EFFECT OF INCREASED DRIVE-TRAIN STIMULUS-INTENSITY ON DISPERSION OF VENTRICULAR REFRACTORINESS

Background Most studies evaluating the effects of high-intensity drive -train (S-1) stimulation on the measurement of the ventricular effecti ve refractory period (VERP) demonstrated a shortening of the VERP. Bec ause this effect may be due to the local release of catecholamines, VE RP shortening would be expected to occur only near the site of stimula tion. Local shortening in the VERP should then result in an increased dispersion of refractoriness during high-intensity drive-train stimula tion. Thus, this study evaluated the spatial distribution of the VERP shortening resulting from high-intensity S-1 stimulation and its effec t on dispersion of refractoriness. Methods and Results Three groups of patients were studied. In group 1, 10 subjects without structural hea rt disease had VERP determinations performed at the right ventricular apex (RVA) and outflow tract (RVOT) while the S-1 site was changed to evaluate the effects of low-intensity S-1 stimulation on the measured VERP. In group 2, the effect of high-intensity S-1 stimulation on the VERP was studied 0, 7, 14, and 21 mm away from the S-1 site to measure the spatial distribution of VERP shortening and the effect on dispers ion of refractoriness; 10 additional subjects without structural heart disease made up group 2. Because increased dispersion of refractorine ss may be deleterious in certain clinical situations, the effect of hi gh-intensity S-1 stimulation was studied in group 3, which comprised 1 0 subjects with chronically implanted transvenous defibrillators; noni nvasive measurements of the VERP through the chronic lead were made wh ile the S-1 stimulus intensity was varied from low to high intensity. All VERP determinations were performed during continuous pacing by use of an incremental method and a low stimulus intensity for the extrast imulus. In group 1, the RVA VERPs were 218+/-9 and 214+/-10 ms when th e S-1 site was the RVA and RVOT, respectively (P=NS). The RVOT VERPs w ere also unchanged when the S-1 site was changed from the RVOT to the RVA. In group 2, high-intensity S-1 changed the VERP from 224+/- 8 (at twice the threshold) to 203+/-10 ms (P<.01), 220+/-11 to 2091+/-12 ms (P<.01), 222+/-12 to 221+/-12 ms, and 220+/-11 to 221+/-11 ms at 0, 7 , 14, and 21 mm away from the S-1 site, respectively. High-intensity S -1 stimulation led to an increase in the dispersion of refractoriness from 13+/-4 to 22+/-9 ms (P=.006). In group 3, high-intensity S-1 stim ulation shortened the VERP from 309+/-23 to 285+/-30 ms (P=.0003). Con clusions Low-intensity S-1 stimulation has no significant effect on th e VERP. High-intensity S-1 stimulation shortens the refractory period maximally at the site of stimulation; the VERP shortening dissipates b etween 7 and 14 mm away from the site of S-1 stimulation, resulting in an increased dispersion of refractoriness. The local VERP shortening with high-intensity stimulation is noted in patients with chronically implanted defibrillator leads, which may have implications for the mec hanism of proarrhythmia during high-intensity stimulation.