Reverse electrical remodeling following pressure unloading in a rat model of myocardial hypertrophy
█ Original article
DOI: 10.26430/CHUNGARICA.2018.48.2.118
Authors:
Ruppert Mihály1,2*, Barta Bálint András2*, Korkmaz-Icöz Sevil1, Li Shiliang1, Oláh Attila2, Mátyás Csaba2, Németh Balázs Tamás2, Benke Kálmán2, Sayour Alex Ali2, Karck Matthias1, Merkely Béla2, Radovits Tamás2*, Szabó Gábor1*
1Ruprecht-Karls Egyetem Szívsebészeti Klinika, Kísérleti Kutató Laboratórium, Heidelberg
2Semmelweis Egyetem, Kísérleti Kutató Laboratórium, Városmajori Szív- és Érsebészeti Klinika, Budapest
*A szerzők azonos mértékben járultak hozzá a közleményhez
Készült Ruppert et al. Hypertens Res 2017; 40: 637–645. közleményének felhasználásával a SpringerNature Kiadó írásos engedélyével (1)
Summary
Introduction: 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.
Methods: 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.
Results: 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 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 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 vs. AB week 12, P<0.05) in parallel with the attenuation of interstitial collagen accumulation.
Conclusions: The regression of LVH with maintained cardiac function and decreased myocardial fibrosis contributes to pressure unloading-induced reverse electrical remodeling.
ISSUE: CARDIOLOGIA HUNGARICA | 2018 | VOLUME 48, ISSUE 2
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