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Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3651_Библиотеки_им_академика_М_И_Перельмана

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R. Le Bouar et al.
Fig. 18.9 A 12-lead ECG showing induction of a wide QRS complex tachycardia during programmed ventricu­lar stimulation, with a heart rate of 187bpm, right bundle branch block morphology, and inferior axis, compatible
the left ventricle. Therefore, mapping of the LV was decided.
Access to the left ventricle was obtained using a retrograde approach by puncturing the right common femoral artery using the modied Seldinger technique, under Doppler ultrasound guidance. A Pentaray catheter (Biosense Webster, Johnson & Johnson) was introduced in a 9F 20 cm vascular sheath and was subsequently advanced via the aorta to the LV.It was used to perform the anatomical map, the bipolar voltage map, and the activation map of the LV. The Biosense Webster® SmartTouch SF open­irrigated 3.5mm tip with double curve was used to perform RF ablation.
An anatomical map of the LV was rst cre­ated, which showed a mildly dilated LV, with a volume of 209mL.
with VT.The QRS width was 130ms, suggestive of a sep­tal origin. Of note, the aspect of this VT is different from that of the clinical VT
A bipolar voltage map was subsequently cre­ated during sinus rhythm, which showed the presence of an area of low-voltage electrograms at the level of the septal and inferior wall of the LV, measuring 22.3 cm2, representing 11.3% of the total LV surface, compatible with scar post­myocardial infarction (Fig.18.10).
The unipolar voltage map is presented in com­parison to the bipolar voltage map in Fig.18.11. The area of low voltage (dened as a value of less than
8.3mV) corresponds well to the area of low voltage on the bipolar voltage map, being a little wider.
Programmed ventricular stimulation was per­formed once again, with induction of the previ­ously induced VT (Fig. 18.12). This was hemodynamically tolerated by the patient, which allowed the creation of an activation map with the Pentaray catheter. The activation map of the
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Fig. 18.10 CARTO image in RAO 58° caudal 49° show­ing the septal and the inferior wall of the left ventricle. Bipolar voltage map of the left ventricle revealing an area of low voltage (< 0.5mV, red color) at the level of the septal and inferior wall, compatible with myocardial scar post-myocardial infarction. The low-voltage area repre­sents 22.3 cm2 or 11.3% of the entire surface of the LV.The orange dots represent the bundle of His, continu­ing with the proximal part of the left bundle branch
LV during VT is presented in Figs. 18.13 and
18.14. This was in favor of a double-loop macro-
reentry circuit, forming a “gure of 8,” each of the two loops using the same critical isthmus at the level of the mid-septal LV wall. The length of the VT isthmus was 28 mm, with a width of 22mm, and it was situated at a distance of 21mm from the bundle of His.
Figure 18.15 shows the relationship between the anatomical substrate of the tachycardia (the low-voltage area situated at the level of the septal LV wall, seen on the bipolar voltage map of the LV, right panel) and the critical components of the VT: the two outer loops and the VT isthmus superposed on the activation map of the LV.
Having identied the critical components of the VT, RF ablation was performed during VT by
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creating several ablation lesions at the level of the VT isthmus (Fig.18.16). The target parameters were power 30W and ablation index 550. VT is terminated during RF application at this level, conrming the ndings of the activation map. This is shown in Fig.18.17.
Programmed ventricular stimulation was per­formed after the ablation, with induction of a dif­ferent VT. This was identical to the clinical VT (Fig.18.18).
Mapping and ablation of the clinical VT were subsequently decided. Given the fact that this VT was also hemodynamically tolerated, an activa­tion map of the VT was subsequently begun. However, placing the Pentaray catheter at the level of the basal septal LV systematically termi­nated the VT (Fig.18.19). Therefore, the activa­tion map for this VT was not complete.
A pacemap was therefore created, according to the technique described by de Chillou et al. [1].
The pacemap was created by pacing from the distal electrode of the roving/ablation catheter at a xed coupling interval of 600 ms in several areas of the LV, with emphasis on areas situated in or close to the myocardial scar at the level of the septal LV wall. The PASO module of the CARTO system was used to compare the result­ing 12-lead ECG during local pacing with the morphology of the PVC.A superposed correla­tion of 99.4% was observed in an area of high septal wall, at the level of the myocardial scar, close to the mitral valve, at 13mm distance from the His bundle and 8 mm distance from the entrance zone of the previously ablated VT, iden­tifying the exit zone of the VT (Fig.18.20). This is explained by the fact that activation of the LV during pacing proceeds from this site in a manner similar as that during VT. The resulting QRS morphology is therefore identical to the QRS morphology during VT.
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R. Le Bouar et al.
Fig. 18.11 CARTO image in RAO 70° caudal 30° show­ing the presence of a low-voltage area at the level of the septal and inferior wall of the LV (red color). Left panel shows the bipolar voltage map, with scar being dened at a value of <0.5mV; right panel shows the unipolar volt­age map, with scar being dened as <8.3mV.The yellow,
Fig. 18.12 A 12-lead ECG recorded after reinduction of VT 1 at programmed ventricular stimulation
green, and blue areas represent areas with borderline val­ues, between 0.5mV and 1.5 mV on the bipolar voltage map and between 3.5 and 8.3mV on the unipolar voltage map. The orange dots represent the bundle of His, con­tinuing with the proximal part of the left bundle branch
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Fig. 18.13 CARTO image of the left ventricle in RAO 70° caudal 30° showing the activation map of the LV dur­ing VT 1. The exit zone (red color), the two outer loops (represented in yellow, green, and blue, indicated by the curved and straight red arrows), and the entrance zone (in violet) are shown. The VT isthmus is delineated by the
Pacing the LV in adjacent zones of the exit zone identied sites with slightly different corre­spondence percentages, until a site was found where the morphology of the paced QRS com­plex differed signicantly from the morphology of the QRS during VT. This identied the area corresponding to the entrance zone during VT.This is explained by the fact that during ven­tricular pacing, the depolarization of the LV takes place in the direction opposite to that of the VT isthmus (where slow conduction is present), toward healthy ventricular myocardium, where the conduction velocity is superior to the conduc­tion at the level of the VT isthmus. The resulting morphology is therefore very different (Fig.18.21).
two narrow white lines (manually added for learning pur­pose). Upper right corner of the image: surface ECG lead II and intracavitary electrograms recorded by the elec­trodes 1–2 of the Pentaray catheter, recording a low­amplitude fragmented signal, present in mid- and late diastole
Once the exit zone and the entrance zone were identied, the VT isthmus was considered pres­ent between these two zones. The VT was likely a macro-reentry around the mitral valve.
RF ablation was performed by creating an ablation line joining the mitral annulus and the lines of ablation performed for the ablation of the rst VT (Fig.18.22). The target parameters were power=30W and ablation index 550.
The bipolar and the unipolar voltage map of the LV with superposed RF ablation lesions are presented in Fig.18.23.
Programmed ventricular stimulation was per­formed after the ablation, before and after iso­prenaline infusion, this time without induction of any ventricular arrhythmia (Fig.18.24).
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R. Le Bouar et al.
Fig. 18.14 CARTO image of the left ventricle in RAO 70° caudal 30° (same as in Fig.18.12) showing the septal LV wall. Activation map of the LV during ventricular tachycardia, showing the critical components of the VT: the exit zone (red color), the two outer loops (represented in yellow, green, and blue, indicated by the curved and straight red arrows), and the entrance zone (in violet). The
There were no complications related to the
procedure.
The 12-lead ECG recorded after the ablation
is shown in Fig.18.25.
Given the presence of ventricular tachycardia and of a myocardial scar post-myocardial infarc­tion, the decision to implant an ICD was taken. Given the good result of the ablation procedure and the young age of the patient, after discussion of the patient’s case by the heart team, a subcuta­neous ICD was implanted (Fig.18.26).
The patient was discharged from the hospital 48h later after the ICD implantation.
ICD interrogation 4 months post-ablation showed no recurrent episodes of ventricular tachycardia.
VT isthmus is delineated by the two narrow white lines (manually added for learning purpose). Upper right corner of the image: surface ECG lead II and intracavitary elec­trograms recorded by the electrodes 1–2 of the Pentaray catheter, recording a local signal, present in mid-diastole. The Pentaray catheter is placed in the entrance zone of the VT
Answers
Question 1: C.Ventricular tachycardia.
Question 2: B. Infero-septal left
ventricle.
Clues: 1. The presence of a LBBB pat­tern during VT can indicate either an origin in the right ventricle or an origin at the level of the LV septum.
2. The presence of a “QS” aspect in the inferior leads during VT orients the origin of the tachycardia at the level of the inferior wall of the heart.
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Fig. 18.15 CARTO image in RAO 70° caudal 30° show­ing the activation map of the LV during VT (left panel) and its anatomical relationship with the VT substrate shown on the bipolar voltage map of the LV (right panel),
3. The presence of a “double QRS axis transition” in the precordial leads is also an argument in favor of a septal origin.
Question 3: A.Yes. This should also be ablated, since the goal of a catheter ablation procedure for VT is ablation of all monomorphic sustained VTs.
Question 4: C.LV Inferior wall.
corresponding to the junction of the area of low voltage with normal myocardial tissue. The red arrows indicate the two outer loops of the VT
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R. Le Bouar et al.
Fig. 18.16 CARTO image of the left ventricle in RAO 70° caudal 30° (same as in Fig.18.12) showing the activation map of the LV during VT with superposed RF lesions at the level of the VT isthmus
Fig. 18.17 A 12-lead ECG showing VT termination during RF ablation of the critical isthmus
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Fig. 18.18 A 12-lead ECG showing the induction of the clinical VT during programmed ventricular stimulation
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Fig. 18.19 A 12-lead ECG showing the termination of the clinical VT by a mechanically induced PVC (red arrow) created by the Pentaray catheter situated at the level of the basal and septal LV wall
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Fig. 18.20 Left panel: CARTO image showing the sep- tal wall of the left ventricle. Pacemap of the left ventricle during sinus rhythm performed with the roving/ablation catheter identifying the exit zone of the clinical VT (in
red). Pacing at this site (yellow star) reproduces the QRS morphology of the VT with a concordance of 99.4% (right panel)
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Fig. 18.21 CARTO image showing the same view of the left ventricular septal wall as in Fig.18.20. Pacemap of the left ventricle in sinus rhythm identifying the entrance zone of the clinical VT (violet zone, adjacent to the entrance zone, in red). Pacing with the roving/ablation catheter at this site (yellow star) reproduces a QRS mor­phology very different from the morphology of the clini­cal VT (0%), even though the catheter is situated at a very
Fig. 18.22 CARTO image showing the septal wall of the left ventricle in RAO 98° caudal 27° showing the pacemap of the LV for the clinical VT with superposed RF ablation lesions (pink and red dots)
short distance compared to its position in Fig.18.18 (see text for further explanation). This is due to the fact that the activation wavefront from this site propagates not through the VT isthmus where slow-conducting myocardial bers are found, but in the opposite direction, through myocar­dial bers that conduct the activation wavefront faster, therefore creating a QRS morphology different from the QRDS morphology during VT