Wolff–Parkinson–White syndrome (WPW).

Patient Sh., 24 years old admitted to the tachyarrhythmia surgical treatment unit at the Medical Center with the diagnosis "Demonstrating WPW syndrome". AAVC of the left lower paraseptal location. Paroxysmal orthodromic АВ reciprocal tachycardia".
The patient underwent Non-invasive EPI using the "AMYCARD 01 C" system.
At the beginning activation mapping is carried out on epicardial model of the entire heart.  Isopotential and "dichromatic" maps were built.  Early activation of the left ventricle in the paraseptal region of АV-furrow was found (Fig. 1). The beginning of activation in the region of АV-furrow testifies the diagnosis of WPW syndrome.  The location of activation break zone points to the left paraseptal location of additional atrioventricular conjugation (AAVC).
To determine the location of AAVC towards the endocardium and epicardium, activation mapping on an endo-epicardial model of the ventricles is carried out.
On the endocardial surface of paraseptal region of the lateral wall of the left ventricle an isopotential map reveals  the region of early activation in the form of concentrically spreading region of negative potential that appears earlier that the epicardial one (Fig. 2).
Dichromatic maps in the FND mode show that the endocardial break of activation advances the epicardial break of 24 seconds that testifies endocardial location of the additional atrioventricular conjugation (Fig. 3).

   

Fig. 1.  Patient Sh. WPW syndrome of the left lower paraseptal location. Polygonal (to the left) and voxel (to the right) epicardial models of the heart. "Dichromatic" map in the FND mode.  The initial moment of ventricular activation.  The zone of an early activation is highlighted with a marker.  Activation of the left ventricle appears in the left paraseptal area in the region of atrioventricular furrow.

 

 

Fig. 2.  Patient Sh. WPW syndrome of the left lower paraseptal location.  Endo-epicardial polygonal model. Isopotential map. View of the side of the endocardium and epicardium.  Area of concentrically spreading negative potential, the sign of an early activation of myocardium, appears earlier in the endocardium than in the epicardium.

   
   
   

Fig. 3.  Patient Sh. WPW syndrome of the lower paraseptal location.  Endo-epicardial polygonal model. "Dichromatic" map in the FND mode. Initial period of ventricular activation.  Endocardial activation of the left ventricle advances epicardial activation of 24 milliseconds that testifies endocardial location of AAVC.

Maps of activation direction (the ADM mode) reveal typical areas of divergence of vector of myocardium activation direction from the regions of activation breaks (Fig.4).
Isochronous maps and maps of activation spread in the ADM mode shows the dynamics of full ventricular activation.  The sequence of ventricular activation is of a complicated character: pathologic wave of activation from AAVC meets "normal" wave of activation that appears due to ventricular activation by Kent-His’ bundle (Fig. 5, Fig. 6).


 
 

Fig. 4.  Patient Sh. WPW syndrome of the left paraseptal location.  Polygonal endo-epicardial ventricular model.  Map of myocardium activation direction in the ADM mode.  A typical picture of divergent vectors of activation direction from the points of activation break.

 
 

Fig. 5.  Patient Sh. WPW syndrome of the left paraseptal location.  Polygonal endo-epicardial ventricular model. Isochronous map in the ADM mode. Activation appears in the endocardium of posterior paraseptal region of the left ventricle and in 24 milliseconds it breaks in the epicardium in this region.  Approximately at the same time activation reaches basal parts of the interventricular septum to the left.  A little earlier, at the 20th millisecond activation of septum-apical region of the right ventricle (by the right pedicle of Kent-His’ bundle) begins.

   
   
   

Fig. 6.   Patient Sh. WPW syndrome of the left paraseptal location.  Polygonal endo-epicardial model of the heart.  Activation spread maps in the ADM mode.  Activation wave from AAVC meets activation wave from Kent-His’s bundle.

An invasive EPI of the heart proved this location of AAVC.  The patient has received a successful RFA of the left lower AAVC through transseptal access (Fig. 7).
 During postoperative period the signs of ventricular pre-excitation in ECG were not observed, transesophageal EPI did not evoked orthodromic tachycardia.


Fig. 7.  Patient Sh. The effective zone of RFА. (CS – coronary sinus, Abl – ablative electrode, RA - electrode in the right atrium, the region of effective RFA is marked with a star). Panel А – the left oblique projection (30 degrees), panel B – the right oblique projection (45 degrees)

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