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5.8 Ventricular Tachycardia (VT) 329,330,331,332

Ventricular tachycardia (VT) is a rapid heartbeat that can lead to sudden cardiac death.

Broadly, VT can be divided into two types, focal and reentrant, based on mechanisms and
patterns of excitation spread. The arrhythmia mechanisms can be determined during invasive
electrophysiology (EP) study based on the heart’s response to ventricular pacing at a faster rate
than the tachycardia and resetting of the VT, a process known as entrainment. Focal VT is
characterized by activation starting from a focal site and cannot be reproducibly entrained.

Reentrant VT is activation forming a rotational wave that can be successfully entrained. ECGI
was applied in a series of 25 patients undergoing EP studies and catheter ablation procedures for
various forms of VT. The results revealed diverse activation patterns, mechanisms and sites of

initiation of human VT 329 .

Location of VT Origin

On the basis of invasive EP studies, 11 patients had their origin in the RV, including

9 patients in which the origin was in the RVOT. ECGI located the site of origin in 10 of 11 RV sites
(91%) and in 11 of 12 LV sites (92%). Examples of ECGI localization are shown in Figure 5.26.

Mechanisms of VT

Based on invasive EP studies, 18 patients had focal VT, whereas five patients had a reentrant
mechanism. For the patients with focal VT, activation maps uniformly showed a radial activation
pattern emerging from the site of origin. In all the patients with reentrant VT, ECGI showed a

rotational wave front with a high degree of curvature, with the wave front returning to the
initiation site. Examples of these two distinct patterns are shown in Figure 5.27.

Examples of Focal VT

We reported a case of a 29-years-old athlete who had frequent PVCs and who developed a
spontaneous, sustained VT during exercise testing 330 . The ECG morphologies of the VT and PVCs
were very similar (if not identical). Therefore, ECGI was performed during a single PVC (ECGI is

performed during a single beat; there is no need to collect data from multiple beats as in catheter
mapping). The ECGI isochrones map (Figure 5.28A) localized the origin of the PVC to the LV apex,
to an area of a small diverticulum (CT image in Figure 5.28C). Based on the pure Q morphology

of the ECGI-reconstructed EGM from that site, it was determined that the initiation site was
epicardial. Guided by the ECGI data, invasive electroanatomic mapping (CARTO) of the LV was
performed during PVCs (Figure 5.28B) and during VT (induced with isoproterenol). The non-
invasive ECGI map was consistent with the invasive catheter map (compare Figures 5.28 A and B)
and epicardial cryoablation procedure was performed through a subxiphoid puncture.