The comparative effects of drive and test stimulus intensity on myocardialexcitability and vulnerability

Citation
Hs. Friedman et al., The comparative effects of drive and test stimulus intensity on myocardialexcitability and vulnerability, PACE, 23(1), 2000, pp. 84-95
Citations number
17
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
PACE-PACING AND CLINICAL ELECTROPHYSIOLOGY
ISSN journal
01478389 → ACNP
Volume
23
Issue
1
Year of publication
2000
Pages
84 - 95
Database
ISI
SICI code
0147-8389(200001)23:1<84:TCEODA>2.0.ZU;2-7
Abstract
The number and intensity of stimuli that set basic cycle length in cardiac electrophysiological studies can influence the electrical properties assess ed by extrastimuli. The relative contribution of drive (S-1) and test (S-2) stimulus intensity in defining myocardial excitability and vulnerability h as not been reported. The purpose of this investigation was to assess this interaction and to determine whether atrial and ventricular findings differ ed. The effects of S-1 and S-2 intensity On atrial and ventricular stimulus -in tensity-refractory-period curves were determined in open-chest dogs: co mparisons were made between curves with S-1 intensity varied between diasto lic threshold (DT) and 10 mA and S-2 intensity maintained at DT and those w ith S-2 intensity maintained at DT and S-2 intensity varied between DT and 10 mA. S-1-S-1 was held constant and S-1-S-2 varied. The effects of differe nt stimulation sites, cycle length, number of stimulations, and neural bloc kade were assessed. S-1 intensity amplification shifted atrial stimulus-int ensity-refractory period curves in the direction of increased excitability and vulnerability the changes were more pronounced than those obtained by m odulating S-2 intensity The changes produced by increasing S-1 intensity we re evident at different cycle lengths and were enhanced by an increased num ber of stimulations, but were not evident when S-1 and S-2 were delivered a t different atrial sites. Although beta-blockade attenuated the effects of increasing S-1 intensity somewhat, the addition of cholinergic blockade vir tually abolished it. Ventricular refractoriness was also changed by modulat ion of S-1 intensity, but the changes were less striking. In the atrium, mo dulation of S-1 intensity has greater effects of stimulus-intensity-refract ory-period relations than modulation of S-2 intensity; in the ventricle, th e converse is true.