Pace Mapping

During VT, the electrical wavefront circulates through a protected channel within scar tissue. At the point where the wavefront exits this channel into healthy myocardium, it spreads outward freely. The direction and speed of that spread determine the QRS morphology we see on the surface ECG.

The critical insight: the QRS shape depends almost entirely on where the wavefront enters normal myocardium, and on the angle of that entry. Two circuits with different internal paths but the same exit site will produce nearly identical QRS complexes. The exit is the signature.

When we pace from that same exit site, we bypass the circuit entirely but recreate the identical activation sequence through the rest of the ventricle. If all 12 surface leads show a matching morphology, we have confirmed the location.

We compare the paced QRS to the clinical VT QRS in all 12 leads, one by one. Each lead is scored as a match or a mismatch based on overall morphology, axis, and amplitude.

When we pace from normal myocardium, the QRS begins almost immediately after the pacing stimulus. The stimulus-to-QRS interval (stim-to-QRS) is short, typically less than 40 ms.

When we pace from within scar tissue, the story changes. The electrical impulse must first travel through the slow-conducting channel inside the scar before it reaches healthy myocardium and generates a QRS on the surface. This produces a measurable delay between the stimulus artifact and the QRS onset.

A long stim-to-QRS interval tells us something important: the catheter is deep within the isthmus of the reentrant circuit, surrounded by scar. The wavefront has to traverse that protected corridor before it exits. We may have a perfect 12/12 QRS match, but the delay reveals that we are pacing from within the channel rather than from the exit itself.

This distinction matters for ablation planning. The exit site is one valid target. The protected isthmus is another. The stim-to-QRS interval helps us distinguish between them.

Activation mapping requires the VT to be running. We move the catheter point by point, recording the local activation time at each location. The site with the earliest presystolic signal is closest to the origin. It is the gold standard for localizing the circuit, but it has a strict prerequisite: the VT must be sustained and hemodynamically tolerated long enough to complete the map.

Pace mapping works in sinus rhythm. We do not need the VT to be running at all. This makes it indispensable in two common scenarios: when VT is not inducible in the lab, and when VT causes hemodynamic collapse that forces us to terminate it immediately.

In practice, the two approaches complement each other. Activation mapping finds the earliest site during VT; pace mapping confirms the exit site from sinus rhythm. When both point to the same location, confidence is high. When we cannot perform activation mapping at all, pace mapping becomes the primary localization tool.

Pace mapping has real constraints. The most common pitfall involves pacing output. Higher pacing output captures a larger volume of myocardium around the catheter tip, which can alter the QRS morphology slightly compared to the clinical VT. The general practice is to pace at the lowest output that achieves consistent capture, reducing the radius of captured tissue.

Epicardial VT exit sites pose a different problem. If the exit is on the outer surface of the heart, pacing from the endocardial surface may never replicate the morphology accurately. The wavefront would have to traverse the full wall thickness before exiting, producing a different activation pattern.

Patients with multiple VT morphologies require separate pace maps for each one. Each morphology represents a different exit site (and often a different circuit), so a single 12/12 match confirms only one of them.

Finally, pace mapping identifies the exit site, not the full isthmus. The protected channel through which the wavefront circulates during VT may extend several centimeters beyond the exit. A successful ablation often requires targeting the isthmus itself, which demands additional mapping strategies such as substrate mapping or entrainment.