Goldberger J J, Smith J R, Kim Y H, Damle R S, Kadish A H
Division of Cardiology, Northwestern University Medical School, Chicago, Ill, USA.
Circulation. 1995 Aug 15;92(4):875-80. doi: 10.1161/01.cir.92.4.875.
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.
大多数评估高强度驱动序列（S1）刺激对心室有效不应期（VERP）测量影响的研究表明VERP缩短。由于这种效应可能是由于儿茶酚胺的局部释放，预计VERP缩短仅会在刺激部位附近发生。VERP的局部缩短应会导致高强度驱动序列刺激期间不应期离散度增加。因此，本研究评估了高强度S1刺激导致的VERP缩短的空间分布及其对不应期离散度的影响。
对三组患者进行了研究。在第1组中，10名无结构性心脏病的受试者在右心室心尖（RVA）和流出道（RVOT）测定VERP，同时改变S1部位以评估低强度S1刺激对所测VERP的影响。在第2组中，研究了距S1部位0、7、14和21毫米处高强度S1刺激对VERP的影响，以测量VERP缩短的空间分布及其对不应期离散度的影响；另外10名无结构性心脏病的受试者组成第2组。由于不应期离散度增加在某些临床情况下可能有害，在第3组中研究了高强度S1刺激的影响，该组由10名长期植入经静脉除颤器的受试者组成；在将S1刺激强度从低强度变化到高强度时，通过慢性电极进行VERP的无创测量。所有VERP测定均在连续起搏期间采用递增法并使用低强度的额外刺激进行。在第1组中，当S1部位为RVA和RVOT时，RVA的VERP分别为218±9和214±10毫秒（P = 无显著性差异）。当S1部位从RVOT改变为RVA时，RVOT的VERP也未改变。在第2组中，高强度S1使VERP从224±8（阈值的两倍）变为203±10毫秒（P <.01），在距S1部位0、7、14和21毫米处分别从220±11变为209±12毫秒（P <.01），从222±12变为221±12毫秒，从220±11变为221±11毫秒。高强度S1刺激导致不应期离散度从13±4增加到22±9毫秒（P =.006）。在第3组中，高强度S1刺激使VERP从309±23缩短至285±30毫秒（P =.0003）。
低强度S1刺激对VERP无显著影响。高强度S1刺激在刺激部位最大程度地缩短不应期；VERP缩短在距S1刺激部位7至14毫米之间消散，导致不应期离散度增加。在长期植入除颤器电极的患者中观察到高强度刺激导致的局部VERP缩短，这可能对高强度刺激期间的致心律失常机制有影响。
