Prolongation of conduction time during premature stimulation in the human atrium is primarily caused by local stimulus response latency

Document Type

Journal Article

Publication Date

1-1-1995

Journal

European Heart Journal

Volume

16

Issue

12

DOI

10.1093/oxfordjournals.eurheartj.a060848

Keywords

Conduction time; Extrastimulation; Human atrium; Stimulus response latency

Abstract

Background: Conventional clinical electrophysiological techniques cannot accurately differentiate between local stimulus response latency and propagation time of the atrial response. The purpose of this study was to identify and distinguish local stimulus response latency from impulse propagation time in the human right atrium during programmed electrical stimulation. Methods: Pacing was performed from two atrial sites (high and low right atrium) in 19 patients, using monophasic action potential recording/pacing combination catheters (interelectrode distance < 2mm). Local stimulus response latency (interval between stimulus artifact and upstroke of the local monophasic action potential), and propagation time (interval between local and remote monophasic action potential upstroke) were evaluated at a basic cycle length (S1-S1) of 600 ms and as a function of the extrastimulus proximity (interval between extrastimulus and effective refractory period). Data are presented as means ± SEM. Results: During basic stimulation, local latency was very small (3.8 ± 1.7 ms). During premature extrastimulation (proximity < 70 ms), local latency increased progressively with decreasing coupling intervals. Prolongation of local latency was most pronounced during stimulation close to the effective refractory period with local stimulus response latency increasing to 18.3 ± 1.4 ms (380 ± 7.9%) at 10 ms proximity (P<0.002) and to 27.9 ± 3.7 ms (630 ± 13.2%) at 5 ms proximity, respectively (P<0.0001). The impulse propagation time between the stimulation site and the remote recording site was on average 54.5 ± 14.3 ms during basic stimulation, and increased up to 62.1 ± 13.5 ms (14.0 ± 8.4%), which was not significant. Conclusions: The intra-atrial impulse propagation remained essentially unchanged during the entire range of premature stimulation. Local stimulus response latency was negligible and constant during late coupling intervals but increased dramatically when extrastimulation approached the preceding repolarization phase. This has the following clinical impact: first, local stimulus response latency during premature extrastimulation curbs the targeted atrial response interval; second, local stimulus response latency, not propagation time, seems responsible for the greater functional than effective refractory period during electrical stimulation; third, local stimulus response latency should be considered in pace mapping for accurate comparison of conduction time before pacing with that during pacing.

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