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disopyramide (Disopyramide Dumles / Dirythmin SA / Dirytmin)

✓ Approved

AstraZeneca UK Limited · SCN5A · 小分子

什么是 disopyramide？

disopyramide 是一种小分子，由AstraZeneca UK Limited研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名Disopyramide Dumles, Dirythmin SA, Dirytmin
公司AstraZeneca UK Limited
药物类别小分子
分子靶点SCN5A
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, AstraZeneca UK Limited

作用机制

分子靶点

disopyramide 作用于 1 个分子靶点：

SCN5Asodium voltage-gated channel alpha subunit 5 (CMD1E, SSS1)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

disopyramide 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Cardiac disordersArrhythmia✓ Approved

相关研究文献

PubMedHeart & lung : the journal of critical care2026-09-04

Association of common QT-prolonging medications with arrhythmic risk in patients with bundle branch block: A stratified cohort analysis in left bundle branch block vs. right bundle branch block phenotypes.

Derector Evan E, DO Tirth Patel TP, Watanabe Hiroto H, Solomon Diana D et al.

Bundle branch block (BBB) affects 11-17% of adults over 80 and is associated with mortality and heart failure. Conventional QTc formulae overestimate repolarization in wide QRS complexes, with clinicians holding symptom-management therapies based on inaccurate measurements. This retrospective study utilized the MIMIC-IV database to examine arrhythmogenic risk by drug class and BBB phenotype. Adult ICU admissions with BBB were stratified by drug exposure: amiodarone, high-risk anti-arrhythmics (sotalol, dofetilide, procainamide, ibutilide, quinidine, disopyramide), and common non-cardiac QT-prolonging agents (haloperidol, ondansetron, quetiapine, methadone, levofloxacin, azithromycin). The primary outcome was a composite of ventricular arrhythmia and cardiac arrest; a sensitivity analysis restricted to ventricular arrhythmia was performed. Propensity score matching (1:1) with time-varying Cox regression addressed confounding and immortal time bias. The matched cohort included 1722 admissions (LBBB =1252; RBBB =470). Common non-cardiac agents were not associated with the composite outcome in LBBB (HR 0.96, p = 0.83) or RBBB (HR 0.61, p = 0.24; 28 events, hypothesis-generating). Amiodarone was associated with the composite (LBBB: HR 3.63, p < 0.01; RBBB HR: 3.90, p < 0.01), but not the LBBB sensitivity analysis (HR 1.61, p = 0.19), suggesting confounding by indication. Among patients with QTc >500 ms, common agents remained non-significant. Common non-cardiac QT-prolonging medications were not associated with increased risk in patients with BBB, even with prolonged QTc. The divergence between composite and sensitivity results for amiodarone highlights the influence of confounding by indication. Medication alerts should incorporate stratification by drug class rather than QTc alone.

PMID 42697068
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PubMedAmerican heart journal plus : cardiology research and practice2026-07-12

Ice-cold beer-triggered swallow syncope with reproducible supra-Hisian AV block documented by intracardiac recordings.

Sato Daisuke D, Uchimura Kumi K, Katashima Takashi T, Matsui Yumie Y et al.

Swallow syncope is a rare situational syncope caused by an exaggerated vagal reflex and may result in bradyarrhythmia or atrioventricular block. A 63-year-old man with recurrent syncope triggered by beer ingestion underwent cardiovascular, gastrointestinal, ambulatory electrocardiographic, and electrophysiological evaluation, including provocation testing. Only ice-cold beer reproducibly induced transient AH block. Other foods and beverages, including cold soda, cold sake, and room-temperature beer, were negative. Ambulatory monitoring documented a symptomatic 7.9-second pause. Disopyramide was ineffective. Permanent pacemaker implantation prevented recurrent symptoms despite repeat provocation. This case highlights a highly specific trigger for swallow syncope and the diagnostic value of targeted provocation testing.

PMID 42437181
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PubMedIndian heart journal2026-06-19

Medical management of hypertrophic cardiomyopathy.

Gupta Mohit D MD, Goel Vrinda V, Girish M P MP

Hypertrophic cardiomyopathy (HCM) is a genetically determined myocardial disease in which symptoms are driven not simply by ventricular hypertrophy, but by a combination of dynamic left ventricular outflow tract obstruction (LVOTO), impaired diastolic filling and other factors.The therapy for HCM differs fundamentally from routine heart failure management and must be mechanism based. In obstructive HCM, the pharmacologic objective is to blunt hypercontractility, lengthen diastole, preserve loading conditions, and reduce the LVOT gradient. In non-obstructive HCM, management is focused on symptom control, heart-rate moderation, careful volume management, and treatment of arrhythmias and congestion. Non-vasodilating beta-blockers, non-dihydropyridine calcium-channel blockers, and disopyramide have constituted the foundation of medical therapy. The contemporary era has added sarcomere-directed treatment with cardiac myosin inhibitors, particularly mavacamten and aficamten, The present review provides a pragmatic algorithm for publication-level clinical use in contemporary practice.

PMID 42314796
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PubMedJournal of clinical medicine2026-06-12

Use of Disopyramide in Obstructive Hypertrophic Cardiomyopathy: A European Insight.

Charron Philippe P, Osman Faizel F, Trochu Jean-Noel JN, Zema Carla C et al.

Background/Objectives: Guidelines for obstructive hypertrophic cardiomyopathy (HCM) recommend treatment with disopyramide as an add-on to beta-blockers or calcium-channel blockers when symptoms persist. Data pertaining to effective disopyramide use in practice beyond single-center experience are very limited. This study aimed to quantify disopyramide use in patients with obstructive HCM in England, France and Germany, before the availability of cardiac myosin inhibitors. Methods: This retrospective study used nationally representative databases from England (Clinical Practice Research Datalink and Hospital Episode Statistics, 2010-2019), France (National Healthcare Data System, 2012-2019) and Germany (German statutory health insurance, 2011-2019). Adults (18+) with obstructive HCM were included, based on diagnostic codes for obstructive HCM or any HCM with septal reduction therapy. Disopyramide usage was defined as ≥1 prescription for a patient in a calendar year. Results: Overall, 3730, 6823 and 1141 patients diagnosed with obstructive HCM were identified in the English, French and German databases, respectively. In England, disopyramide use ranged from 4.7% to 5.6% per year with use generally stable over time. The equivalent usage for France was 1.7% to 2.6% per year. As expected, no recorded reimbursed use was reported in Germany during the study period. Conclusions: Disopyramide use is very low in patients with obstructive HCM, possibly due to treatment-related issues, availability or lack of reimbursement. These barriers may drive the uptake of alternative guideline recommended therapies for obstructive HCM treatment.

PMID 42279095
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PubMedArchives of gerontology and geriatrics2026-06-07

Microglial PICALM: A novel genetic driver and therapeutic target in vascular dementia.

Chai Zhaohui Z, Xu Qiuhan Q, Cheng Dan D, Zhang Yuning Y et al.

Vascular dementia (VaD) lacks well-defined genetic mechanisms. Cell-type-specific effects of GWAS loci remain unexplored. We integrated single‑cell eQTL data (183 donors, eight cell types) with VaD GWAS (3624 cases, 475,484 controls) using Mendelian randomization and Bayesian colocalization, replicated in an independent cohort (2074 cases, 456,366 controls). Subtype, snRNA‑seq, cell‑cell communication, PheWAS, expression profiling, and drug prediction with BBB permeability assessment were performed. Microglial PICALM was the only robustly replicated signal (OR = 0.8334, p = 5.3 × 10⁻⁴; colocalization PP.H4 > 0.75). The effect was strongest in multiple infarctions dementia (OR = 0.7746). Exploratory snRNA-seq analysis (4 VaD vs. 4 controls; GSE282111) provided supporting evidence for microglial PICALM enrichment and downregulation (p < 0.001). PICALM‑high microglia showed enhanced neurovascular‑ and phagocytosis‑related communication (e.g., SPP1, GAS6, GRN). PheWAS revealed no pleiotropy. In silico drug repurposing prioritised three FDA-approved BBB-penetrant compounds (disopyramide, benzocaine, amantadine) as candidates warranting further mechanistic validation. Microglial PICALM is identified as a likely genetic determinant of VaD, especially in the multiple infarctions subtype. Upregulating PICALM may be associated with a neuroprotective microglial phenotype, highlighting PICALM as a candidate therapeutic target warranting further experimental validation.

PMID 42250393
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PubMedJRSM cardiovascular disease2026-05-29

Pharmacologic therapies for hypertrophic cardiomyopathy: The past, the present, and the future.

Halațiu Vasile-Bogdan VB, Cozac Dan Alexandru DA, Scridon Alina A

Hypertrophic cardiomyopathy (HCM) stands as the most common monogenic cardiac disease, with an estimated prevalence historically reported as 1:500, but likely closer to 1:200 based on contemporary population studies in the general population. The past decade has marked a fundamental shift in therapeutic strategy: from symptomatic relief toward interventions directly targeting pathological sarcomeric hypercontractility. Conventional therapy relies on beta-blockers and non-dihydropyridine calcium channel antagonists, which provide symptomatic benefits through negative inotropic effects. For refractory left ventricular outflow tract obstruction, disopyramide constitutes an effective third-line option, although its anticholinergic profile requires cautious administration. Cardiac myosin inhibitors, mavacamten and aficamten, have introduced a novel therapeutic paradigm through direct modulation of actin-myosin cross-bridge formation. Pivotal clinical trials have demonstrated significant improvements in exercise capacity, reduction in obstruction severity, and enhancement of functional status, validating for the first time a therapeutic strategy that directly targets the underlying sarcomeric mechanism of hypercontractility. The therapeutic horizon includes next-generation myosin modulators, metabolic pathway interventions, and gene-based strategies. Current challenges involve accessibility to these therapies, substantial costs, and the requirement for mandatory regular echocardiographic monitoring. Future perspectives are oriented toward precision personalized medicine, integrating molecular therapeutics with genetic profiling to enable increasingly individualized risk stratification and therapeutic decision making.

PMID 42210975
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