Treatment of pyridostigmine-induced AV block with hyoscyamine in a patient with myasthenia gravis

Anil Gehi, Michael G Benatar, Jonathan Langberg

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Treatment of Pyridostigmine-Induced AV Block. Myasthenia gravis is an autoimmune disorder of the nervous system typically mediated by antibodies against the nicotinic acetylcholine receptor at the neuromuscular junction. Treatment of myasthenia gravis frequently involves the use of cholinesterase inhibitors such as pyridostigmine. Treatment with these agents has been associated with bradycardia and syncope requiring pacemaker implantation. We report a case of a 60-year-old man with a 1-year history of myasthenia gravis treated with pyridostigmine who presented with syncope due to high degree AV block. Before committing the patient to a permanent pacemaker, a trial of medical therapy with hyoscyamine was attempted. Hyoscyamine is a muscarinic antagonist commonly used to block cholinergic side effects associated with pyridostigmine without reducing its efficacy at the neuromuscular junction. Treatment with hyoscyamine resulted in complete resolution of AV block, thereby avoiding pacemaker implantation.

Original languageEnglish
Pages (from-to)214-216
Number of pages3
JournalJournal of Cardiovascular Electrophysiology
Volume19
Issue number2
DOIs
StatePublished - Feb 1 2008
Externally publishedYes

Fingerprint

Hyoscyamine
Pyridostigmine Bromide
Atrioventricular Block
Myasthenia Gravis
Neuromuscular Junction
Syncope
Autoimmune Diseases of the Nervous System
Therapeutics
Muscarinic Antagonists
Cholinesterase Inhibitors
Nicotinic Receptors
Bradycardia
Cholinergic Agents
Antibodies

Keywords

  • Heart block
  • Myasthenia gravis
  • Syncope

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Physiology

Cite this

Treatment of pyridostigmine-induced AV block with hyoscyamine in a patient with myasthenia gravis. / Gehi, Anil; Benatar, Michael G; Langberg, Jonathan.

In: Journal of Cardiovascular Electrophysiology, Vol. 19, No. 2, 01.02.2008, p. 214-216.

Research output: Contribution to journalArticle

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