부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.yjmcc.2007.05.010 Byline: Wim Anne (a), Rik Willems (a), Patricia Holemans (a), Frank Beckers (a), Tania Roskams (b), Ilse Lenaerts (a), Hugo Ector (a), Hein Heidbuchel (a) Keywords: Angiotensin; Arrhythmia (mechanisms); Fibrosis; Remodeling; Matrix metalloproteinases Abstract: The development of atrial fibrillation (AF) is associated with electrical and structural remodeling. The aim of this study was to assess the contribution of electrical and structural remodeling to the development of AF in a rapid atrially paced ovine model with and without His bundle ablation and to determine the role of the angiotensin pathway and matrix metalloproteinases in this process. Thirty-five sheep were rapidly paced in the atrium and were randomized to undergo His bundle ablation (HBA) (21 sheep; HBA sheep) or not (14 sheep; non-HBA sheep). After HBA the ventricles were paced at 80 bpm. Both groups were subdivided to receive active treatment (quinapril+losartan) or placebo. Sheep were followed for 15 weeks. Inducible AF was defined as a rapid irregular atrial rhythm lasting >1 min. Inducible AF was considered to be persistent if during further follow-up no sinus rhythm (SR) was documented anymore. The inducibility of AF with atrial tachypacing was not different between the 4 groups. On the other hand, non-HBA sheep developed persistent AF significantly earlier than HBA sheep (p =0.028). They had elevated ventricular rates, diminished atrial MMP-2, increased TIMP-2 expression, and more extensive atrial fibrosis. Active treatment in these sheep significantly lowered AT-II (p =0.018), prevented atrial fibrogenesis (p Author Affiliation: (a) Department of Cardiology, University Hospital Gasthuisberg, University of Leuven, Leuven, Belgium (b) Department of Pathology, University Hospital Gasthuisberg, University of Leuven, Leuven, Belgium Article History: Received 10 October 2006; Revised 28 April 2007; Accepted 14 May 2007