.001) and conduction slowing (53 ± 3 cm/s vs. 64 ± 3 cm/s; p = 0.005). CONCLUSIONS: Pressure-induced RVF is associated with electrophysiologic remodeling of the atrophic LV. |
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Authors:
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Maxim Hardziyenka; Maria E Campian; Arie O Verkerk; Sulaiman Surie; Antoni C G van Ginneken; Sara Hakim; André C Linnenbank; H A C M Rianne de Bruin-Bon; Leander Beekman; Mart N van der Plas; Carol A Remme; Toon A B van Veen; Paul Bresser; Jacques M T de Bakker; Hanno L Tan |
Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Journal of the American College of Cardiology Volume: 59 ISSN: 1558-3597 ISO Abbreviation: J. Am. Coll. Cardiol. Publication Date: 2012 Jun |
Date Detail:
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Created Date: 2012-06-08 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8301365 Medline TA: J Am Coll Cardiol Country: United States |
Other Details:
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Languages: eng Pagination: 2193-202 Citation Subset: AIM; IM |
Copyright Information:
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Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. |
Affiliation:
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Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; Interuniversity Cardiology Institute of the Netherlands, Utrecht, the Netherlands. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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