title: Impact of catheter ablation on pulmonary vein morphology and mechanical function.
abstract: BACKGROUND
  Previous reports have documented that radiofrequency catheter ablation of pulmonary veins induces a significant increase in the peak velocity of transvenous blood flow. Although the magnitude of the increase infers a state of pulmonary vein stenosis, there have been no reports of direct visualization of the ablation zone.
  
  
  RESULTS
  In each of 23 subjects, the myocardium investing one or more pulmonary veins (total of 42 veins) was electrically isolated by applying a confluent circumferential ablation lesion to the atrial side of the venoatrial junction. Doppler measurements of transvenous flow velocity were made before and after ablation using phased-array intracardiac echocardiography. Direct visualization of the ablation zone was performed using rotating intracardiac echocardiography, permitting assessment of shape, cross-sectional area, phasic variation in cross-sectional area, and wall thickness. In a subset of 5 subjects, a more detailed assessment of the ablation and contiguous regions was performed using three-dimensional echocardiography (rotating transducer). Prior to ablation, venoatrial junctions demonstrated noncircular shape and marked phasic variation in cross-sectional area. There was a trivial transvenous pressure gradient. After ablation, there was a significant increase in both anterograde and retrograde flow velocities and pressure gradient, the magnitudes of which were inversely proportional to the preablation and postablation areas. Direct visualization of the ablation zone revealed circumferential wall swelling, reduced cross-sectional area, and diminishment in phasic variation in cross-sectional area. Similar observations were made at contiguous nonablated sites, diminishing in magnitude as a function of distance.
  
  
  CONCLUSIONS
  Pulmonary vein ablation induces significant acute changes in morphology and mechanical function that extend beyond the ablation zone.
authors.affiliation: University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA. schwartzmand@msx.upmc.edu
authors.forename: David
authors.initials: D
authors.lastname: Schwartzman
authors.forename: Hideaki
authors.initials: H
authors.lastname: Kanzaki
authors.forename: Raveen
authors.initials: R
authors.lastname: Bazaz
authors.forename: John
authors.initials: J
authors.lastname: Gorcsan
mesh_terms: D000328:Adult; D001281:Atrial Fibrillation / Q000503:physiopathology / Q000601:surgery; D016275:Atrial Function / Q000502:physiology; D001783:Blood Flow Velocity / Q000502:physiology; D017115:Catheter Ablation; D015150:Echocardiography, Doppler; D005260:Female; D006325:Heart Atria / Q000000981:diagnostic imaging / Q000503:physiopathology / Q000601:surgery; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology / Q000601:surgery; D008297:Male; D008875:Middle Aged; D011667:Pulmonary Veins / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000601:surgery*; D013223:Statistics as Topic; D016896:Treatment Outcome