Chronic rapid atrial pacing. Structural, functional, and electrophysiological characteristics of a new model of sustained atrial fibrillation. Morillo, C. A., Klein, G. J., Jones, D. L., & Guiraudon, C. M. j-C, 91(5):1588–1595, 1995.
abstract   bibtex   
BACKGROUND: Despite the clinical importance of atrial fibrillation (AF), the development of chronic nonvalvular AF models has been difficult. Animal models of sustained AF have been developed primarily in the short-term setting. Recently, models of chronic ventricular myopathy and fibrillation have been developed after several weeks of continuous rapid ventricular pacing. We hypothesized that chronic rapid atrial pacing would lead to atrial myopathy, yielding a reproducible model of sustained AF. METHODS AND RESULTS: Twenty-two halothane-anesthetized mongrel dogs underwent insertion of a transvenous lead at the right atrial appendage that was continuously paced at 400 beats per minute for 6 weeks. Two-dimensional echocardiography was performed in 11 dogs to assess the effects of rapid atrial pacing on atrial size. Marked biatrial enlargement was documented; after 6 weeks of continuous rapid atrial pacing, the left atrium was 7.8 +/- 1 cm2 at baseline versus 11.3 +/- 1 cm2 after pacing, and the right atrium was 4.3 +/- 0.7 cm2 at baseline versus 7.2 +/- 1.3 cm2 after pacing. An increase in atrial area of at least 40% was necessary to induce sustained AF and was strongly correlated with the inducibility of AF (r =.87). Electron microscopy of atrial tissue demonstrated structural changes that were characterized by an increase in mitochondrial size and number and by disruption of the sarcoplasmic reticulum. After 6 weeks of continuous rapid atrial pacing, sustained AF was induced in 18 dogs (82%) and nonsustained AF was induced in 2 dogs (9%). AF occurred spontaneously in 4 dogs (18%). Right atrial ERP, measured at cycle lengths of 400 and 300 milliseconds at baseline, was significantly shortened after pacing, from 150 +/- 8 to 127 +/- 10 milliseconds and from 147 +/- 11 to 123 +/- 12 milliseconds, respectively (P <.001). This finding was highly predictive of inducibility of AF (90%). Increased atrial area (40%) and ERP shortening were highly predictive for the induction of sustained AF (88%). Local epicardial ERP correlated well with local AFCL (R2 =.93). Mean AFCL was significantly shorter in the left atrium (81 +/- 8 milliseconds) compared with the right atrium 94 +/- 9 milliseconds (P <.05). An area in the posterior left atrium was consistently found to have a shorter AFCL (74 +/- 5 milliseconds). Cryoablation of this area was attempted in 11 dogs. In 9 dogs (82%; mean, 9.0 +/- 4.0; range, 5 to 14), AF was terminated and no longer induced after serial cryoablation. CONCLUSIONS: Sustained AF was readily inducible in most dogs (82%) after rapid atrial pacing. This model was consistently associated with biatrial myopathy and marked changes in atrial vulnerability. An area in the posterior left atrium was uniformly shown to have the shortest AFCL. The results of restoration of sinus rhythm and prevention of inducibility of AF after cryoablation of this area of the left atrium suggest that this area may be critical in the maintenance of AF in this model.
@Article{RSM:Mor95,
  author =       "C. A. Morillo and G. J. Klein and D. L. Jones and C.
                 M. Guiraudon",
  title =        "Chronic rapid atrial pacing. Structural, functional,
                 and electrophysiological characteristics of a new model
                 of sustained atrial fibrillation",
  journal =      j-C,
  volume =       "91",
  number =       "5",
  pages =        "1588--1595",
  abstract =     "BACKGROUND: Despite the clinical importance of atrial
                 fibrillation (AF), the development of chronic
                 nonvalvular AF models has been difficult. Animal models
                 of sustained AF have been developed primarily in the
                 short-term setting. Recently, models of chronic
                 ventricular myopathy and fibrillation have been
                 developed after several weeks of continuous rapid
                 ventricular pacing. We hypothesized that chronic rapid
                 atrial pacing would lead to atrial myopathy, yielding a
                 reproducible model of sustained AF. METHODS AND
                 RESULTS: Twenty-two halothane-anesthetized mongrel dogs
                 underwent insertion of a transvenous lead at the right
                 atrial appendage that was continuously paced at 400
                 beats per minute for 6 weeks. Two-dimensional
                 echocardiography was performed in 11 dogs to assess the
                 effects of rapid atrial pacing on atrial size. Marked
                 biatrial enlargement was documented; after 6 weeks of
                 continuous rapid atrial pacing, the left atrium was 7.8
                 +/- 1 cm2 at baseline versus 11.3 +/- 1 cm2 after
                 pacing, and the right atrium was 4.3 +/- 0.7 cm2 at
                 baseline versus 7.2 +/- 1.3 cm2 after pacing. An
                 increase in atrial area of at least 40\% was necessary
                 to induce sustained AF and was strongly correlated with
                 the inducibility of AF (r =.87). Electron microscopy of
                 atrial tissue demonstrated structural changes that were
                 characterized by an increase in mitochondrial size and
                 number and by disruption of the sarcoplasmic reticulum.
                 After 6 weeks of continuous rapid atrial pacing,
                 sustained AF was induced in 18 dogs (82\%) and
                 nonsustained AF was induced in 2 dogs (9\%). AF
                 occurred spontaneously in 4 dogs (18\%). Right atrial
                 ERP, measured at cycle lengths of 400 and 300
                 milliseconds at baseline, was significantly shortened
                 after pacing, from 150 +/- 8 to 127 +/- 10 milliseconds
                 and from 147 +/- 11 to 123 +/- 12 milliseconds,
                 respectively (P <.001). This finding was highly
                 predictive of inducibility of AF (90\%). Increased
                 atrial area (40\%) and ERP shortening were highly
                 predictive for the induction of sustained AF (88\%).
                 Local epicardial ERP correlated well with local AFCL
                 (R2 =.93). Mean AFCL was significantly shorter in the
                 left atrium (81 +/- 8 milliseconds) compared with the
                 right atrium 94 +/- 9 milliseconds (P <.05). An area in
                 the posterior left atrium was consistently found to
                 have a shorter AFCL (74 +/- 5 milliseconds).
                 Cryoablation of this area was attempted in 11 dogs. In
                 9 dogs (82\%; mean, 9.0 +/- 4.0; range, 5 to 14), AF
                 was terminated and no longer induced after serial
                 cryoablation. CONCLUSIONS: Sustained AF was readily
                 inducible in most dogs (82\%) after rapid atrial
                 pacing. This model was consistently associated with
                 biatrial myopathy and marked changes in atrial
                 vulnerability. An area in the posterior left atrium was
                 uniformly shown to have the shortest AFCL. The results
                 of restoration of sinus rhythm and prevention of
                 inducibility of AF after cryoablation of this area of
                 the left atrium suggest that this area may be critical
                 in the maintenance of AF in this model.",
  keywords =     "Animals Atrial
                 Fibrillation/etiology/pathology/*physiopathology
                 Baroreflex/physiology *Cardiac Pacing, Artificial
                 Disease Models, Animal Dogs Echocardiography
                 Electrocardiography Electrophysiology Heart
                 Atria/ultrasonography Microscopy, Electron
                 Myocardium/pathology Time Factors",
  year =         "1995",
}
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