Hydroquinidine therapy in Brugada syndrome

Hermida, Jean‐Sylvain; Denjoy, Isabelle; Clerc, Jérôme; Extramiana, Fabrice; Jarry, G; Milliez, Paul; Guicheney, Pascale; Fusco, Stefania Di; Rey, Jean‐Luc; Cauchemez, B; Leenhardt, Antoine

doi:10.1016/j.jacc.2003.12.046

Cited by 237 publications

(133 citation statements)

References 26 publications

Supporting

Mentioning

123

Contrasting

Unclassified

Order By: Relevance

“…The authors concluded that quinidine effectively suppresses VF induction as well as spontaneous arrhythmias in patients with Brugada syndrome and may be useful as an adjunct to ICD therapy or as an alternative to ICD in cases in which an ICD is refused, unaffordable, or not feasible for any reason. These results are consistent with those reported the same group in prior years (Belhassen et al 1999(Belhassen et al 2002 and more recently by other investigators (Hermida et al 2004;Mok et al 2004). The data highlight the need for randomized clinical trials to assess the effectiveness of quinidine, preferably in patients with frequent events who have already received an ICD.…”

Section: Pharmacologic Approach To Therapysupporting

confidence: 91%

“…a Control, BCL 800 ms. b Terfenadine (5 μM) induces ST segment elevation as a result of heterogeneous loss of the epicardial action potential dome, leading to phase 2 reentry3 which triggers a closely coupled extrasystole (BCL = 800 ms). c Addition of AVEO 118 (7 μM) prevents loss of the epicardial action potential dome and phase 2 reentry-induced arrhythmias (BCL = 800 ms) Table 2 Device nad pharmacologic apaproach to therapy of the Brugada syndrome Devices and Ablation ICD (Brugada et al 2000a) ?Ablation or Cryosurgery (Haissaguerre et l. 2003) ?Pacemaker (vn den Berg et al 2001) Pharmcaologic Approach to Therapy Ineffective Amiodarone β-Blockers (Brugadaa et al 1998) Class iC antiarrhythmics Flecainide (Shimizu et al 2000a) Propafenone (Matana et al 2000) ?Disopyramide (Chinushi et al 1997) Class IA aaantiarrhythmics Procainaamide (Brugada et al 2000c) Effective for treatment of electrical storms β-Adrenergic agonists-isoproterenol (Miyazaki et al 1996;Shihmizu et al 2000b) Phosphodiesterase III inhibitors-cilostazol (Tsuchiya et al 2002) Effective general therapy Class IA antiarrythmics Quinidine (Belhassen and Viskin 2004;Alings et al 2001;Belhassen et al 1999Belhassen et al , 2002Yan and Antzelevitch 1999;Hermida et al 2004;Mok et al 2004) Experimental therapy I to blockers-cardioselective and ion channel specific Quinidine (Yan and Antzelevitch 1999) 4-Aaminopyridine (Yan and Antzelevitch 1999) Tedisamil (Fish et al 2004b) AVE0118 (Fish et al 2004a) …”

Section: Pharmacologic Approach To Therapymentioning

confidence: 99%

See 1 more Smart Citation

Therapy for the Brugada Syndrome

Antzelevitch

Fish

Basis and Treatment of Cardiac Arrhythmias

View full text Add to dashboard Cite

The Brugada syndrome is a congenital syndrome of sudden cardiac death first described as a new clinical entity in 1992. Electrocardiographically characterized by a distinct coved-type ST segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children. The ECG manifestations of the Brugada syndrome are often dynamic or concealed and maybe revealed or modulated by sodium channel blockers. The syndrome may also be unmasked or precipitated by a febrile state, vagotonic agents, α-adrenergic agonists, β-adrenergic blockers, tricyclic ortetracyclic antidepressants, a combination of glucose and insulin, and hypokalemia, as well as by alcohol and cocaine toxicity. An implantable cardioverter-defibrillator (ICD) is the most widely accepted approach to therapy. Pharmacological therapy aimed at rebalancing the currents active during phase 1 of the right ventricular action potential is used to abort electrical storms, as an adjunct to device therapy, and as an alternative to device therapy when use of an ICD is not possible. Isoproterenol and cilostazol boost calcium channel current, and drugs like quinidine inhibit the transient outward current, acting to diminish the action potential notch and thus suppress the substrate and trigger for ventricular tachycardia/fibrillation (VT/VF). KeywordsBrugada syndrome; Phase 2 reentry; ST segment elevation; I Na ; I to ; Implantable cardioverterdefibrillator (ICD); VT; SCN5A mutations; Sudden death; Bradycardia Clinical Characteristics and Diagnostic CriteriaThe Brugada syndrome typically manifests in the third or fourth decade of life (average age of 41±15 years), although patients have been diagnosed with the syndrome at an age as young as 2 days and as old as 84 years. The prevalence of the disease is estimated to be at least 5 per 10,000 inhabitants in Southeast Asia, where the syndrome is endemic (Nademanee et al. 1997). In Japan, a Brugada syndrome ECG (type 1) is observed in 12 per 10,000 inhabitants; type 2 and type 3 ECGs, which are not diagnostic of Brugada syndrome, are much more prevalent, appearing in 58 per 10,000 inhabitants (Miyasaka et al. 2001). The true prevalence of the disease in the general population is difficult to estimate because the ECG pattern is often concealed (Brugada et al. 2003). Sudden unexplained nocturnal death syndrome (SUNDS also known as SUDS) and Brugada syndrome have been shown to be phenotypically, genetically, and functionally the same disorder (Vatta et al. 2002).Although syncope and sudden death are a consequence of ventricular tachycardia/fibrillation (VT/VF), approximately 20% of Brugada syndrome patients also develop supraventricular arrhythmias (Morita et al. 2002). Atrial fibrillation (AF) is reported in approximately 10%-20% of cases. Atrio-ventricular (AV) nodal reentrant tachycardia (AVNRT) and Wolf-ParkinsonWhite (WPW) syndrome have been described as well (Eckardt et al. 2001 et al. 2004)...

show abstract

Section: Pharmacologic Approach To Therapysupporting

confidence: 91%

Section: Pharmacologic Approach To Therapymentioning

confidence: 99%

Therapy for the Brugada Syndrome

Antzelevitch

Fish

Basis and Treatment of Cardiac Arrhythmias

View full text Add to dashboard Cite

show abstract

“…12) A number of reports have shown the effectiveness of quinidine in treatment of Brugada syndrome. [13][14][15][16][17][18][19] Because the typical features of Brugada syndrome were not observed in this case, it is unclear whether quinidine would have been effective. If VF storms occur despite the administration of quinidine, we are considering EPS and ablation under alcohol administration.…”

Section: Discussionmentioning

confidence: 99%

Alcohol‐induced Ventricular Fibrillation in Brugada Syndrome

Hayashi

Mitani

Goto

et al. 2009

Journal of Arrhythmia

View full text Add to dashboard Cite

A 37-year-old man lost consciousness suddenly due to ventricular fibrillation (VF). After cardioversion, twelve-lead ECG showed a pattern characteristic of type 1 Brugada. An implantable cardioverter defibrillator (ICD) was implanted for Brugada syndrome. In the following three years, VF occurred eight times after consumption of alcohol. Association between the Brugada syndrome and alcohol consumption has rarely been reported. Recently, it was reported that alcohol has inhibitory effect on single cardiac sodium channel gating and it may be that alcohol acted as a sodium channel blocker in this patient. Here we report a case of alcohol-induced VF in Brugada syndrome. (J Arrhythmia 2009; 25: 32-35)

show abstract

“…Additionally, they both respond well to quinidine, isoproterenol and cilostazol, explained by the effect of these agents on inhibition of potassium currents or increase of calcium currents. 37 Apart from the similar ECG and clinical phenotype, some differences can be also appreciated between the two entities. They include: …”

Section: Overlapping Features Of Brugada and Early Repolarisation Synmentioning

confidence: 99%

Brugada Syndrome and Early Repolarisation: Distinct Clinical Entities or Different Phenotypes of the Same Genetic Disease?

Conte

Caputo

Regoli

et al. 2016

Arrhythmia &Amp; Electrophysiology Review

View full text Add to dashboard Cite

General understanding of early repolarisation (ER) has dramatically changed in the last decade. For several years, ER has been considered a benign electrocardiographic (ECG) finding with high prevalence in the general population. Recently different studies have challenged this view and showed a significant association with life-threatening arrhythmias. [1][2][3][4][5] In 2008 Haïssaguerre et al. first reported an increased prevalence of a particular pattern of ER on the resting 12-lead ECG of patients with history of idiopathic ventricular fibrillation (VF) (see Figure 1). 2 In these patients, ER was characterised by elevation of the QRS-ST segment junction of at least 0.1 mV above the baseline level, manifesting as QRS slurring (a smooth transition from the QRS complex to the ST segment) or notching (a positive J deflection of at least 1 mm inscribed on the S wave) in two adjacent inferior (II, III and aVF), lateral (I, aVL, and V4-V6), or infero-lateral leads. The ER pattern was observed in 31 % of patients with idiopathic VF and in 5 % of healthy control subjects.Moreover, patients with idiopathic VF and ER pattern presented a higher risk of experiencing an arrhythmic recurrence during a 5-year follow-up.2 This observation was confirmed by a case-control study showing that J-point elevation in the inferior and lateral leads is more frequent in patients with idiopathic VF than in matched control subjects (27 % versus 8 % in inferior leads; 13 % versus 1 % in lateral leads).3 Conversely, ER localised exclusively in V4 to V6 occurs with similar frequency among patients and healthy subjects.

show abstract

Hydroquinidine therapy in Brugada syndrome

Cited by 237 publications

References 26 publications

Therapy for the Brugada Syndrome

Therapy for the Brugada Syndrome

Alcohol‐induced Ventricular Fibrillation in Brugada Syndrome

Brugada Syndrome and Early Repolarisation: Distinct Clinical Entities or Different Phenotypes of the Same Genetic Disease?

Contact Info

Product

Resources

About