Key result
The lidocaine analog Kö 1173 (1-8 mg/kg) significantly raised the threshold for repetitive ventricular extrasystoles and prevented its decrease during acute coronary insufficiency.
Why the study?
Does the lidocaine analog Kö 1173 improve the threshold for repetitive ventricular extrasystoles in a canine model of acute coronary insufficiency?
Does the lidocaine analog Kö 1173 improve the threshold for repetitive ventricular extrasystoles in a canine model of acute coronary insufficiency?
The lidocaine analog Kö 1173 prevents the decrease in ventricular fibrillation threshold during acute coronary insufficiency in dogs without affecting cardiac conduction.
Hypothesis-generating in canine ischemia; leaves open translation of Kö 1173 to clinical antiarrhythmic use.
The electrophysiologic properties of a lidocaine analog (Kö 1173) was experimentally studied in 41 mongrel dogs. The threshold for occurrence of repetitive ventricular extrasystoles was significantly raised by the administration of 2, 4, and 8 mg/kg of the drug, while atrioventricular and intraventricular conduction times were not affected. After ligation of the anterior descending branch of the left coronary artery, the threshold for occurrence of repetitive ventricular extrasystoles was significantly lowered before the administration of Kö 1173 but it returned to control values after the administration 1 mg/kg of the drug. The strength-interval curve shifted profressively to the right when the dose was increased from 2 to 4 and 8 mg/kg. These results indicate that Kö 1173 prevents the decrease in threshold for occurrence of repetitive ventricular extrasystoles in acute coronary insufficiency at a dose which does not affect the conduction system.
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kuma et al. (2008) studied Acute coronary insufficiency (n=41). Lidocaine analog (Kö 1173) vs. Baseline/control values was evaluated on Threshold for occurrence of repetitive ventricular extrasystoles. The lidocaine analog Kö 1173 (1-8 mg/kg) significantly raised the threshold for repetitive ventricular extrasystoles and prevented its decrease during acute coronary insufficiency.
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