Isolated Potentials During Sinus Rhythm and Pace-Mapping Within Scars as Guides for Ablation of Post-Infarction Ventricular Tachycardia
Male
Myocardial Infarction
Action Potentials
Stroke Volume
Middle Aged
Cicatrix
Electrocardiography
03 medical and health sciences
0302 clinical medicine
Heart Conduction System
Heart Rate
Catheter Ablation
Tachycardia, Ventricular
Humans
Female
Cardiology and Cardiovascular Medicine
Electrophysiologic Techniques, Cardiac
Aged
DOI:
10.1016/j.jacc.2005.12.062
Publication Date:
2006-05-03T13:21:07Z
AUTHORS (12)
ABSTRACT
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).Pace-mapping has been used in the scar border zone to identify the exit site of post-infarction VT.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.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 > or =1 isthmus was identified and ablated were free of arrhythmic events during a mean follow-up of 10 months.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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