title: ACE-inhibitor treatment attenuates atrial structural remodeling in patients with lone chronic atrial fibrillation.
abstract: OBJECTIVE
  Chronic atrial fibrillation (AF) is characterized by a remodeling process which involves the development of fibrosis. Since angiotensin II has been suspected to be involved in this process, the aim of our study was to investigate a possible influence of an ACE-I therapy in patients with chronic AF regarding the occurrence of left atrial structural remodeling.
  
  
  METHODS
  Atrial tissue samples were obtained from patients with lone chronic AF or sinus rhythm (SR). Collagen I, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) protein expression were measured by quantitative Western Blotting techniques and calculated as mean +/- SEM. Histological tissue samples were used for calculating microvessel density (microvessel/mm(2) +/- SEM).
  
  
  RESULTS
  In AF, the collagen amount was higher (1.78 +/- 0.21; p = 0.01) vs. SR (0.37 +/- 0.07) accompanied by declining microcapillary density (AF: 145 +/- 13 vs. SR: 202 +/- 9; p = 0.01). Additionally, a negative correlation (p = 0.01) between collagen content and microcapillary density was observed. To investigate the influence of an ACE-I therapy on this remodeling process, patient groups were divided into AF and SR both with or without ACE-I. Interestingly, there was a significantly lower expression of collagen I in AF with ACE-I (1.04 +/- 0.26) vs. AF without ACE-I treatment (2.07 +/- 0.24, p = 0.02). The microcapillaries were not diminished in AF with ACE-I (180 +/- 15) vs. SR with ACE-I (196 +/- 9), but there was a significant rarification in AF without ACE-I (123 +/- 18; p = 0.03). The expression of VEGF and bFGF did not reveal any significant differences.
  
  
  CONCLUSIONS
  In patients undergoing ACE-I treatment: atrial structural remodeling was attenuated and the loss of atrial microcapillaries was prevented.
authors.affiliation: University of Leipzig-Heart Center, Department of Cardiac Surgery, Strümpellstrasse 19, 04289 Leipzig, Germany. andreasboldt@web.de
authors.forename: A
authors.initials: A
authors.lastname: Boldt
authors.forename: A
authors.initials: A
authors.lastname: Scholl
authors.forename: J
authors.initials: J
authors.lastname: Garbade
authors.forename: M E
authors.initials: ME
authors.lastname: Resetar
authors.forename: F W
authors.initials: FW
authors.lastname: Mohr
authors.forename: J F
authors.initials: JF
authors.lastname: Gummert
authors.forename: St
authors.initials: S
authors.lastname: Dhein
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D015153:Blotting, Western; D002196:Capillaries / Q000187:drug effects; D002908:Chronic Disease; D003094:Collagen / Q000378:metabolism; D003331:Coronary Vessels / Q000187:drug effects; D003720:Densitometry; D016222:Fibroblast Growth Factor 2 / Q000032:analysis; D005355:Fibrosis; D006325:Heart Atria / Q000187:drug effects* / Q000473:pathology; D006801:Humans; D008875:Middle Aged; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D016222:Fibroblast Growth Factor 2; D003094:Collagen