title: Persistent lone atrial fibrillation: clinicopathologic study of 19 cases.
abstract: BACKGROUND
  The extent to which atrial myocardium is remodeled in patients with persistent lone atrial fibrillation (LAF) is largely unknown.
  
  
  OBJECTIVE
  The purpose of this study was to perform a clinicopathologic investigation in patients with persistent LAF.
  
  
  METHODS
  We characterized structural and molecular remodeling in atrial biopsies from 19 patients (17 males, mean age 49 years) with persistent (>7 days; n = 8) or long-lasting persistent (>1 year; n = 11) LAF who underwent surgical ablation. Atrial tissue from 15 autopsy samples without clinicopathologic evidence of heart disease served as controls.
  
  
  RESULTS
  Morphometric analysis showed cardiomyocyte hypertrophy and greater amounts of myolytic damage and interstitial fibrosis in persistent LAF patients compared to controls (P <.0001). Atrial tissue levels of heme oxygenase-1 and 3-nitrotyrosine were increased in persistent LAF patients (P <.001), consistent with oxidative stress. Levels of superoxide dismutase-2, interleukin-8, interleukin-10, tumor necrosis factor-α, and thiobarbituric acid reactive substance were greater in controls than in persistent LAF patients. Immunoreactive signal for connexin43 was reduced more frequently in persistent LAF patients than controls. There was no correlation between features of structural or molecular remodeling and clinical parameters, including persistent LAF duration.
  
  
  CONCLUSIONS
  In persistent LAF patients, the atria are modified by structural remodeling and molecular changes of oxidative stress. Tissue changes in persistent LAF appear to occur early after its onset and are qualitatively no different than those observed in patients with atrial fibrillation related to conventional risk factors. These findings suggest that different types of atrial fibrillation are associated with the same spectrum of tissue lesions. Early intervention to restore sinus rhythm in persistent LAF patients may prevent irreversible tissue change, especially interstitial fibrosis.
authors.affiliation: Department of Biomedical, Biotechnological, and Translational Sciences (S.Bi.Bi.T.), Unit of Pathology, University of Parma, Parma, Italy. Electronic address: domenico.corradi@unipr.it.
authors.forename: Domenico
authors.initials: D
authors.lastname: Corradi
authors.affiliation: Division of Cardiology, Vaio Hospital, Fidenza, Italy.
authors.forename: Sergio
authors.initials: S
authors.lastname: Callegari
authors.affiliation: Department of Biomedical, Biotechnological, and Translational Sciences (S.Bi.Bi.T.), Unit of Pathology, University of Parma, Parma, Italy.
authors.forename: Laura
authors.initials: L
authors.lastname: Manotti
authors.affiliation: Cardiothoracic Surgery Unit, Department of Cardiology, San Raffaele University Hospital, Milan, Italy.
authors.forename: David
authors.initials: D
authors.lastname: Ferrara
authors.affiliation: Department of Clinical and Experimental Medicine, Laboratory of Industrial Toxicology, University of Parma, Parma, Italy.
authors.forename: Matteo
authors.initials: M
authors.lastname: Goldoni
authors.affiliation: Department of Clinical and Experimental Medicine, Laboratory of Industrial Toxicology, University of Parma, Parma, Italy.
authors.forename: Rossella
authors.initials: R
authors.lastname: Alinovi
authors.affiliation: Department of Clinical and Experimental Medicine, Laboratory of Industrial Toxicology, University of Parma, Parma, Italy.
authors.forename: Silvana
authors.initials: S
authors.lastname: Pinelli
authors.affiliation: Department of Clinical and Experimental Medicine, Laboratory of Industrial Toxicology, University of Parma, Parma, Italy; Italian Workers' Compensation Authority (INAIL) Research Center at the University of Parma, Parma, Italy.
authors.forename: Paola
authors.initials: P
authors.lastname: Mozzoni
authors.affiliation: Department of Clinical and Experimental Medicine, Laboratory of Industrial Toxicology, University of Parma, Parma, Italy; Italian Workers' Compensation Authority (INAIL) Research Center at the University of Parma, Parma, Italy.
authors.forename: Roberta
authors.initials: R
authors.lastname: Andreoli
authors.affiliation: Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
authors.forename: Angeliki
authors.initials: A
authors.lastname: Asimaki
authors.affiliation: Cardiothoracic Surgery Unit, Department of Cardiology, San Raffaele University Hospital, Milan, Italy.
authors.forename: Alberto
authors.initials: A
authors.lastname: Pozzoli
authors.affiliation: Department of Biomedical, Biotechnological, and Translational Sciences (S.Bi.Bi.T.), Unit of Pathology, University of Parma, Parma, Italy.
authors.forename: Gabriella
authors.initials: G
authors.lastname: Becchi
authors.affiliation: Department of Clinical and Experimental Medicine, Laboratory of Industrial Toxicology, University of Parma, Parma, Italy.
authors.forename: Antonio
authors.initials: A
authors.lastname: Mutti
authors.affiliation: Cardiothoracic Surgery Unit, Department of Cardiology, San Raffaele University Hospital, Milan, Italy.
authors.forename: Stefano
authors.initials: S
authors.lastname: Benussi
authors.affiliation: Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
authors.forename: Jeffrey E
authors.initials: JE
authors.lastname: Saffitz
authors.affiliation: Cardiothoracic Surgery Unit, Department of Cardiology, San Raffaele University Hospital, Milan, Italy.
authors.forename: Ottavio
authors.initials: O
authors.lastname: Alfieri
mesh_terms: D000328:Adult; D000368:Aged; D001281:Atrial Fibrillation / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D064752:Atrial Remodeling; D015415:Biomarkers / Q000378:metabolism; D005260:Female; D006325:Heart Atria / Q000473:pathology* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000473:pathology*; D018384:Oxidative Stress
chemical_list: D015415:Biomarkers
keywords: Atrial cardiomyocyte; Lone atrial fibrillation; Pathology; Remodeling; Structure