title: Contraction-excitation feedback in human atrial fibrillation.
abstract: BACKGROUND
  Contraction-excitation feedback, that is, electrophysiologic changes that are caused or preceded by mechanical changes of the myocardium, has been extensively studied in the ventricles. The role of contraction-excitation feedback in the atria, and more particularly in the genesis and maintenance of atrial fibrillation, has been less adequately investigated.
  
  
  OBJECTIVE
  The aim of the present study was to determine whether increased right atrial pressure (RAP) facilitates the induction of atrial fibrillation (AF) in patients with a history of lone AF.
  
  
  METHODS
  Sixteen patients with a history of paroxysmal AF but without structural heart disease were included in the study. All patients underwent electrophysiologic study at both a lower (3.1 +/- 2.0 mmHg) and (in 13 cases) a higher (6.4 +/- 2.5 mmHg) RAP. "Higher" was considered the pressure following rapid (in about 30 min) intravenous administration of normal saline or before the administration of a diuretic.
  
  
  RESULTS
  Rapid atrial pacing induced AF in 19 of 29 attempts. At a lower pressure, rapid pacing induced brief (3 s to 3 min) AF in 3 of 16 patients, long-lasting (> 3 min) AF in 3 of 16 patients, and no AF in 10 of 16 patients. At a higher pressure, brief AF was induced in 3 of 10 patients in whom no AF could be induced at a lower pressure, and long-lasting AF in 10 patients in whom either brief AF (3 cases) or no AF (7 cases) was induced at a lower pressure. In 11 patients, in whom Wenckebach periodicity was determined at both higher and lower pressure, the critical cycle length at which atrioventricular block appeared was significantly (p < 0.001, paired t-test) longer (349.1 +/- 44.4 ms, i.e., +15.5 +/- 11.3 ms) at higher than at lower atrial pressure (333.6 +/- 41.0 ms). In nine patients, in whom Wenckebach periodicity was determined and two rhythms occurred at different pressures, the critical cycle length was 332.2 +/- 45.8 ms when associated with sinus rhythm, and significantly (p < 0.01) longer (344.4 +/- 48.0 ms, i.e., +12.2 +/- 8.3 ms) when associated with induction of AF.
  
  
  CONCLUSIONS
  In patients with lone atrial fibrillation, modest increases in atrial pressure may facilitate the induction of atrial fibrillation.
authors.affiliation: Department of Clinical Therapeutics, Medical School of Athens University, Greece.
authors.forename: A
authors.initials: A
authors.lastname: Antoniou
authors.forename: D
authors.initials: D
authors.lastname: Milonas
authors.forename: J
authors.initials: J
authors.lastname: Kanakakis
authors.forename: S
authors.initials: S
authors.lastname: Rokas
authors.forename: D A
authors.initials: DA
authors.lastname: Sideris
mesh_terms: D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000628:therapy; D001794:Blood Pressure / Q000502:physiology; D006328:Cardiac Catheterization; D002304:Cardiac Pacing, Artificial; D004232:Diuretics / Q000008:administration & dosage / Q000627:therapeutic use; D004562:Electrocardiography; D005246:Feedback / Q000502:physiology*; D005665:Furosemide / Q000008:administration & dosage / Q000627:therapeutic use; D006325:Heart Atria / Q000503:physiopathology*; D006801:Humans; D007262:Infusions, Intravenous; D008875:Middle Aged; D009200:Myocardial Contraction / Q000502:physiology*
chemical_list: D004232:Diuretics; D005665:Furosemide