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J. Am. Coll. Cardiol. · May 2006
Isolated potentials during sinus rhythm and pace-mapping within scars as guides for ablation of post-infarction ventricular tachycardia.
- Frank Bogun, Eric Good, Stephen Reich, Darryl Elmouchi, Petar Igic, Kristina Lemola, David Tschopp, Krit Jongnarangsin, Hakan Oral, Aman Chugh, Frank Pelosi, and Fred Morady.
- University of Michigan Medical Center, Ann Arbor, Michigan, USA. fbogun@umich.edu
- J. Am. Coll. Cardiol. 2006 May 16; 47 (10): 2013-9.
ObjectivesThe purpose of this study was to identify ventricular tachycardia (VT) isthmus sites by pace-mapping within scar tissue and to identify electrogram characteristics that are helpful in identifying VT isthmus sites during sinus rhythm (SR).BackgroundPace-mapping has been used in the scar border zone to identify the exit site of post-infarction VT.MethodsIn 19 consecutive patients (18 men, mean age 66 +/- 9 years, mean ejection fraction 0.24 +/- 0.12) with post-infarction VT, a left ventricular voltage map was generated during SR. Pace-mapping was performed at sites with abnormal electrograms or isolated potentials. Radiofrequency ablation was performed at isthmus sites as defined by pace-mapping (perfect pace-map = 12/12 matching electrocardiogram leads; good pace-map = 10/12 to 11/12 matching electrocardiogram leads) and/or entrainment mapping.ResultsA total of 81 VTs (mean cycle length 396 +/- 124 ms) were inducible. In 16 of the 19 patients, a total of 41 distinct isthmus areas of 41 distinct VTs were identified and successfully ablated. All but one displayed isolated potentials during SR. Furthermore, 22 of the 81 VTs (27%) for which no isthmus was identified became noninducible after ablation of a targeted VT. The 16 patients in whom > or =1 isthmus was identified and ablated were free of arrhythmic events during a mean follow-up of 10 months.ConclusionsDuring SR, excellent or good pace-maps at sites of isolated potentials within areas of scar identify areas of fixed block that are protected and part of the critical isthmus of post-infarction VT. Shared common pathways might explain why non-targeted VTs might become noninducible after ablation of other VTs.
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