ISSN:
1432-1912
Keywords:
Key words Fluvoxamine
;
Amitriptyline
;
Canine myocardial infarction
;
Epicardial activation delay
;
Arrhythmia
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract We studied the effects of fluvoxamine and amitriptyline on epicardial activation delay of premature excitations, the effective refractory period, and the incidence of ventricular arrhythmias by programmed electrical ventricular stimulation in the canine heart after myocardial infarction. Additionally, we investigated whether the inhibition of norepinephrine reuptake by amitriptyline contributes to epicardial activation delay or arrhythmias by combination with propranolol pretreatment. Amitriptyline, at a dose of 3 mg/kg, significantly prolonged epicardial activation delay of premature excitations in the infarcted zone in a frequency-dependent manner (n=10). Amitriptyline also prolonged epicardial activation delay of premature excitations in the normal zone (n=10). The effective refractory period in the infarcted zone was significantly prolonged by amitriptyline at a dose of 3 mg/kg (n=8). Amitriptyline increased the incidence of ventricular arrhythmias induced by programmed electrical ventricular stimulation (n=8). Propranolol did not affect the epicardial activation delay caused by amitriptyline or the incidence of ventricular arrhythmias induced by programmed electrical ventricular stimulation (n=6). Fluvoxamine, on the other hand, had no significant effect on epicardial activation delay of premature excitations (n=10) or the effective refractory period (n=8) in both the infarcted and normal zones. Fluvoxamine did not increase the incidence of ventricular arrhythmias induced by programmed electrical ventricular stimulation (n=8). From the present results, fluvoxamine seems to have lower cardiac toxicity than amitriptyline. Moreover, the electrophysiological effects of amitriptyline in this model may be due to a direct cardiac depressive action, but not to the inhibition of norepinephrine reuptake.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00168703
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