Atrial and ventricular fibrosis induced by atrial fibrillation: Evidence to support early rhythm control

Boaz Avitall*, Jian Bi, Andrew Mykytsey, Alex Chicos

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

63 Scopus citations

Abstract

Background: Atrial fibrillation (AF) with poorly controlled ventricular response is known to be detrimental to ventricular function, conversely, heart failure (HF) increases susceptibility to AF. Objective: This study sought to examine the electropathological effects of 3 months of atrial fibrillation (AF) in dogs with and without concomitant ventricular dysfunction. Methods: Three groups of dogs were studied: dogs with chronic AF induced by rapid pacing and concomitant ventricular dysfunction induced by rapid ventricular response with intact atrioventricular node (AVN), dogs with ablated AVN and AF while the ventricle was paced at 80 beats/min, and normal sham dogs. After 3 months of AF, the first 2 groups underwent direct current cardioversion (DCCV) to normal sinus rhythm and were monitored for 3 months, followed by retesting of AF susceptibility. Tissue fibrosis was assessed at various sites by trichrome staining and quantitative immunohistochemistry. Results: AF was induced within 12 ± 4 days and 30 ± 13 days, respectively, in the intact and ablated AVN groups (P <.01). After 3 months of AF, left ventricular ejection fraction was 30.4% ± 10.1% and 55% ± 5% in the intact and ablated AVN groups (P <.01), respectively. After 3 months of normal sinus rhythm, AF was reinduced after 4 ± 2 and 7.2 ± 2 days, respectively (P = NS). There were no regional differences and an abundance of fibrosis within atria. Atrial fibrosis was significantly increased in intact AVN versus ablated AVN and sham groups, and also was greater in AVN-ablated versus sham dogs. Ventricular fibrosis was increased in intact AVN versus ablated AVN and sham groups and was not significantly different in ablated AVN and sham groups. Conclusion: AF without ventricular dysfunction results in atrial fibrosis and increased susceptibility to AF, suggesting that AF alone causes atrial fibrosis. AF with rapid ventricular response further increases atrial and ventricular fibrosis. Conversion to normal sinus rhythm should be done as early as possible to avoid atrial and ventricular fibrosis and increased susceptibility to AF.

Original languageEnglish (US)
Pages (from-to)839-845
Number of pages7
JournalHeart rhythm
Volume5
Issue number6
DOIs
StatePublished - Jun 1 2008

Keywords

  • AV nodal ablation
  • Atrial fibrillation
  • Fibrosis
  • Heart failure

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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