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J Am Coll Cardiol, 2006; 47:2013-2019, doi:10.1016/j.jacc.2005.12.062
(Published online 24 April 2006). © 2006 by the American College of Cardiology Foundation |
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University of Michigan Medical Center, Ann Arbor, Michigan
Manuscript received September 19, 2005; revised manuscript received November 4, 2005, accepted December 5, 2005.
* Reprint requests and correspondence: Dr. Frank Bogun, Division of Cardiology, University of Michigan Health System, TC B1 140, 1500 East Medical Center Drive, Ann Arbor, Michigan 48109-0366 (Email: fbogun{at}umich.edu).
OBJECTIVES: The 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).
BACKGROUND: Pace-mapping has been used in the scar border zone to identify the exit site of post-infarction VT.
METHODS: In 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.
RESULTS: A 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
1 isthmus was identified and ablated were free of arrhythmic events during a mean follow-up of 10 months.
CONCLUSIONS: During 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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