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Background: Disopyramide is used to treat heart failure symptoms in patients with obstructive hypertrophic cardiomyopathy (HCM) with known medium-term efficacy and safety, while long-term outcomes are unknown.

Methods And Results: A total of 92 consecutive patients with symptomatic obstructive HCM with peak left ventricular outflow tract gradients of ≥30 mm Hg at rest or with provocation who were maintained on disopyramide for ≥5 years at 2 dedicated HCM centers were included: 92 patients; mean age, 62.5 years; 54% women; treated with disopyramide for median 7.

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Background: Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular outflow tract obstruction (LVOTO), leading to symptoms and adverse outcomes. Disopyramide, with its negative inotropic effects, is commonly used to reduce LVOTO in obstructive HCM (HOCM). This study evaluates the impact of disopyramide on functional capacity in HOCM patients.

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Disclaimer: In an effort to expedite the publication of articles, AJHP is posting manuscripts online as soon as possible after acceptance. Accepted manuscripts have been peer-reviewed and copyedited, but are posted online before technical formatting and author proofing. These manuscripts are not the final version of record and will be replaced with the final article (formatted per AJHP style and proofed by the authors) at a later time.

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Stereoselective block of the hERG potassium channel by the Class Ia antiarrhythmic drug disopyramide.

Cell Mol Life Sci

November 2024

School of Physiology, Pharmacology and Neuroscience, Biomedical Sciences Building, University of Bristol, University Walk, Bristol, BS8 1TD, UK.

Article Synopsis
  • Potassium channels from the human hERG gene are affected by various drugs, and this study specifically investigates the effects of chiral disopyramide, a Class Ia antiarrhythmic, on hERG currents in HEK 293 cells.* -
  • The findings show that the S(+) enantiomer of disopyramide is more potent at inhibiting hERG current compared to the R(-) form, with IC values of 3.9 µM and 12.9 µM respectively, and certain mutations in hERG alter these effects.* -
  • Molecular simulations indicate that the S(+) form binds more effectively to specific residues in the hERG channel, while the R(-)
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Background: Standard-of-care (SoC) medications for the treatment of obstructive hypertrophic cardiomyopathy (oHCM) are recommended as first-line therapy despite the lack of evidence from controlled clinical trials and well known off-target side effects.

Objectives: We describe the impact of SoC therapy downtitration and withdrawal in patients already receiving aficamten in FOREST-HCM (Follow-Up, Open-Label, Research Evaluation of Sustained Treatment with Aficamten in Hypertrophic Cardiomyopathy; NCT04848506).

Methods: Patients receiving SoC therapy (beta-blocker, nondihydropyridine calcium-channel blocker, and/or disopyramide) were eligible for protocol-guided SoC downtitration and withdrawal at the discretion of the investigator and after achieving a stable dose of aficamten for ≥4 weeks.

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