Effect of increased drive-train stimulus intensity on dispersion of ventricular refractoriness.

Abstract

Most studies evaluating the effects of high-intensity drive-train (S1) stimulation on the measurement of the ventricular effective refractory period (VERP) demonstrated a shortening of the VERP. Because this effect may be due to the local release of catecholamines, VERP shortening would be expected to occur only near the site of stimulation. Local shortening in the VERP should then result in an increased dispersion of refractoriness during high-intensity drive-train stimulation. Thus, this study evaluated the spatial distribution of the VERP shortening resulting from high-intensity S1 stimulation and its effect on dispersion of refractoriness. Three groups of patients were studied. In group 1, 10 subjects without structural heart disease had VERP determinations performed at the right ventricular apex (RVA) and outflow tract (RVOT) while the S1 site was changed to evaluate the effects of low-intensity S1 stimulation on the measured VERP. In group 2, the effect of high-intensity S1 stimulation on the VERP was studied 0, 7, 14, and 21 mm away from the S1 site to measure the spatial distribution of VERP shortening and the effect on dispersion of refractoriness; 10 additional subjects without structural heart disease made up group 2. Because increased dispersion of refractoriness may be deleterious in certain clinical situations, the effect of high-intensity S1 stimulation was studied in group 3, which comprised 10 subjects with chronically implanted transvenous defibrillators; noninvasive measurements of the VERP through the chronic lead were made while the S1 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 extrastimulus. In group 1, the RVA VERPs were 218 +/- 9 and 214 +/- 10 ms when the S1 site was the RVA and RVOT, respectively (P = NS). The RVOT VERPs were also unchanged when the S1 site was changed from the RVOT to the RVA. In group 2, high-intensity S1 changed the VERP from 224 +/- 8 (at twice the threshold) to 203 +/- 10 ms (P < .01), 220 +/- 11 to 209 +/- 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 S1 site, respectively. High-intensity S1 stimulation led to an increase in the dispersion of refractoriness from 13 +/- 4 to 22 +/- 9 ms (P = .006). In group 3, high-intensity S1 stimulation shortened the VERP from 309 +/- 23 to 285 +/- 30 ms (P = .0003). Low-intensity S1 stimulation has no significant effect on the VERP. High-intensity S1 stimulation shortens the refractory period maximally at the site of stimulation; the VERP shortening dissipates between 7 and 14 mm away from the site of S1 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 mechanism of proarrhythmia during high-intensity stimulation.