Key result
Sympathetic denervation combined with norepinephrine infusion or sympathetic stimulation significantly increased the incidence of ventricular fibrillation in dogs (p<0.001).
Why the study?
Does sympathetic denervation supersensitivity increase the risk of ventricular fibrillation in a canine model of myocardial infarction?
Population
69 dogs
Comparison
Programmed ventricular stimulation during… vs Control period and sham-operated dogs
Design
Preclinical
Follow-up
4 to 22 days after the first operation
Authors
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Supports denervation supersensitivity as VF trigger in canine MI; leaves open human translation and beta-blockade effects.
Does sympathetic denervation supersensitivity increase the risk of ventricular fibrillation in a canine model of myocardial infarction?
p-value: p=<0.001
In a canine model, sympathetic denervation supersensitivity following myocardial infarction or phenol application is arrhythmogenic, increasing the vulnerability to ventricular fibrillation, which can be attenuated by beta-blockade.
Inoue et al. (1987) studied Sympathetic denervation and myocardial infarction (n=69). Sympathetic stimulation and norepinephrine infusion vs. Control state / sham-operated dogs was evaluated on Incidence of ventricular fibrillation elicited by programmed ventricular stimulation (p=<0.001). Sympathetic denervation combined with norepinephrine infusion or sympathetic stimulation significantly increased the incidence of ventricular fibrillation in dogs (p<0.001).
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