The comparative effects of drive and test stimulus intensity on myocardial excitability and vulnerability.
The number and intensity of stimuli that set basic cycle length in cardiac electrophysiological studies can influence the electrical properties assessed by extrastimuli. The relative contribution of drive (S1) and test (S2) stimulus intensity in defining myocardial excitability and vulnerability has not been reported. The purpose of this investigation was to assess this interaction and to determine whether atrial and ventricular findings differed. The effects of S1 and S2 intensity on atrial and ventricular stimulus-intensity-refractory-period curves were determined in open-chest dogs: comparisons were made between curves with S1 intensity varied between diastolic threshold (DT) and 10 mA and S2 intensity maintained at DT and those with S1 intensity maintained at DT and S2 intensity varied between DT and 10 mA. S1-S1 was held constant and S1-S2 varied. The effects of different stimulation sites, cycle length, number of stimulations, and neural blockade were assessed. S1 intensity amplification shifted atrial stimulus-intensity-refractory period curves in the direction of increased excitability and vulnerability; the changes were more pronounced than those obtained by modulating S2 intensity. The changes produced by increasing S1 intensity were evident at different cycle lengths and were enhanced by an increased number of stimulations, but were not evident when S1 and S2 were delivered at different atrial sites. Although beta-blockade attenuated the effects of increasing S1 intensity somewhat, the addition of cholinergic blockade virtually abolished it. Ventricular refractoriness was also changed by modulation of S1 intensity, but the changes were less striking. In the atrium, modulation of S1 intensity has greater effects of stimulus-intensity-refractory-period relations than modulation of S2 intensity; in the ventricule, the converse is true.
Friedman
H S
HS
Department of Medicine, Long Island College Hospital, New York, USA.
Wattanasuwan
N
N
Sharafkhaneh
A
A
Win
M
M
Mallipeddi
D
D
Khan
I A
IA
Dai
C P
CP
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology* / Q000628:therapy; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography; D006325:Heart Atria / Q000503:physiopathology; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D006352:Heart Ventricles / Q000503:physiopathology; D009200:Myocardial Contraction / Q000187:drug effects; D014693:Ventricular Fibrillation / Q000503:physiopathology* / Q000628:therapy
D000319:Adrenergic beta-Antagonists