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Department of Anesthesia Royal Victoria Hospital, McGill University Montreal, Quebec
In the review article by Dr. Kostopanagiotou et al. (1) concerned with transplant recipients undergoing non-transplant surgery, it is indicated that "neostigmine usually has no effect in the denervated heart." This opinion, espoused in many earlier reviews on pharmacological considerations of the transplanted heart, has little evidence to support it. I wish to challenge this opinion which continues to be expressed despite recent evidence to the contrary. Neostigmine produces a dose-dependent, atropine-sensitive reduction in heart rate in cardiac transplants, and patients who have received transplants more than six months before the administration of neostigmine may be particularly sensitive to its bradycardic effect (2–4). Edrophonium also evokes a reduction in heart rate in cardiac transplants, although the magnitude of the bradycardia is smaller and less variable (5). Animal studies suggest anticholinesterases produce bradycardia in the denervated heart by their direct stimulation of cholinergic receptors in the peripheral cardiac parasympathetic pathway or by their anticholinesterase action, which protects the hydrolysis of acetylcholine tonically released from cardiac parasympathetic postganglionic cells (6,7). I believe the anticholinesterase effects on the transplanted heart are not merely curiosities without clinical significance. A case report attributes bradycardia and cardiac arrest in two cardiac transplant patients to the parasympathomimetic effects of neostigmine (8). These findings have prompted us to caution that when administering anticholinesterases to heart transplant patients, a muscarinic antagonist should always be coadministered to block the cardiac and other muscarinic side effects (9).
References
Department of Anaesthesia University of Athens, Medical School Athens, Greece
We would like to thank Dr. Backman for his comments on our review article. Indeed, Dr. Backman’s research (1) contradicts traditional knowledge that anticholinesterases have no effect on the rate of a denervated heart (2,3). Although reinnervation of the transplanted heart rarely, if ever, occurs, it seems that, given enough time posttransplantation, other receptor-related mechanisms may take over and allow neostigmine to exert its bradycardic effect. We certainly agree that, however remote, the possibility of bradycardic response should be considered when administering neostigmine to cardiac transplant recipients and that coadministration of a muscarinic antagonist may prevent this serious complication.
References
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