Voltage mapping in VT: Let’s talk Fidelity

Controversial point #1:

• Identifying low voltage tissue is a proxy for identifying slow velocity tissue (which may participate as the slow limb of reentry VT)
  • Perhaps an oversimplification since low voltage also is an indirect measure of fibrofatty infiltration & thinning.

 

Controversial point #2:

• The historical voltage criteria of 0.5mV – 1.5mV is becoming more and more irrelevant in substrate based VT ablation strategies.

 

• • Critical concept: A 1.2mV signal on a 4mm Navistar catheter may be recorded  as a 0.6mV signal on an Orion basket multielectrode catheter due to the small 0.4mm electrodes providing higher spatial resolution & recording less far-field electrical activity and recording truly local tissue activity.

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Discussing the pitfalls & considerations of voltage mapping

 

Historical basis of bipolar voltage cut-offs

Ventricular voltage cut-offs of 0.5-1.5mV was grounded in the study of x6 structurally normal patients where:

1. 95% of EGMs>1.55mV. This is why 1.5mV is used as the cut-off value for “normal” voltage, annotated as purple on 3D maps
2.  0.5mV was chosen arbitrarily to reflect tissue that was severely diseased or electrically inert.

 

This is the original quote from the 2000 paper  (1st reference below): “On the basis of our previous experience with catheter and intraoperative mapping, we then arbitrarily designated a value of <0.5 mV as consistent with “densely scarred” endocardium.”

 

Equipment used to perform this historical voltage mapping was 4mm electrode Navistar catheter without contact force.

 

The inadequacies of voltage mapping

1. Poor differentiation of electrically inert vs diseased but viable tissue which may participate in reenty
2. Late potentials and pace-capture sites frequently occur in areas <0.5mV – can be missed as these sites are assumed to be “electrically dense”.
3. Does NOT uncover functional substrate
4. Does NOT uncover intramural substrate.

 

 

Tool considerations for Voltage mapping

Current multielectrode mapping catheters bear little resemblance to the 4mm single bipole catheter used to determine our historical voltage cut-offs of 0.5mV to 1.5mV.

We must be aware that the tissue with a voltage of <0.5mV may not be electrically inert, and may house late potentials & diseased but conducting tissue which may participate in re-entry.

 

• Early Navistar maps captured hundreds of points using large electrodes. Today, catheters like Intellemap Orion collect over 10,000 points with electrodes just one-tenth the size – necessitating a more nuanced approach than the standard 0.5mV – 1.5mV cut-offs.

 

• Multielectrode mapping catheters equipped with smaller electrodes and reduced inter-electrode spacing enhance spatial resolution, enabling detection of localized near-field electrograms. In contrast, larger electrodes with wider spacing tend to capture more far-field activity, which may falsely elevate recorded voltage and misclassify heterogeneous or borderline tissue as ‘healthy & high voltage.

 

• This precision is lost if we apply standard voltage cut-offs (0.5–1.5 mV). Lowering the threshold may reveal viable but diseased myocardium often missed at higher cut-offs

Principle: We should all be curious what the voltage map looks like when we lower the voltage threshold. 

 

Bipolar Blindness?

 

How can we optimise voltage maps? – adjusting voltage cut-offs

Adjusting voltage cut-offs to improve differentiation between inert & diseased tissue?

 

Method 1: Gate lower voltage threshold to Late Potentials & Pace-capture

• Lower the low voltage threshold until regions with identifiable late potentials and capturable tissue with pacing is not shown as red

 

• This method may uncover channels of diseased substrate within dense scar which may participate in reentry.

 

 

Software tools which improve voltage mapping

 

 

Unipolar LV Voltages

• One of the pitfalls of Bipolar voltage maps, is that it only detects subendocardial disease substrate & misses intramural & epicardial disease substrate.

 

• Unipolar voltage maps may assist in uncovering intramural or epicardial disease when the bipolar voltage appears normal & is sometimes used as a surrogate marker of intramural disease.

 

• Unipolar voltage measures voltage between the catheter electrode and the return/indifferent electrode – meaning it measures the full thickness of myocardial voltage making it an indicator of intramural/epicardial disease when the bipolar endocardial voltage is “normal”.

 

The diagram below describes the principle behind unipolar voltage detection & how unipolar low voltage collected on the endocardial surface correlates with direct bipolar mapping of the epicardium. 

 

My two cents:

• Identifying low voltage tissue is a PROXY for identifying slowly conducting tissue (which may participate as the slow limb in reentry VT).

 

• We should all be curious what voltage maps look like if we adjust the voltage threshold beyond the historically accepted 0.5mV – 1.5mV.

 

• Adjusting voltage maps based on sites of local capture & fractionated late potentials is one method of improving differentiation between electrically inert scar & diseased substrate potentially participating in VT.

 

• Multipolar mapping catheters & software solutions improve spatial resolution & bipolar voltage fidelity, however, we are still missing intramural, epicardial, functional & decremental substrate when only relying on a bipolar voltage map.

 

• Unipolar voltage maps can identify intramural/epicardial substate in the context of “normal” bipolar endocardial voltage.

 

• The inadequacies of voltage mapping is why other forms of substrate mapping including ILAM, DeEP, S2/S3 & ICE mapping exist…more on these in future BeatBox Blog posts :)

 

Cheers
Mitch & CPiP Team

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