title: Effects of acute atrial dilation on heterogeneity in conduction in the isolated rabbit heart.
abstract: BACKGROUND
  Atrial dilation plays an important role in the development and persistence of atrial fibrillation (AF). The mechanisms by which atrial dilation increases the vulnerability to AF are not fully understood.
  
  
  RESULTS
  In 11 isolated rabbit hearts, the right atrium was acutely dilated by increasing the intra-atrial pressure from 2 to 9 and 14 cm H2O. A rectangular mapping array of 240 electrodes (spatial resolution 0.5 mm) was positioned on the free wall of the right atrium. The atrium was paced from four different sites at intervals of 240 and 125 msec. At normal atrial pressure (2 cm H2O), conduction was uniform in all directions with an anisotropy ratio between 1.5 and 1.7. Increasing the pressure to 9 cm H2O decreased the normalized conduction velocity during rapid pacing by 18%. The incidence of areas of slow conduction and conduction block increased from 6.6% and 1.6% to 10.2% and 3.3%. At 14 cm H2O, conduction velocity decreased by 31% and the percentage of slow conduction and block further increased to 11.5% and 6.6% (P < 0.001). The appearance of lines of intra-atrial block was largely dependent on the pacing site. Whereas during pacing at the cranial part of the crista terminalis no increase in conduction delays occurred, pacing from the low right atrium unmasked several lines of block oriented parallel to the major trabeculae and the crista terminalis. In an additional series of six hearts the left atrium also was mapped. The effect of dilation of the left atrium was comparable to that of the right atrium. Increasing the atrial pressure to 14 cm H2O increased the amount of intra-atrial conduction block threefold to fourfold.
  
  
  CONCLUSIONS
  Acute atrial dilation results in slowing of conduction and an increase of the amount of intra-atrial conduction block. The increase in spatial heterogeneity in conduction was related to the anisotropic properties of the atrial wall.
authors.affiliation: Department of Physiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
authors.forename: Sabine C M
authors.initials: SC
authors.lastname: Eijsbouts
authors.forename: Mohamed
authors.initials: M
authors.lastname: Majidi
authors.forename: Marc
authors.initials: M
authors.lastname: van Zandvoort
authors.forename: Maurits A
authors.initials: MA
authors.lastname: Allessie
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology* / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D006325:Heart Atria / Q000473:pathology / Q000503:physiopathology*; D006329:Heart Conduction System / Q000503:physiopathology*; D011312:Pressure; D011817:Rabbits