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).
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.
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.
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). 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.
During postoperative period the signs of ventricular pre-excitation in ECG were not observed, transesophageal EPI did not evoked orthodromic tachycardia.