Mechanism of arrhythmogenicity of the short–long cardiac sequence that precedes ventricular tachyarrhythmias in the long QT syndrome
Nabil El-Sherif, MDa,
Edward B. Caref, PhDa,
Masaomi Chinushi, MDa and
Mark Restivo, PhDa
a Cardiology Division, Department of Medicine, State University of New York Health Science Center and Veterans Affairs Medical Center, Brooklyn, New York, USA
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Figure 1 Electrocardiographic recordings from a short–long cardiac sequence in which the occurrence of a second subendocardial focal beat from a different site initiated ventricular tachyarrhythmia after a stable unifocal bigeminal rhythm. The stars refer to beats of focal origin; R refers to reentrant beats.
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Figure 2 Tridimensional activation of the V1 and V2 beats of the nonsustained ventricular tachyarrhythmia shown in Figure 1 (left) and selected electrograms along the reentrant pathway of the V2 beat (right). For diagrammatic illustration of tridimensional activation, the heart is cut transversely into five sections oriented with the basal section on top and the apical section on the bottom and labeled 1 to 5. The V1 and V2 beats arose from different subendocardial sites (marked by stars). Note that the V2 beat initiated reentry. Isochrones of activation are drawn at 20-ms intervals and labeled 1, 2, 3 and so on, and functional conduction block is represented by heavy solid lines.
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Figure 3 Electrocardiographic recordings from a different experiment in which ventricular tachyarrhythmia was initiated by the ventricular premature beat (V2) that followed the first short–long cardiac sequence. The latter was due to the occurrence of a ventricular premature beat (V1, the short cycle) followed after a compensatory pause by a sinus beat (the long cycle). Note that V1 followed a sudden lengthening of the sinus cycle length. The numbers represent cardiac cycle length in ms.
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Figure 4 Tridimensional activation maps of the V1 and V2 beats shown in Figure 3 (top) and selected electrograms along the reentrant pathway induced by the V2 beat (bottom). The two V beats arose from different sites in section 3 (marked by stars on the maps and electrograms) and had different local coupling intervals. See text for details. CL = cycle length.
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Figure 5 Top: Sections 1 and 3 of the activation maps of beats V1 and V2 from the short–long sequence shown in Figures 3 and 4. Bottom: Unipolar electrograms recorded from two plunge needle electrodes, A and B, from sections 1 and 3, respectively. The numbers represent local activation–recovery intervals (ARI) in ms. The numbers in parentheses are the cardiac cycle length in ms. Note the development of conduction block between electrode sites #5 and #4 during V2 in needle B. The changes in a preceding cardiac cycle were associated with significant changes in local ARIs that were more marked in midmyocardial (Mid) and endocardial (End) zones compared with epicardial (Epi) zones. See text for details. E = electrotonic potential.
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Figure 6 Electrocardiographic recording from a different experiment showing constant coupling intervals of ventricular premature beats but gradual lengthening of the last two returning sinus cycles before the onset of ventricular tachyarrhythmia. Numbers are in ms. The artifacts in the electrocardiographic leads were due to vagal stimulation. The stars refer to beats of focal origin; R refers to reentrant beats.
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Figure 7 Right panel illustrates the activation map of section 3 of the penultimate bigeminal beat (A) and the last bigeminal beat that initiated ventricular tachyarrhythmia (B) from the experiment shown in Figure 6. Isochrones of activation are drawn at 20-ms intervals and labeled 1, 2, 3 and so on, and functional conduction block is represented by heavy solid lines. Left panel illustrates electrograms from selected sites on the two maps (A1 to A4 and B1 to B4). The electrograms labeled A* and B* were recorded at the site of origin of bigeminal beat A and B, respectively. Both beats arose from the same right ventricular subendocardial site in section 2 (not shown in the figure). The numbers in parentheses represent the local activation–recovery intervals (ARI) at each site. Note that the ARIs of B1 to B4 were 19 to 37 ms longer compared with A1 to A4. Functional conduction developed between sites B3 and B4 because of increased dispersion of repolarization (DR).
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