Role of atrial arrhythmia and ventricular response in atrial fibrillation induced atrial remodelling. Issue 2 (24th January 2020)

• Record Type: Journal Article
• Authors: Guichard, Jean-Baptiste; Xiong, Feng; Qi, Xiao-Yan; L'Heureux, Nathalie; Hiram, Roddy; Xiao, Jiening; Naud, Patrice; Tardif, Jean-Claude; Da Costa, Antoine; Nattel, Stanley
• Is Part Of: Cardiovascular research. Volume 117:Issue 2(2021)
• Page Start: 462
• Page End: 471
• Publication Date: 2020-01-24
• Subjects: Atrial fibrillation -- Atrial remodelling -- Fibrosis -- Arrhythmia-induced cardiomyopathy -- Ventricular response; Cardiovascular system -- Diseases -- Periodicals; Cardiovascular system -- Periodicals; 616.1
• DOI: 10.1093/cvr/cvaa007
• Languages: English
• ISSNs: 0008-6363

Abstract

Abstract: Aims: No studies have assessed the specific contributions of atrial fibrillation (AF)-related atrial vs. associated ventricular arrhythmia to remodelling. This study assessed the roles of atrial arrhythmia vs. high ventricular rate in AF-associated remodelling. Methods and results: Four primary dog-groups (12/group) were subjected to 3-week pacing: 600-b.p.m. atrial tachypacing maintaining AF [AF w/o- atrioventricular block (AVB)]; atrial tachypacing with atrioventricular-node ablation (AF+AVB) and ventricular-demand pacing (80 b.p.m.); 160-b.p.m. ventricular-tachypacing (V160) reproducing the response rate during AF; and sinus rhythm with AVB/ventricular-pacing at 80-b.p.m. (control group). At terminal study, left-atrial (LA) effective refractory period (ERP) was reduced equally in both AF groups (w/o-AVB and AF+AVB). AF-inducibility was increased strongly in AF groups (w/o-AVB and AF+AVB) and modestly in V160. AF duration was significantly increased in AF w/o-AVB but not in AF+AVB or V160. Conduction velocity was decreased in AF w/o-AVB, to a greater extent than in AF+AVB and V160. Atrial fibrous-tissue content was increased in AF w/o-AVB, AF+AVB and V160, with collagen-gene up-regulation only in AF w/o-AVB. Connexin43 gene expression was reduced only in AF w/o-AVB. An additional group of 240-b.p.m. ventricular tachypacing dogs (VTP240; to induce heart failure) was studied: vs. other tachypaced groups, VTP240 caused greater fibrosis, but no change in LA-ERP or AF-inducibility. VTP240 also increased AF duration, strongly decreased left ventricular ejection fraction, and was the only group with LA natriuretic-peptide activation. Conclusion: The atrial tachyarrhythmia and rapid ventricular response during AF produce distinct atrial remodelling; both contribute to the arrhythmogenic substrate, providing new insights into AF-related remodelling and novel considerations for ventricular rate-control. Graphical Abstract: