Upstream stimulation versus downstream stimulation
arrhythmogenesis based on repolarization dispersion in the human heart
Frank Bode, MD* ,
Pamela Karasik, MD, FACC*,
Hugo A. Katus, MD, FESC and
Michael R. Franz, MD, PhD, FACC*,*
* Veteran Affairs and Georgetown University Medical Centers, Washington, DC, USA
Medizinische Klinik II, Universitaetsklinikum Luebeck, Germany
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Figure 1 Simultaneous monophasic action potential recording from the right ventricular outflow tract (RVOT) and right ventricular apex (RVA). The pacing sequence that initiates ventricular tachycardia (VT) at the successful stimulation site (RVA in this example) is compared to a corresponding pacing sequence at the noninducing stimulation site (RVOT). Intervals are given in milliseconds. (A) Pacing sequence prompting VT induction. Programmed electrical stimulation is performed in the RVA using three extra-stimuli (coupling intervals between stimuli (S): S1-S1 400 ms, S1-S2 290 ms, S2-S3 250 ms, S3-S4 240 ms). Action potential durations (APDs) were measured from the upstroke in phase 0 to the 90% repolarization level (Repol). During baseline stimulation (S1), APD is shorter at the RVA stimulation site than the RVOT site (284 vs. 302 ms). Upon introduction of premature stimuli, APDs shorten and conduction time (CT) from the RVA to the RVOT site increases. Dispersion of repolarization (Disp) measured between the time of 90% repolarization in the RVA and the time of 90% repolarization in the RVOT increases from 86ms at baseline (S1) to 92 ms with the last extra-stimulus applied (S4). (B) Closest coupled stimulation in the RVOT using three extra-stimuli (coupling intervals between stimuli: S1-S1 400 ms, S1-S2 290 ms, S2-S3 250 ms, S3-S4 215 ms). No VT is induced. In accordance with A, PD is longer at the RVOT stimulation site than the RVA site (300 ms vs. 282 ms). Conduction time between sites increases and APDs shorten upon introduction of premature stimuli, comparable to RVA pacing. Dispersion of repolarization is 50 ms during RVOT pacing at baseline (S1) and enhances to 82 ms with the last extra-stimulus applied (S4). Thus, stimulation of the RVOT site with longer APD produces less dispersion of repolarization than stimulation at the RVA site with shorter APD.
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Figure 2 Site specific difference in action potential duration (APD) and effective refractory period (ERP) during stimulation at basic cycle lengths (BCLs) of 600 ms and 400 ms. Action potential duration and ERP were significantly shorter at the inducing site (black bar) as compared to the noninducing site (white bar). *p < 0.05; **p < 0.01.
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Figure 3 Corresponding action potential durations (APDs) at the inducing (black bar) and noninducing site (white bar) during programmed stimulation. The APD decreased at both sites when premature extra-stimuli (S2-S4) were introduced at short coupling intervals. The APD was consistently shorter at the inducing site. *p < 0.05.
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Figure 4 Conduction time between the two ventricular sites. Impulses required progressively more time to propagate from the stimulation site to the remote site upon introduction of an increasing number of closely coupled extra-stimuli. No difference in intersite conduction time was found between stimulation at the ventricular tachycardia inducing site (black bar) vs. stimulation at the noninducing site (white bar). *p < 0.05.
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Figure 5 Dispersion of repolarization between the two ventricular sites. During baseline (S1) stimulation at the ventricular tachycardia-inducing site repolarization dispersion was larger than during stimulation at the noninducing site. Extra-stimulus application increased the dispersion of repolarization at both sites. Maximal dispersion produced by extra-stimulation at the noninducing site (white bar) only approached the amount of repolarization dispersion that was present during baseline stimulation at the inducing site (black bar). The largest repolarization dispersion was measured during extra-stimulation at the inducing site upon ventricular tachycardia initiation. *p < 0.05.
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