Shock Reduction With Long-Term Quinidine in Patients With Brugada Syndrome and Malignant Ventricular Arrhythmia Episodes

Anguera, Ignasi; García‐Alberola, Arcadio; Dallaglio, Paolo; Toquero, Jorge; Pérez, Lidia Sanz; Martínez, Juan G.; Peinado, Rafaél; Rubín, José M.; Brugada, Josép; Cequier, Ángel

doi:10.1016/j.jacc.2016.01.042

Cited by 31 publications

(14 citation statements)

References 4 publications

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“…. Anguera33 et al noted that quinidine could be useful to reduce, but not supress, the burden of ventricular arrhythmias with still few patients who experienced ICD shocks.…”

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confidence: 99%

The QUIDAM study: Hydroquinidine therapy for the management of Brugada syndrome patients at high arrhythmic risk

et al. 2017

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Although HQ seems to be effective in preventing life-threatening ventricular arrhythmia, it could not be an alternative for ICD implantation. Its frequent side effects greatly reduce its probable compliance and therefore do not reveal a significant effect. HQ increases repolarization dispersal with no changes in BrS pattern, which could indicate a more complex action of HQ than its I blocking effect alone.

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“…. Anguera33 et al noted that quinidine could be useful to reduce, but not supress, the burden of ventricular arrhythmias with still few patients who experienced ICD shocks.…”

mentioning

confidence: 99%

The QUIDAM study: Hydroquinidine therapy for the management of Brugada syndrome patients at high arrhythmic risk

et al. 2017

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“…Quinidine is moderately effective in unselected patients with atrial arrhythmias, but is associated with a significant increase in mortality. 4 , 5 , 7 For this reason, quinidine has fallen out of favor in the treatment of AF in patients without associated BrS. However, in the cases described, quinidine effectively suppressed atrial and ventricular arrhythmias in 2 patients with BrS without mutations in SCN5A .…”

Section: Discussionmentioning

confidence: 99%

“…Hydroquinidine has been identified as the AAD of choice for preventing recurrent ventricular arrhythmias in patients with BrS. 4 , 5 Hydroquinidine has also been used safely in a limited number of patients with concomitant ventricular and atrial arrhythmias. 3 The recent QUIDAM study randomized 50 high-risk patients to hydroquinidine or placebo to determine the impact on life-threatening arrhythmias.…”

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confidence: 99%

Quinidine effective for the management of ventricular and atrial arrhythmias associated with Brugada syndrome

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et al. 2018

HeartRhythm Case Reports

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“…In consideration of the favorable pharmacodynamic profile in Brugada syndrome ( 14 ), an oral regimen of hydroquinidine, that is a class 1A anti-arrhythmic drug, was introduced as a potential anti-myotonic agent and was titrated up to 150 mg bid in a few days. This regimen appreciably reduced myotonia, but had to be interrupted due to the appearance of diarrhea.…”

Section: Case Presentationmentioning

confidence: 99%

Flecainide-Induced Brugada Syndrome in a Patient With Skeletal Muscle Sodium Channelopathy: A Case Report With Critical Therapeutical Implications and Review of the Literature

et al. 2018

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Skeletal muscle sodium channelopathies are a group of neuromuscular disorders associated with mutations in the SCN4A gene. Because principal sodium channel isoforms expressed in the skeletal muscles and the heart are distinct one from the other, this condition usually spares cardiac functioning. Nonetheless, evidence on a possible link between skeletal muscle and cardiac sodium channelopathies has emerged in recent years. To date, eight patients bearing pathogenetic mutations in the SCN4A gene and manifesting cardiac electrophysiological alterations have been reported in literature. Among these patients, three presented a phenotype compatible with Brugada syndrome. We report the case of a 29-year-old patient affected by non-dystrophic myotonia associated with a p.G1306E mutation in the SCN4A gene, who presented symptoms of syncope and palpitation after the introduction of flecainide as an anti-myotonic agent. ECG and ajmaline challenge were consistent with the diagnosis of Brugada syndrome, leading to the implantation of a cardioverter defibrillator. No mutation in causative genes for Brugada syndrome was detected. Mexiletine treatment reduced myotonia without any cardiac adverse events. This case report highlights the clinical relevance of the recognition of cardiac electrophysiological alterations in skeletal muscle sodium channelopathies. The discovery of a possible pathogenetic linkage between skeletal muscle and cardiac sodium channelopathies may have significant implications in patients' management, also in light of the fact that class 1C anti-arrhythmics are potential triggers for life-threatening arrhythmias in patients with Brugada syndrome.

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Shock Reduction With Long-Term Quinidine in Patients With Brugada Syndrome and Malignant Ventricular Arrhythmia Episodes

Cited by 31 publications

References 4 publications

The QUIDAM study: Hydroquinidine therapy for the management of Brugada syndrome patients at high arrhythmic risk

The QUIDAM study: Hydroquinidine therapy for the management of Brugada syndrome patients at high arrhythmic risk

Quinidine effective for the management of ventricular and atrial arrhythmias associated with Brugada syndrome

Flecainide-Induced Brugada Syndrome in a Patient With Skeletal Muscle Sodium Channelopathy: A Case Report With Critical Therapeutical Implications and Review of the Literature

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