title: Electroanatomic remodeling of the left atrium in paroxysmal and persistent atrial fibrillation patients without structural heart disease.
abstract: BACKGROUND
  The nature of the atrial substrate thought to contribute toward maintaining atrial fibrillation (AF) outside the pulmonary veins remains poorly defined. Therefore, our objective was to determine whether patients with paroxysmal and persistent AF have an abnormal electroanatomic substrate within the left atrium (LA).
  
  
  RESULTS
  Thirty-one patients with AF (17 paroxysmal AF and 14 persistent AF) were compared with 15 age-matched controls with left-sided supraventricular tachycardia (SVT). High-density 3-dimensional electroanatomic maps were created and the LA was divided into 8 segments for regional analysis. Bipolar voltage, conduction, and effective refractory periods (ERPs) of the posterior LA, left atrial appendage (LAA), and distal coronary sinus (CSd) and percentage complex signals were assessed. In the majority of LA regions, compared with controls, AF patients had: (1) lower mean voltage and a higher percentage low voltage; (2) slower conduction; and (3) more prevalent complex signals. Many of these changes were more marked in the persistent than the paroxysmal AF group.
  
  
  CONCLUSIONS
  Patients with AF have lower regional voltage, increased proportion of low voltage, slowed conduction, and increased proportion of complex signals compared to controls. Many of these changes are more pronounced in persistent AF patients, suggesting there may be a progressive nature to the changes. Differences occurred in the absence of structural heart disease. These substrate abnormalities provide further insight into the progressive nature of atrial remodeling and the mechanisms involved in maintenance of AF.
authors.affiliation: Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia.
authors.forename: Andrew W
authors.initials: AW
authors.lastname: Teh
authors.forename: Peter M
authors.initials: PM
authors.lastname: Kistler
authors.forename: Geoffrey
authors.initials: G
authors.lastname: Lee
authors.forename: Caroline
authors.initials: C
authors.lastname: Medi
authors.forename: Patrick M
authors.initials: PM
authors.lastname: Heck
authors.forename: Steven J
authors.initials: SJ
authors.lastname: Spence
authors.forename: Paul B
authors.initials: PB
authors.lastname: Sparks
authors.forename: Joseph B
authors.initials: JB
authors.lastname: Morton
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Kalman
mesh_terms: D000368:Aged; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D020517:Atrial Appendage / Q000503:physiopathology; D001281:Atrial Fibrillation / Q000473:pathology* / Q000503:physiopathology / Q000601:surgery; D016279:Atrial Function, Left; D018780:Body Surface Potential Mapping; D017115:Catheter Ablation; D054326:Coronary Sinus / Q000473:pathology / Q000503:physiopathology; D004351:Drug Resistance; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D005355:Fibrosis; D006321:Heart / Q000503:physiopathology*; D006325:Heart Atria / Q000473:pathology* / Q000503:physiopathology*; D006329:Heart Conduction System / Q000502:physiology; D006331:Heart Diseases / Q000150:complications; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D012032:Refractory Period, Electrophysiological / Q000502:physiology; D013617:Tachycardia, Supraventricular / Q000503:physiopathology
chemical_list: D000889:Anti-Arrhythmia Agents