Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antagonism of neuromuscular block using cholinesterase inhibitors and atropine is charged with several risks, which are at least partly caused by pharmacological characteristics of the anticholinergic drugs, e.g. short duration of action causing secondary bradycardia. Compared to atropine, ipratropium bromide, a new anticholinergic drug, is--due to its quarternary ammonium compound--characterized by longer duration of action. In contrast to atropine, this substance does not penetrate the blood-brain and placental barrier. Our present study was designed to compare the haemodynamic effects of both substances, using invasive monitoring, during antagonism of neuromuscular block with pyridostigmine. In contrast to atropine, ipratropium bromide induced a higher degree of initial tachycardia but did not allow secondary reduction of heart rate by rebound vagal stimulation. While cardiac output was almost constant, ipratropium bromide caused changes in stroke volume, which were due to alterations in heart rate. There were no clinically relevant changes of the other haemodynamic parameters. Cardiac arrhythmia were observed more often after administration of atropine and were of longer duration. In conclusion, ipratropium bromide is a useful alternative to atropine in patients with pre existing low heart rate and bradyarrhythmia.
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PMID:[Hemodynamic effects in antagonism of neuromuscular blockage: atropine-pyridostigmine versus ipratropium bromide-pyridostigmine]. 623 62

We describe three cases of patients with Alzheimer's disease who presented with cardiac syncope soon after initiation of a cholinesterase inhibitor therapy (donepezil). Bradyarrhythmia was documented in two patients, considered probable in one, and was presumed related to the cholinergic therapy. Pacemaker implantation seemed justified rather than donepezil cessation. More over, it permitted an increase in donepezil dosage.
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PMID:Significance of syncope in patients with Alzheimer's disease treated with cholinesterase inhibitors. 1475 43

Dementia with Lewy bodies (DLB) is a neurodegenerative condition that results in loss of mesopontine cholinergic neurons and sympathetic deinnervation. Although acetylcholinesterase inhibitors have been shown to improve cognitive and behavioral deficits in DLB, these patients may be more susceptible to bradyarrhythmic side effects from this class of drugs due to the autonomic insufficiency associated with the disease. We present a patient who experienced a dose-dependent, symptomatic sinus bradyarrhythmia with donepezil doses at and greater than 5 mg. Owing to underlying autonomic dysfunction, patients with DLB may be at increased risk of bradyarrhythmia resulting from treatment with acetylcholinesterase inhibitors.
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PMID:Donepezil-associated bradyarrhythmia in a patient with dementia with Lewy bodies (DLB). 2050 40

Herein we describe 6 cases of patients with Alzheimer's disease presented with syncope, dizziness, and dyspnea soon after the initiation of cholinesterase inhibitor therapy. All patients had bradyarrhythmia on electrocardiogram (ECG). Two patients had complete atrioventricular block, 2 pateints had 2/1 type atrioventricular block, 1 patient had sinus bradycardia and hypersensitive carotid sinus syndrome, and 1 had sick sinus syndrome. All these patients were treated with pacemaker implantation and the cholinesterase inhibitor therapy continued. At 13-month follow-up, no syncope, dizziness, or dyspnea was reported.
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PMID:Anticholinesterase-induced symptoms improved by pacemaker implantation in patients with Alzheimer's disease: analysis of 6 cases. 2281 79

A 58-year-old woman complained of general fatigue and was diagnosed with sick sinus syndrome (SSS) by ambulatory electrocardiogram, which demonstrated sinus arrest at midnight and paroxysmal atrial fibrillation (AF) at nighttime. Since her plasma cholinesterase (ChE) activity had been persistently zero, she was diagnosed with ChE deficiency. She refused permanent pacemaker implantation, and treatment with positive chronotropic drugs is ongoing. A novel association of ChE deficiency with SSS is theoretically possible rather than coincident, considering that ChE plays a key role in cholinergic influences on the sinus node leading to sinus bradyarrhythmia and on the atria, causing vagally mediated AF.
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PMID:Sick Sinus Syndrome Observed in a Patient with Cholinesterase Deficiency. 3044 82