The R″ wave in V1 and the negative terminal QRS vector in aVF combine to a novel 12-lead ECG algorithm to identify slow conducting anatomical isthmus 3 in patients with tetralogy of Fallot

Figures

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  Figure 1. ECG examples. (A–C) Examples of QRS morphologies in lead V1. No R″ (A) and R″ (B, C) are illustrated (arrow points to R″). (D–E) Examples of lead aVF with the isoelectric line extended through the QRS complexes (dotted lines). The final time the QRS complex passes this line towards negative is defined as the beginning of the negative terminal portion (NTP). (D) Absence of NTP, in contrast to (E) and (F) where NTP is present with a duration of 54 and 100 ms, respectively (see time calliper).

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  Figure 2. Flowchart of included patients. rTOF, repaired tetralogy of Fallot; EAM, electroanatomical mapping; Vp, ventricular pacing; AF, atrial fibrillation; RBBB, right bundle branch block; rest as in Table 1.

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  Figure 3. Scatterplot and ROC curve of duration of NTP in aVF. Absence of an NTP in aVF was scored as 0 in the ROC curve analysis (A) and the scatterplot (B). ROC, receiver operating characteristics; AUC, area under the curve; rest as in earlier tables/figures.

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  Figure 4. Diagnostic algorithm of derivation cohort.

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  Figure 5. EAM activation and voltage mapping and correspondence with QRS characteristics. (A) RV activation map of a 36-year-old rTOF patient with a TAP and normal conducting AI 3. Activation times are colour-coded (8 isochrones) according to bar. The RV activation originates in the septum and the wavefront propagates over the RV free wall (left; anterior view) and through the fast conducting AI 3 (right; posterior view) with late activation of the basal lateral peri-tricuspid RV (arrows). No R″ or negative terminal deflection in aVF was observed (see inset with QRS complexes). (B) Bipolar voltage maps of the same patient (same views) showing high voltages at AI 3 (colour-coded according to bar). (C) Activation maps as in (A) showing the terminal activation pattern directed towards basal–lateral and inferior: activation after R′ peak in V1 is colour-coded according to five isochrones (right, modified posterior view). (D) RV activation maps of a 57-year-old rTOF patient with a TAP and SCAI 3 (conduction velocity 0.38 m/s). The terminal activation has shifted superiorly towards the lateral RV outflow tract leading to an R″ in V1 and a negative terminal QRS portion in aVF (inset). The views…

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  Figure 6. (A) Diagnostic flowchart and (B) scatterplot of duration of NTP stratified per presence of SCAI 3 in the validation cohort.

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  Figure 7. Expected RV activation in hypothetical scenarios. (A–C) Schematics of expected RV activation in hypothetical patients with SCAI 3 and an additional (slow conducting) AI. The arrows indicate the direction of RV activation, the waved arrows indicate slow conduction through a SCAI, and the circle indicates the terminal RV activation. (A) Simultaneous presence of a normal conducting AI 4 can counteract for the slow conduction though SCAI 3 and would lead to an RV activation similar to patients without SCAI 3. (B) In case of a SCAI 3 and a SCAI 2, the high lateral RVOT will remain the latest activated part of the RV (SCAI 3 not shown; RVOT indicates RVOT patch). (C) Similarly, the presence of SCAI 1 and SCAI 3 will lead to late activation of the lateral RVOT. Abbreviations as in earlier figures/tables.