ArticleCurrent therapeutic research, clinical and experimental2025
Pharmacodynamics, Safety, and Tolerability of Pyridostigmine Bromide in Heart Failure.
Article in Current therapeutic research, clinical and experimental, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01415921 (Augmentation of Parasympathetic Signaling With Pyridostigmine in Heart Failure), which is not on this map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Augmentation of Parasympathetic Signaling With Pyridostigmine in Heart Failure
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14 authors.
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Abstract
Background: Pyridostigmine bromide is a short-acting carbamate acetylcholinesterase inhibitor that has been shown to acutely augment parasympathetic signaling in cardiovascular disease populations. Objective: This study was undertaken to characterize pharmacodynamics, safety, and tolerability of pyridostigmine during repeated dosing in patients with heart failure. Methods: A prospective ascending-dose, forced titration, double-blind Phase II randomized clinical trial was conducted to compare the effects of pyridostigmine bromide (15, 30, and 60 mg TID over 8 weeks) versus matching placebo on red blood cell (RBC) acetylcholinesterase activity, cholinergic side effects, and physiologic measures of parasympathetic heart rate modulation and sympathovagal balance in ambulatory patients with chronic systolic heart failure. Results: Fifty subjects were screened, and 33 eligible subjects were randomly assigned (mean age, 55 years; mean left ventricular ejection fraction, 23%). Pyridostigmine bromide significantly decreased RBC acetylcholinesterase activity ( Conclusions: Pyridostigmine bromide administered over 8 weeks was associated with a significant reduction of RBC acetylcholinesterase activity and relatively mild symptoms of cholinergic excess, but changes in parasympathetic signaling in the sinoatrial node previously reported after acute administration were not observed. Further investigations are needed to delineate pharmacodynamic and pathobiological factors contributing to these findings. ClinicalTrials.gov identifier: NCT01415921.
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