title: Electrical and contractile remodeling during the first days of atrial fibrillation go hand in hand.
abstract: BACKGROUND
  The mechanisms of the atrial contractile dysfunction induced by atrial fibrillation (AF) are not completely understood. In particular, the relation between the atrial dysfunction and electrical remodeling has not yet been studied.
  
  
  RESULTS
  Seven goats were chronically instrumented with electrodes sutured to the atria and with ultrasonic piezoelectric crystals to record the atrial diameters. A pressure transducer was implanted in the right atrium. After 5 minutes, 3 hours, and throughout the first 5 days of artificially maintained AF, atrial contractile function was measured and the atrial effective refractory period (AERP) was monitored for comparison. Also, the positive inotropic effects of the L-type Ca2+-channel agonist BayY5959 and short trains of rapid atrial pacing were studied. After resumption of sinus rhythm, the recovery of atrial contractile function was followed. After 5 minutes of AF, atrial contractility was decreased by approximately 55% but recovered completely within 10 minutes. Five days of AF nearly completely abolished the atrial contractile function, and recovery took 2 days. During the first days of AF, the development of the contractile dysfunction followed the same time course as the shortening of AERP (electrical remodeling). In remodeled atria, BayY5959 increased atrial contractility to the same extent as it prolonged AERP. The inotropic effect of short trains of rapid atrial pacing was similar in normal and remodeled atria.
  
  
  CONCLUSIONS
  Depending on the duration of AF, different mechanisms contribute to the AF-induced atrial hypocontractility. Atrial contractile remodeling during several days of AF goes hand in hand with electrical remodeling and might be caused by a reduction of the L-type Ca2+-current.
authors.affiliation: Department of Physiology, University of Maastricht, The Netherlands. Schotten@fys.unimaas.nl
authors.forename: Ulrich
authors.initials: U
authors.lastname: Schotten
authors.forename: Mattias
authors.initials: M
authors.lastname: Duytschaever
authors.forename: Jannie
authors.initials: J
authors.lastname: Ausma
authors.forename: Sabine
authors.initials: S
authors.lastname: Eijsbouts
authors.forename: Hans-Ruprecht
authors.initials: HR
authors.lastname: Neuberger
authors.forename: Maurits
authors.initials: M
authors.lastname: Allessie
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002304:Cardiac Pacing, Artificial; D004095:Dihydropyridines / Q000494:pharmacology; D004553:Electric Conductivity; D004594:Electrophysiology; D006041:Goats; D006325:Heart Atria / Q000503:physiopathology; D007700:Kinetics; D009200:Myocardial Contraction; D010507:Periodicity; D012032:Refractory Period, Electrophysiological
chemical_list: C109289:BAY y 5959; D002120:Calcium Channel Agonists; D004095:Dihydropyridines