title: Diffuse ventricular fibrosis in atrial fibrillation: noninvasive evaluation and relationships with aging and systolic dysfunction.
abstract: OBJECTIVE
  The purpose of this study was to evaluate diffuse myocardial fibrosis of the left ventricle (LV) in patients with atrial fibrillation (AF).
  
  
  BACKGROUND
  Diffuse myocardial fibrosis is a hallmark of cardiomyopathy. Unlike replacement fibrosis, it is not visualized on delayed-enhancement cardiac magnetic resonance (CMR) imaging, but may be quantified with contrast-enhanced T(1) mapping methods. In atrial fibrillation (AF), it may be induced by arrhythmia or reflect pre-existing cardiomyopathy.
  
  
  METHODS
  Ninety subjects underwent CMR using a clinical 1.5-T scanner: 23 controls, 40 paroxysmal AF patients, and 27 persistent AF patients. Cardiac morphology and function was evaluated from CMR cine imaging. A histologically validated T(1) mapping sequence was used to calculate post-contrast T(1) relaxation time (T(1) time) of the LV myocardium as an index of diffuse myocardial fibrosis.
  
  
  RESULTS
  Age was similar across controls, paroxysmal AF patients, and persistent AF patients (54 ± 12 years, 58 ± 9 years, and 56 ± 10 years, p = NS). Persistent AF patients had larger indexed left atrium volume (55 ± 18 ml vs. 41 ± 12 ml and 47 ± 14 ml) and lower ejection fraction (54 ± 10% vs. 65 ± 6% and 61 ± 8%) than controls and paroxysmal AF patients (p < 0.05). Post-contrast ventricular T(1) time differed across all groups (controls, 535 ± 86 ms; paroxysmal AF, 427 ± 95 ms; persistent AF, 360 ± 84 ms; p < 0.001). Univariate predictors of post-contrast ventricular T(1) time included age, sex, AF category, ejection fraction, LV mass, congestive heart failure, and body mass index. After multivariate analysis, age, AF category, and ejection fraction remained independent predictors.
  
  
  CONCLUSIONS
  Post-contrast ventricular T(1) mapping identifies diffuse LV fibrosis in patients with AF and provides new insights into the association between AF and adverse ventricular remodeling.
authors.affiliation: Alfred Hospital and Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
authors.forename: Liang-Han
authors.initials: LH
authors.lastname: Ling
authors.forename: Peter M
authors.initials: PM
authors.lastname: Kistler
authors.forename: Andris H
authors.initials: AH
authors.lastname: Ellims
authors.forename: Leah M
authors.initials: LM
authors.lastname: Iles
authors.forename: Geraldine
authors.initials: G
authors.lastname: Lee
authors.forename: Gerard L
authors.initials: GL
authors.lastname: Hughes
authors.forename: Jonathan M
authors.initials: JM
authors.lastname: Kalman
authors.forename: David M
authors.initials: DM
authors.lastname: Kaye
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Taylor
mesh_terms: D000368:Aged; D000375:Aging; D001281:Atrial Fibrillation / Q000175:diagnosis / Q000209:etiology*; D009202:Cardiomyopathies / Q000150:complications* / Q000175:diagnosis; D018450:Disease Progression; D005260:Female; D005355:Fibrosis / Q000150:complications / Q000175:diagnosis; D005500:Follow-Up Studies; D006801:Humans; D019028:Magnetic Resonance Imaging, Cine / Q000379:methods*; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D012189:Retrospective Studies; D013599:Systole; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000175:diagnosis