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
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.