@Article{RSM:Ver2003,
  author =       "S. Verheule and E. Wilson and T. th Everett and S.
                 Shanbhag and C. Golden and J. Olgin",
  title =        "Alterations in atrial electrophysiology and tissue
                 structure in a canine model of chronic atrial
                 dilatation due to mitral regurgitation",
  journal =      j-C,
  volume =       "107",
  number =       "20",
  pages =        "2615--2622",
  scinote =         "1524-4539 (Electronic) Journal Article Research
                 Support, U.S. Gov't, P.H.S.",
  abstract =     "BACKGROUND: Clinically, chronic atrial dilatation is
                 associated with an increased incidence of atrial
                 fibrillation (AF), but the underlying mechanism is not
                 clear. We have investigated atrial electrophysiology
                 and tissue structure in a canine model of chronic
                 atrial dilatation due to mitral regurgitation (MR).
                 METHODS AND RESULTS: Thirteen control and 19 MR dogs (1
                 month after partial mitral valve avulsion) were
                 studied. Dogs in the MR group were monitored using
                 echocardiography and Holter recording. In open-chest
                 follow-up experiments, electrode arrays were placed on
                 the atria to investigate conduction patterns, effective
                 refractory periods, and inducibility of AF. Alterations
                 in tissue structure and ultrastructure were assessed in
                 atrial tissue samples. At follow-up, left atrial length
                 in MR dogs was 4.09+/-0.45 cm, compared with
                 3.25+/-0.28 at baseline (P<0.01), corresponding to a
                 volume of 205+/-61\% of baseline. At follow-up, no
                 differences in atrial conduction pattern and conduction
                 velocities were noted between control and MR dogs.
                 Effective refractory periods were increased
                 homogeneously throughout the left and right atrium.
                 Sustained AF (>1 hour) was inducible in 10 of 19 MR
                 dogs and none of 13 control dogs (P<0.01). In the
                 dilated MR left atrium, areas of increased interstitial
                 fibrosis and chronic inflammation were accompanied by
                 increased glycogen ultrastructurally. CONCLUSIONS:
                 Chronic atrial dilatation in the absence of overt heart
                 failure leads to an increased vulnerability to AF that
                 is not based on a decrease in wavelength.",
  keywords =     "Animals Atrial Fibrillation/etiology/physiopathology
                 Chronic Disease Dilatation,
                 Pathologic/etiology/pathology/*physiopathology Disease
                 Models, Animal Disease Susceptibility Dogs
                 Echocardiography, Transesophageal Electrocardiography,
                 Ambulatory *Electrophysiologic Techniques, Cardiac
                 Heart Atria/pathology/*physiopathology/ultrasonography
                 Heart Conduction System/physiopathology Microscopy,
                 Electron Mitral Valve
                 Insufficiency/complications/*physiopathology/ultrasonography
                 Myocardium/pathology/ultrastructure Ventricular
                 Function, Left",
  year =         "2003",
}

{"_id":"3Y3qnahuqWtnM9FZc","bibbaseid":"verheule-wilson-theverett-shanbhag-golden-olgin-alterationsinatrialelectrophysiologyandtissuestructureinacaninemodelofchronicatrialdilatationduetomitralregurgitation-2003","downloads":0,"creationDate":"2016-07-01T21:38:42.281Z","title":"Alterations in atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation","author_short":["Verheule, S.","Wilson, E.","th Everett, T.","Shanbhag, S.","Golden, C.","Olgin, J."],"year":2003,"bibtype":"article","biburl":"http://www.sci.utah.edu/~macleod/Bibtex/biglit.bib","bibdata":{"bibtype":"article","type":"article","author":[{"firstnames":["S."],"propositions":[],"lastnames":["Verheule"],"suffixes":[]},{"firstnames":["E."],"propositions":[],"lastnames":["Wilson"],"suffixes":[]},{"firstnames":["T."],"propositions":["th"],"lastnames":["Everett"],"suffixes":[]},{"firstnames":["S."],"propositions":[],"lastnames":["Shanbhag"],"suffixes":[]},{"firstnames":["C."],"propositions":[],"lastnames":["Golden"],"suffixes":[]},{"firstnames":["J."],"propositions":[],"lastnames":["Olgin"],"suffixes":[]}],"title":"Alterations in atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation","journal":"j-C","volume":"107","number":"20","pages":"2615–2622","scinote":"1524-4539 (Electronic) Journal Article Research Support, U.S. Gov't, P.H.S.","abstract":"BACKGROUND: Clinically, chronic atrial dilatation is associated with an increased incidence of atrial fibrillation (AF), but the underlying mechanism is not clear. We have investigated atrial electrophysiology and tissue structure in a canine model of chronic atrial dilatation due to mitral regurgitation (MR). METHODS AND RESULTS: Thirteen control and 19 MR dogs (1 month after partial mitral valve avulsion) were studied. Dogs in the MR group were monitored using echocardiography and Holter recording. In open-chest follow-up experiments, electrode arrays were placed on the atria to investigate conduction patterns, effective refractory periods, and inducibility of AF. Alterations in tissue structure and ultrastructure were assessed in atrial tissue samples. At follow-up, left atrial length in MR dogs was 4.09+/-0.45 cm, compared with 3.25+/-0.28 at baseline (P<0.01), corresponding to a volume of 205+/-61% of baseline. At follow-up, no differences in atrial conduction pattern and conduction velocities were noted between control and MR dogs. Effective refractory periods were increased homogeneously throughout the left and right atrium. Sustained AF (>1 hour) was inducible in 10 of 19 MR dogs and none of 13 control dogs (P<0.01). In the dilated MR left atrium, areas of increased interstitial fibrosis and chronic inflammation were accompanied by increased glycogen ultrastructurally. CONCLUSIONS: Chronic atrial dilatation in the absence of overt heart failure leads to an increased vulnerability to AF that is not based on a decrease in wavelength.","keywords":"Animals Atrial Fibrillation/etiology/physiopathology Chronic Disease Dilatation, Pathologic/etiology/pathology/*physiopathology Disease Models, Animal Disease Susceptibility Dogs Echocardiography, Transesophageal Electrocardiography, Ambulatory *Electrophysiologic Techniques, Cardiac Heart Atria/pathology/*physiopathology/ultrasonography Heart Conduction System/physiopathology Microscopy, Electron Mitral Valve Insufficiency/complications/*physiopathology/ultrasonography Myocardium/pathology/ultrastructure Ventricular Function, Left","year":"2003","bibtex":"@Article{RSM:Ver2003,\n author = \"S. Verheule and E. Wilson and T. th Everett and S.\n Shanbhag and C. Golden and J. Olgin\",\n title = \"Alterations in atrial electrophysiology and tissue\n structure in a canine model of chronic atrial\n dilatation due to mitral regurgitation\",\n journal = j-C,\n volume = \"107\",\n number = \"20\",\n pages = \"2615--2622\",\n scinote = \"1524-4539 (Electronic) Journal Article Research\n Support, U.S. Gov't, P.H.S.\",\n abstract = \"BACKGROUND: Clinically, chronic atrial dilatation is\n associated with an increased incidence of atrial\n fibrillation (AF), but the underlying mechanism is not\n clear. We have investigated atrial electrophysiology\n and tissue structure in a canine model of chronic\n atrial dilatation due to mitral regurgitation (MR).\n METHODS AND RESULTS: Thirteen control and 19 MR dogs (1\n month after partial mitral valve avulsion) were\n studied. Dogs in the MR group were monitored using\n echocardiography and Holter recording. In open-chest\n follow-up experiments, electrode arrays were placed on\n the atria to investigate conduction patterns, effective\n refractory periods, and inducibility of AF. Alterations\n in tissue structure and ultrastructure were assessed in\n atrial tissue samples. At follow-up, left atrial length\n in MR dogs was 4.09+/-0.45 cm, compared with\n 3.25+/-0.28 at baseline (P<0.01), corresponding to a\n volume of 205+/-61\\% of baseline. At follow-up, no\n differences in atrial conduction pattern and conduction\n velocities were noted between control and MR dogs.\n Effective refractory periods were increased\n homogeneously throughout the left and right atrium.\n Sustained AF (>1 hour) was inducible in 10 of 19 MR\n dogs and none of 13 control dogs (P<0.01). In the\n dilated MR left atrium, areas of increased interstitial\n fibrosis and chronic inflammation were accompanied by\n increased glycogen ultrastructurally. CONCLUSIONS:\n Chronic atrial dilatation in the absence of overt heart\n failure leads to an increased vulnerability to AF that\n is not based on a decrease in wavelength.\",\n keywords = \"Animals Atrial Fibrillation/etiology/physiopathology\n Chronic Disease Dilatation,\n Pathologic/etiology/pathology/*physiopathology Disease\n Models, Animal Disease Susceptibility Dogs\n Echocardiography, Transesophageal Electrocardiography,\n Ambulatory *Electrophysiologic Techniques, Cardiac\n Heart Atria/pathology/*physiopathology/ultrasonography\n Heart Conduction System/physiopathology Microscopy,\n Electron Mitral Valve\n Insufficiency/complications/*physiopathology/ultrasonography\n Myocardium/pathology/ultrastructure Ventricular\n Function, Left\",\n year = \"2003\",\n}\n\n","author_short":["Verheule, S.","Wilson, E.","th Everett, T.","Shanbhag, S.","Golden, C.","Olgin, J."],"key":"RSM:Ver2003","id":"RSM:Ver2003","bibbaseid":"verheule-wilson-theverett-shanbhag-golden-olgin-alterationsinatrialelectrophysiologyandtissuestructureinacaninemodelofchronicatrialdilatationduetomitralregurgitation-2003","role":"author","urls":{},"keyword":["Animals Atrial Fibrillation/etiology/physiopathology Chronic Disease Dilatation","Pathologic/etiology/pathology/*physiopathology Disease Models","Animal Disease Susceptibility Dogs Echocardiography","Transesophageal Electrocardiography","Ambulatory *Electrophysiologic Techniques","Cardiac Heart Atria/pathology/*physiopathology/ultrasonography Heart Conduction System/physiopathology Microscopy","Electron Mitral Valve Insufficiency/complications/*physiopathology/ultrasonography Myocardium/pathology/ultrastructure Ventricular Function","Left"],"metadata":{"authorlinks":{}},"downloads":0,"html":""},"search_terms":["alterations","atrial","electrophysiology","tissue","structure","canine","model","chronic","atrial","dilatation","due","mitral","regurgitation","verheule","wilson","th everett","shanbhag","golden","olgin"],"keywords":["animals atrial fibrillation/etiology/physiopathology chronic disease dilatation","pathologic/etiology/pathology/*physiopathology disease models","animal disease susceptibility dogs echocardiography","transesophageal electrocardiography","ambulatory *electrophysiologic techniques","cardiac heart atria/pathology/*physiopathology/ultrasonography heart conduction system/physiopathology microscopy","electron mitral valve insufficiency/complications/*physiopathology/ultrasonography myocardium/pathology/ultrastructure ventricular function","left"],"authorIDs":[],"dataSources":["5HG3Kp8zRwDd7FotB"]}