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Comparison of Oral Procainamide and Mexiletine Treatment of Recurrent and Refractory Ventricular Tachyarrhythmias.
J Clin Med
October 2024
Division of Cardiology, University Hospital "S.Maria della Misericordia", P.le S.Maria della Misericordia 15, 33100 Udine, Italy.
Article Synopsis
- The study investigates the effectiveness and tolerability of oral procainamide versus mexiletine for treating recurrent ventricular arrhythmias in patients who didn't respond to standard therapies like amiodarone and beta-blockers.
- Out of 68 patients treated, approximately 56% experienced a significant reduction in arrhythmia burden, with procainamide showing nearly three times higher efficacy compared to mexiletine.
- Side effects were noted in both treatments, but procainamide had a lower discontinuation rate due to severe side effects, suggesting it may be a preferable option for this patient group.
Preclinical study of the antimyotonic efficacy of safinamide in the myotonic mouse model.
Neurotherapeutics
October 2024
Department of Pharmacy & Drug Sciences, University of Bari Aldo Moro, Bari, Italy. Electronic address:
Mexiletine is the first choice drug in the treatment of non-dystrophic myotonias. However, 30% of patients experience little benefit from mexiletine due to poor tolerability, contraindications and limited efficacy likely based on pharmacogenetic profile. Safinamide inhibits neuronal voltage-gated sodium and calcium channels and shows anticonvulsant activity, in addition to a reversible monoamine oxidase-B inhibition.
View Article and Find Full Text PDFMexiletine versus lamotrigine in non-dystrophic myotonias: a randomised, double-blind, head-to-head, crossover, non-inferiority, phase 3 trial.
Lancet Neurol
October 2024
Centre for Neuromuscular Disorders, The National Hospital for Neurology and Neurosurgery, London, UK; Queen Square Centre for Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK.
Background: Non-dystrophic myotonias are skeletal muscle channelopathies caused by ion channel dysfunction. Symptom onset is frequently in the first decade of life, causing disability in a young cohort. Although there is no cure, symptomatic treatments exist.
View Article and Find Full Text PDFInherited myotonias.
Handb Clin Neurol
August 2024
Centre for Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, United Kingdom. Electronic address:
The inherited myotonias are a complex group of diseases caused by variations in genes that encode or modulate the expression of ion channels that regulate muscle excitability. These variations alter muscle membrane excitability allowing mild depolarization, causing myotonic discharges. There are two groups of inherited myotonia, the dystrophic and the nondystrophic myotonias (NDM).
View Article and Find Full Text PDFBK channels promote action potential repolarization in skeletal muscle but contribute little to myotonia.
Pflugers Arch
November 2024
Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, OH, 45435, USA.
Patients with myotonia congenita suffer from slowed relaxation of muscle (myotonia), due to hyperexcitability caused by loss-of-function mutations in the ClC-1 chloride channel. A recent study suggested that block of large-conductance voltage- and Ca- activated K channels (BK) may be effective as therapy. The mechanism underlying efficacy was suggested to be lessening of the depolarizing effect of build-up of K in t-tubules of muscle during repetitive firing.
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