PMC9596977_01
Results of transthoracic echocardiography. (A) On admission. (B) At the 3-month follow-up.
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F1
Transthoracic echocardiography (TTE) revealed a dilated cardiomyopathy with global hypokinesis, left ventricular end-diastolic diameter (LVEDD) 68 mm, and left ventricular ejection fraction (LVEF) 39% (Figure 1A). LVEF improved to 67% and the LVEDD decreased to 56 mm (Figure 1B).
(A) A 12-lead ECG on admission showed supraventricular tachycardia with alternating RR intervals at a rate of 133 beats/min. The P wave was positive in lead II, negative in aVR, and biphasic in V1, suggesting a sinus rhythm of 66 beats/min. Each sinus beat was simultaneously conducted through the anterograde fast and slow AV nodal pathways, giving rise to a double ventricular response. QRS alternans were present as the first and second QRS complexes during 1:2 AV conduction were of different amplitudes. As shown in the ladder diagram, dots indicate the beginnings of the P waves. Solid oblique and dashed lines in the AV portion of the diagram denote conduction over the fast and slow pathways, respectively. (B) The surface ECG returned to normal after radiofrequency ablation.
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ECG showed a narrow complex tachycardia with 510 and 400 msec alternating R-R intervals. Each P wave was followed by 2 QRS, suggesting 1:2 AV conduction through the fast and slow AV nodal pathways and possible DAVNNT (Figure 2A). Radiofrequency ablation of the slow pathway subsequently eliminated the tachycardia and restored 1:1 AV conduction (Figure 2B).
Seven typical Holter recording strips in lead V1 were shown. The corresponding mechanism was explained in the ladder diagram below each of them. RB, right bundle; LB, left bundle. (A) The sinus P waves (PP intervals 740 msec) were conducted simultaneously over the dual AV nodal pathways, producing a double ventricular response. (B) Group beatings with PP intervals of 1,120 msec were presented. A group of three was seen throughout the tracing follow by a pause, suggesting sinus beats conducted with alternating 1:2 and 1:1 AV ratios with longer PR intervals (160 msec) during 1:1 conduction over the fast pathways. (C) The sinus beats (PP intervals 820 msec) in the group beatings conducted with alternating 1:1 and 1:2 AV ratios with shorter PR intervals (580 msec) during 1:1 conduction over the slow pathways. (D) The front 5 and eleventh P waves were conducted only through the slow pathways, then the sixth to eighth P waves only via the fast pathways, and the ninth, tenth, twelfth, and thirteenth P waves simultaneously over the dual AV pathways. The tenth P wave with a PR interval of 240 msec gave rise to a QRS complex with left bundle branch block (LBBB) morphology, whereas the twelfth and fourteenth P waves with a PR interval of 220 msec produced a QRS wave with right bundle block (RBBB) pattern. The front 7 PP intervals were 720 msec, whereas the remaining PP intervals were approximately 840 msec. (E) The remaining adjacent PP intervals will be determined according to the PP interval of 600 msec consisting of two P waves marked with asterisks. The 2:1 conduction block occurred when the sinus beats were conducted simultaneously via the fast and slow pathways. Additionally, RBBB aberrancy except the sixth QRS complex were presented with conduction through the slow pathways. (F) Single, double, triple, and especially six consecutive QRS complexes with RBBB configuration from the conduction via the fast and slow pathways were shown in the lead V1 rhythm strip. It was the most difficult to identify them due to the superimposition of the P waves (PP intervals 640 msec) on the QRS complexes. (G) As a result of the conduction via the fast and (or) slow pathways, single and double QRS complexes with RBBB pattern as well as six consecutive QRS complexes with LBBB morphology coexisted in the lead V1 rhythm strip. Likewise, the P waves with PP intervals of 620 msec were superimposed on the QRS complexes when LBBB or RBBB occurred, which made them unrecognizable.
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Different patterns of AV conduction recorded from Holter monitoring were displayed in Figure 3. Pattern 1 showed a continuous manifest 1:2 AV conduction over the fast and slow pathways (Figure 3A). Pattern 2 was defined as the slow pathway with a 2:1 conduction block (Figure 3B). Pattern 3 occurred when the conduction of the fast pathway was intermittently blocked (2:1) (Figure 3C). Pattern 4 was classified as the alternating conduction block of the fast and slow pathways (Figure 3D). Pattern 5 was typified by the simultaneous antegrade 2:1 conduction block with the dual AV pathways (Figure 3E). In pattern 6, there was 1:2 conduction with persistent or intermittent left or right bundle branch block (Figures 3F,G).
Findings of the electrophysiological study. The intracardiac recording confirmed the diagnosis of dual AV nodal non-reentrant tachycardia (DAVNNT). (A) One atrial impulse (A) triggered one hissian potential (H1) and one ventricular potential (V1) through the fast pathway, and then one H2 and one V2 through the slow pathway. The time difference between the fast pathway with an AH interval of 96 msec and the slow pathway with an AH interval of 506 msec was long enough to result in a double ventricular response. The HV interval of both fast and slow pathways was 38 msec. This recording was taken at a sweep speed of 100 mm/s. (B) Atrial extra systolic stimulation can reproducibly induce a 1:2 conduction over the fast and slow pathways, corroborating the diagnosis of DAVNNT. A paper speed was 25 mm/s.
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The electrophysiological study (EPS) revealed that each sinus beat was conducted down both the fast and slow pathways, resulting in 2 QRS, which could be reproduced by atrial extra stimulus (Figure 4).