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2016 ; 49
(6
): 887-893
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Noninvasive epicardial and endocardial electrocardiographic imaging of
scar-related ventricular tachycardia
#MMPMID27968777
Wang L
; Gharbia OA
; Horá?ek BM
; Sapp JL
J Electrocardiol
2016[Nov]; 49
(6
): 887-893
PMID27968777
show ga
BACKGROUND: The majority of life-threatening ventricular tachycardias (VTs) are
sustained by heterogeneous scar substrates with narrow strands of surviving
tissue. An effective treatment for scar-related VT is to modify the underlying
scar substrate by catheter ablation. If activation sequence and entrainment
mapping can be performed during sustained VT, the exit and isthmus of the circuit
can often be identified. However, with invasive catheter mapping, only
monomorphic VT that is hemodynamically stable can be mapped in this manner. For
the majority of patients with poorly tolerated VTs or multiple VTs, a close
inspection of the re-entry circuit is not possible. A noninvasive approach to
fast mapping of unstable VTs can potentially allow an improved identification of
critical ablation sites. METHODS: For patients who underwent catheter ablation of
scar-related VT, CT scan was obtained prior to the ablation procedure and
120-lead body-surface electrocardiograms (ECGs) were acquired during induced VTs.
These data were used for noninvasive ECG imaging to computationally reconstruct
electrical potentials on the epicardium and on the endocardium of both
ventricles. Activation time and phase maps of the VT circuit were extracted from
the reconstructed electrograms. They were analyzed with respect to scar substrate
obtained from catheter mapping, as well as VT exits confirmed through ablation
sites that successfully terminated the VT. RESULTS: The reconstructed re-entry
circuits correctly revealed both epicardial and endocardial origins of
activation, consistent with locations of exit sites confirmed from the ablation
procedure. The temporal dynamics of the re-entry circuits, particularly the
slowing of conduction as indicated by the crowding and zig-zag conducting of the
activation isochrones, collocated well with scar substrate obtained by catheter
voltage maps. Furthermore, the results indicated that some re-entry circuits
involve both the epicardial and endocardial layers, and can only be properly
interpreted by mapping both layers simultaneously. CONCLUSIONS: This study
investigated the potential of ECG-imaging for beat-to-beat mapping of unstable
reentrant circuits. It shows that simultaneous epicardial and endocardial mapping
may improve the delineation of the 3D spatial construct of a re-entry circuit and
its exit. It also shows that the use of phase mapping can reveal regions of slow
conduction that collocate well with suspected heterogeneous regions within and
around the scar.