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J Am Coll Cardiol, 2003; 41:802-809, doi:10.1016/S0735-1097(02)02932-7
© 2003 by the American College of Cardiology Foundation
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CLINICAL STUDY: ELECTROPHYSIOLOGIC DISTURBANCE

Relationship of slow conduction detected by pace-mapping to ventricular tachycardia re-entry circuit sites after infarction

Corinna B. Brunckhorst, MD*, William G. Stevenson, MD{dagger},*, Kyoko Soejima, MD{dagger}, William H. Maisel, MD, MPH{dagger}, Etienne Delacretaz, MD{ddagger}, Peter L. Friedman, MD, PhD{dagger} and Shlomo A. Ben-Haim, MD, DSc§

* University of Zurich, Zurich, Switzerland
{dagger} Brigham and Women’s Hospital, Boston, Massachusetts, USA
{ddagger} Swiss Cardiovascular Center, University Hospital, Bern, Switzerland
§ Technion-Israel Institute of Technology, Haifa, Israel

Manuscript received May 21, 2002; revised manuscript received October 6, 2002, accepted November 22, 2002.

* Reprint requests and correspondence: Dr. William G. Stevenson, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis Street, Boston, Massachusetts 02115, USA.
wstevenson{at}partners.org

OBJECTIVES: This study sought to characterize the relationship of conduction delays detected by pace-mapping, evident as a stimulus to QRS interval (S-QRS) delay ≥40 ms, to ventricular tachycardia (VT) re-entry circuit isthmuses defined by entrainment and ablation.

BACKGROUND: Areas of slow conduction and block in old infarcts cause re-entrant VT.

METHODS: In 12 patients with VT after infarction, pace-mapping was performed at 890 sites. Stimulus to QRS intervals were measured and plotted in three-dimensional reconstructions of the left ventricle. Conduction delay was defined as ≥40 ms and marked delay as >80 ms. The locations of conduction delays were compared to the locations of 14 target areas, defined as the region within a radius of 2 cm of a re-entry circuit isthmus.

RESULTS: Pacing captured at 829 sites; 465 (56%) had no S-QRS delay, 364 (44%) had a delay ≥40 ms, and 127 (15%) had a delay >80 ms. Sites with delays were clustered in 14 discrete regions, 13 of which overlapped target regions. Only 1 of the 14 target regions was not related to an area of S-QRS delay. Sites with marked delays >80 ms were more often in the target (52%) than sites with delays 40 to 80 ms (29%) (p < 0.0001).

CONCLUSIONS: Identification of abnormal conduction during pace-mapping can be used to focus mapping during induced VT to a discrete region of the infarct. Further study is warranted to determine if targeting regions of conduction delay may allow ablation of VT during stable sinus rhythm without mapping during VT.

Abbreviations and Acronyms
  ECG
  electrocardiogram
  RF
  radiofrequency
  S-QRS
  stimulus to QRS interval
  VT
  ventricular tachycardia




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