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Verfasst von:Ruppert, Mihály [VerfasserIn]   i
 Korkmaz-İçöz, Sevil [VerfasserIn]   i
 Li, Shiliang [VerfasserIn]   i
 Karck, Matthias [VerfasserIn]   i
 Radovits, Tamás [VerfasserIn]   i
 Szabó, Gábor [VerfasserIn]   i
Titel:Reverse electrical remodeling following pressure unloading in a rat model of hypertension-induced left ventricular myocardial hypertrophy
Verf.angabe:Mihály Ruppert, Sevil Korkmaz-Icöz, Shiliang Li, Béla Merkely, Matthias Karck, Tamás Radovits & Gábor Szabó
E-Jahr:2017
Jahr:July 2017
Umfang:9 S.
Fussnoten:Published online 26 January 2017
Titel Quelle:Enthalten in: Hypertension research
Ort Quelle:[London] : Macmillan Publishers Limited, part of Springer Nature, 1992
Jahr Quelle:2017
Band/Heft Quelle:40(2017), 7, Seite 637-645
ISSN Quelle:1348-4214
Abstract:Pressure overload-induced left ventricular myocardial hypertrophy (LVH) is characterized by increased proarrhythmic vulnerability. In contrast, pressure unloading leads to reverse remodeling and decreases LVH-associated arrhythmogenicity. However, cellular changes that occur during reverse electrical remodeling have been studied less. Therefore, we aimed to provide an electrocardiographic characterization of a rat model of LVH that underwent pressure unloading and to simultaneously identify the underlying cellular and functional alterations. LVH was induced in rats by abdominal aortic banding for 6 or 12 weeks. Sham-operated animals served as controls. Pressure unloading was evoked by removing the aortic constriction after week 6 (debanded). Serial echocardiography and electrocardiography were performed to investigate the development and the regression of LVH. Protein expression levels were detected by western blot. Myocardial fibrosis was assessed by Picrosirius red staining. Pressure unloading resulted in the regression of LVH in correlation with the reversion of the prolonged corrected QT interval (cQT: 68.7±1.6 vs. 91.0±1.9 ms debanded week 12 vs. AB week 12, P<0.05). Furthermore, pressure unloading prevented the functional decompensation of LVH and simultaneously preserved adequate atrioventricular conduction (PQ: 47.5±1.2 vs. 53.8±1.9 ms debanded week 12 vs. AB week 12, P<0.05). Finally, pressure unloading effectively preceded the broadening of the QRS complex (QRS: 21.8±0.5 vs. 24.9±0.7 ms debanded week 12 vs. AB week 12, P<0.05) in parallel with the attenuation of interstitial collagen accumulation. The regression of LVH with maintained cardiac function and decreased myocardial fibrosis contributes to pressure unloading-induced reverse electrical remodeling.
DOI:doi:10.1038/hr.2017.1
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: http://dx.doi.org/10.1038/hr.2017.1
 Volltext: https://www.nature.com/articles/hr20171
 DOI: https://doi.org/10.1038/hr.2017.1
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1575435985
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