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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{"_id":"ridGnAwdtcwRreDR9","bibbaseid":"morillo-klein-jones-guiraudon-chronicrapidatrialpacingstructuralfunctionalandelectrophysiologicalcharacteristicsofanewmodelofsustainedatrialfibrillation-1995","downloads":0,"creationDate":"2016-07-01T21:38:37.901Z","title":"Chronic rapid atrial pacing. Structural, functional, and electrophysiological characteristics of a new model of sustained atrial fibrillation","author_short":["Morillo, C. A.","Klein, G. J.","Jones, D. L.","Guiraudon, C. M."],"year":1995,"bibtype":"article","biburl":"http://www.sci.utah.edu/~macleod/Bibtex/biglit.bib","bibdata":{"bibtype":"article","type":"article","author":[{"firstnames":["C.","A."],"propositions":[],"lastnames":["Morillo"],"suffixes":[]},{"firstnames":["G.","J."],"propositions":[],"lastnames":["Klein"],"suffixes":[]},{"firstnames":["D.","L."],"propositions":[],"lastnames":["Jones"],"suffixes":[]},{"firstnames":["C.","M."],"propositions":[],"lastnames":["Guiraudon"],"suffixes":[]}],"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","bibtex":"@Article{RSM:Mor95,\n author = \"C. A. Morillo and G. J. Klein and D. L. Jones and C.\n M. Guiraudon\",\n title = \"Chronic rapid atrial pacing. Structural, functional,\n and electrophysiological characteristics of a new model\n of sustained atrial fibrillation\",\n journal = j-C,\n volume = \"91\",\n number = \"5\",\n pages = \"1588--1595\",\n abstract = \"BACKGROUND: Despite the clinical importance of atrial\n fibrillation (AF), the development of chronic\n nonvalvular AF models has been difficult. Animal models\n of sustained AF have been developed primarily in the\n short-term setting. Recently, models of chronic\n ventricular myopathy and fibrillation have been\n developed after several weeks of continuous rapid\n ventricular pacing. We hypothesized that chronic rapid\n atrial pacing would lead to atrial myopathy, yielding a\n reproducible model of sustained AF. METHODS AND\n RESULTS: Twenty-two halothane-anesthetized mongrel dogs\n underwent insertion of a transvenous lead at the right\n atrial appendage that was continuously paced at 400\n beats per minute for 6 weeks. Two-dimensional\n echocardiography was performed in 11 dogs to assess the\n effects of rapid atrial pacing on atrial size. Marked\n biatrial enlargement was documented; after 6 weeks of\n continuous rapid atrial pacing, the left atrium was 7.8\n +/- 1 cm2 at baseline versus 11.3 +/- 1 cm2 after\n pacing, and the right atrium was 4.3 +/- 0.7 cm2 at\n baseline versus 7.2 +/- 1.3 cm2 after pacing. An\n increase in atrial area of at least 40\\% was necessary\n to induce sustained AF and was strongly correlated with\n the inducibility of AF (r =.87). Electron microscopy of\n atrial tissue demonstrated structural changes that were\n characterized by an increase in mitochondrial size and\n number and by disruption of the sarcoplasmic reticulum.\n After 6 weeks of continuous rapid atrial pacing,\n sustained AF was induced in 18 dogs (82\\%) and\n nonsustained AF was induced in 2 dogs (9\\%). AF\n occurred spontaneously in 4 dogs (18\\%). Right atrial\n ERP, measured at cycle lengths of 400 and 300\n milliseconds at baseline, was significantly shortened\n after pacing, from 150 +/- 8 to 127 +/- 10 milliseconds\n and from 147 +/- 11 to 123 +/- 12 milliseconds,\n respectively (P <.001). This finding was highly\n predictive of inducibility of AF (90\\%). Increased\n atrial area (40\\%) and ERP shortening were highly\n predictive for the induction of sustained AF (88\\%).\n Local epicardial ERP correlated well with local AFCL\n (R2 =.93). Mean AFCL was significantly shorter in the\n left atrium (81 +/- 8 milliseconds) compared with the\n right atrium 94 +/- 9 milliseconds (P <.05). An area in\n the posterior left atrium was consistently found to\n have a shorter AFCL (74 +/- 5 milliseconds).\n Cryoablation of this area was attempted in 11 dogs. In\n 9 dogs (82\\%; mean, 9.0 +/- 4.0; range, 5 to 14), AF\n was terminated and no longer induced after serial\n cryoablation. CONCLUSIONS: Sustained AF was readily\n inducible in most dogs (82\\%) after rapid atrial\n pacing. This model was consistently associated with\n biatrial myopathy and marked changes in atrial\n vulnerability. An area in the posterior left atrium was\n uniformly shown to have the shortest AFCL. The results\n of restoration of sinus rhythm and prevention of\n inducibility of AF after cryoablation of this area of\n the left atrium suggest that this area may be critical\n in the maintenance of AF in this model.\",\n keywords = \"Animals Atrial\n Fibrillation/etiology/pathology/*physiopathology\n Baroreflex/physiology *Cardiac Pacing, Artificial\n Disease Models, Animal Dogs Echocardiography\n Electrocardiography Electrophysiology Heart\n Atria/ultrasonography Microscopy, Electron\n Myocardium/pathology Time Factors\",\n year = \"1995\",\n}\n\n","author_short":["Morillo, C. A.","Klein, G. J.","Jones, D. L.","Guiraudon, C. 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