Intramural VT: Highlighting the limitations of “Contact Mapping”

Question:

This patient had a prior inferoseptal–apical myocardial infarction. Endocardial and epicardial activation mapping during VT (CL 330ms) demonstrated nearly simultaneous earliest activation on both surfaces with a notable absence of mid diastolic potentials on both surfaces. Given this information & the maps & EGMs below - what can be said about the location of the VT circuit?

(Click to zoom on image)

Answer:

Answer: The mapped sites represented breakout rather than the critical isthmus. Critical isthmus site must be intramural, rather than endo/epicardial.

 

This case highlights a number of interesting points:

  • Firstly, it highlights that ischaemic VT circuitry can be intramural and we cannot make assumptions that ischaemic VT substrate is mostly endocardial.

 

  • Secondly, this case highlights that pseudo-focal activation does not exclude reentry. Simultaneous endo/epi activation/breakout strongly suggests the presence of an intramural circuit.
    • Propagation maps confirmed synchronized ENDO–EPI emergence from deeper tissue.

 

 

Substrate mapping:

  • Voltage mapping demonstrated dense, heterogeneous scar without a clear endocardial conduction corridor – yet this was unlikely the critical isthmus site for the VT due to the lack of diastolic potentials (figure below).

 

  • Programmed stimulation (S2 mapping) unmasked LAVAs and late potentials at the inferoseptal apex, with truly marvelous isochronal crowding indicating critically slow conduction —>which is once again predictive of a VT critical isthmus site -yet this was unlikely the critical isthmus site, as demonstrated by the lack of mid diastolic potentials during VT, and the focal breakout pattern revealed during VT activation mapping

 

  • S2 timing map figure below – indicating late potentials and isochronal crowding.

 

Ablation targeted both endocardial and epicardial breakout regions, resulting in non-inducibility.

 

My Two Cents:

  • Ischaemic substrate can be primarily intramural.

 

  • Late potentials and Iscohronal Crowding are predictive (but not confirmatory) of VT isthmus sites & diastolic corridors – but in this case, they were not part of the VT isthmus site.

 

  • Traditional “contact mapping” mapping is really only a 2-Dimensional surface map of the endocardium or epicardium – we cannot map intramural circuitry with current technology in the EP lab.

 

  • Tools such as Unipolar Voltage, ICE, MRI & educated inferences are our best tools for deducing intramural VT circuitry.

 

  • Ablation at the breakout points was sufficient in abolishing VT in this instance.

 

Thanks for tuning in :)

Regards

Author: Dr Juan. Ismael Almonte G. (MD) with colleagues Dr Rodolfo San Antonio Dharandas (MD) and Judit Mas, Biomedical Engineer – Abbott / EnSite X Specialist.

Edited by Mitch & CPiP Team with permission.

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REFERENCES

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