Abstract
The effect of amitriptyline that leads to ventricular tachycardia was evaluated by the repetitive extrasystole threshold (RET) technique in 18 dogs. The RET was 28.8 +/- 7.9 mamp before and 8.2 +/- 5.3 mamp after amitriptyline, p less than 0.001. Physostigmine, propranolol, sodium bicarbonate, and left stellate ganglionectomy reversed the effect of amitriptyline on RET. We conclude that amitriptyline overdose predisposes to sudden death by lowering the ventricular fibrillation threshold. This cardiotoxic effect is mediated partly through the central nervous system and can be inhibited by increased plasma binding (bicarbonate), cholinergic stimulation (physostigmine), beta adrenergic blockade (propranolol), and sympathetic denervation (left stellate ganglionectomy).
Highlights
The effect of amitriptyline that leads to ventricular tachycardia was evaluated hy the repetitive extrasystole threshold (RET) technique in 18 dogs
The lowered RET is consistent with the clinical finding that tricyclic antidepressant overdoses predispose to ventricular tachycardia
This effect on RET was countered by physostigmine, propranolol, and left stellate ganglionectomy
Summary
For the entire group of 16 dogs RET ± 1 SD was 28.8 ± 7.9 mamp during the control period and 8.2 ± 5.3 mamp after amitriptyline, p < 0.001. Mean RET was 35.6 ± 6.1 mamp before and 5.0 ± 5.2 mamp after amitriptyline, p < 0.001, and 38.0 ± 2.8 mamp after propranolol (control not significantly different). 0.005, and 27.6 ± 9.8 mamp after left stellate ganglionectomy (control not significantly different). 5.8 ± 3.3 mamp after amitriptyline, p < 0.01, and 21.3 ± 16.0 mamp after sodium bicarbonate (control not significantly different). At the time of VFT the mean level of amitriptyline was 971 ± 526 ng/m!
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