title: Substrate characterization of ventricular tachycardia in a porcine model of tetralogy of Fallot using noncontact mapping.
abstract: BACKGROUND
  Ventricular tachycardia (VT) in patients following tetralogy of Fallot (TOF) repair is challenging to map because of the presence of scar, patch material, and hemodynamic residua of surgery. This study investigates whether noncontact mapping can identify the arrhythmia substrate in a porcine model that involves a right ventricular outflow tract (RVOT) patch and either chronic volume or pressure load on the right ventricle.
  
  
  METHODS
  Nine infant pigs (3-5 kg) underwent surgery involving an RVOT patch and creation of pulmonary insufficiency (PI, n = 4) or pulmonary stenosis (PS, n = 5). After a mean of 4.2 months, pigs underwent invasive electrophysiology studies (EPS) with noncontact mapping (Ensite, St. Jude Medical, St. Paul, MN USA) of the right ventricle. Automated, unipolar voltage maps (VM) were constructed during sinus rhythm. Threshold for substrate was set at -0.5 mV and incrementally adjusted to higher values until a contiguous region of low voltage was delineated. Programmed stimulation was performed to induce VT. VT activation was correlated to location of VM defined substrate. Three control pigs underwent EPS and VM.
  
  
  RESULTS
  Free-wall RVOT substrate was identified in each of the model animals, correlating to location of the patch. The mean voltage threshold was -1.1 mV. VT was induced in 6/9 animals. Diastolic activation approximated the inferior or lateral border of the substrate in all animals. No RVOT substrate was identified in the control pigs.
  
  
  CONCLUSIONS
  Automated voltage mapping of sinus beats identifies substrate for VT in a porcine model of TOF. Consistent diastolic activation of the substrate border was found during VT. Targeting this area may be useful in the ablation of VT after repair of TOF.
authors.affiliation: Divisions of Cardiology and Cardiothoracic Surgery, The Children's Hospital of Philadelphia, Philadelphia, PA, USA. jkaltman@cnmc.org
authors.forename: Jonathan R
authors.initials: JR
authors.lastname: Kaltman
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Gillespie
authors.forename: Travis
authors.initials: T
authors.lastname: Seymour
authors.forename: Azeem
authors.initials: A
authors.lastname: Khan
authors.forename: Ilana J
authors.initials: IJ
authors.lastname: Zeltser
authors.forename: Larry A
authors.initials: LA
authors.lastname: Rhodes
authors.forename: Ronn E
authors.initials: RE
authors.lastname: Tanel
authors.forename: Victoria L
authors.initials: VL
authors.lastname: Vetter
authors.forename: J William
authors.initials: JW
authors.lastname: Gaynor
authors.forename: Maully J
authors.initials: MJ
authors.lastname: Shah
mesh_terms: D000818:Animals; D018780:Body Surface Potential Mapping / Q000379:methods*; D004195:Disease Models, Animal; D006329:Heart Conduction System / Q000503:physiopathology*; D013552:Swine; D017180:Tachycardia, Ventricular / Q000209:etiology* / Q000503:physiopathology*; D013771:Tetralogy of Fallot / Q000150:complications* / Q000503:physiopathology*