Time-dependent responses to provocative testing with flecainide in the diagnosis of Brugada syndrome

Calvo, David; Rubín, José M.; Pérez, Diego; Gómez, J.J. Gávira; Flórez, Juan P.; Avanzas, Pablo; García-Ruiz, José M.; Hera, Jesús M. de la; Reguero, Julián R.; Coto, Eliécer; Morı́s, César

doi:10.1016/j.hrthm.2014.10.036

Cited by 17 publications

(13 citation statements)

References 15 publications

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“…Hence, it has been recently reported that those longer periods of ECG recording increase the probability of recognition of the type I ECG. 18 An alternative tool has been proposed for diagnosing BrS: the full stomach test. 19 In this test, ECGs are performed before and after a large meal.…”

Section: Diagnostic Toolsmentioning

confidence: 99%

Brugada syndrome: clinical and genetic findings

Sarquella-Brugada

Campuzano

Arbelo

et al. 2016

Genetics in Medicine

125

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Review ARticleMore than 20 years ago, eight individuals were resuscitated from sudden cardiac death (SCD) caused by documented ventricular fibrillation (VF); all showed a characteristic ST segment elevation in the right precordial leads and a structurally normal heart. 1 In 1996, the term "Brugada syndrome" (BrS) was used to describe what was previously known as "right bundle branch block, persistent ST segment elevation, and sudden death syndrome. " 2 A year later, BrS was reported to be the same disease as sudden unexplained nocturnal death syndrome (SUNDS). In other countries, BrS has different names: Lai Tai (Thailand), Pokkuri (Japan), and Bangungut (Philippines). Currently, the prevalence of BrS is estimated at ~3-5 in 10,000 people, and it is higher in young men of Southeast Asian origin. It is the main cause of death among young healthy men in Southeast Asia. 3 Recent reports suggest that BrS could be responsible for 4% of all SCD and up to 12% of sudden death in patients with structurally normal hearts. The clinical phenotype manifests in adulthood, at a mean age of 41 years, and it is 8-to 10-times more frequent in males. Frequently, sudden death can be the first manifestation of the disease. 4 In 1998, the genetic basis of BrS was established when the sodium channel protein type V subunit α gene (SCN5A), which encodes the α-subunit of the voltage-gated Na v 1.5 cardiac sodium channel responsible for regulating rapid sodium current (I Na ), was associated with the disease. 5 Currently, BrS is recognized as a rare, inherited cardiac channelopathy caused by an alteration of ionic currents that leads to ventricular arrhythmias and SCD. It is clinically characterized by ST segment elevation in leads V1-V3 of the electrocardiogram, but incomplete penetrance and variable expressivity confound the diagnosis. 6 Despite the identification of 18 associated genes, 65-70% of clinically diagnosed cases remain without an identifiable genetic cause. 4 CLINICAL DIAGNOSIS Diagnostic criteriaThe clinical diagnosis of BrS requires the identification of the ST segment elevation in the right precordial leads at baseline or after the use of sodium blockers. Three different electrocardiographic (ECG) patterns can be often observed in families with BrS: type I, which consists of a coved-type ST segment elevation greater than 2 mm followed by a descending negative T wave in at least two right precordial leads (V1 to V3); type II ST elevation, saddleback-shaped patterns with a high initial increase followed by an ST elevation greater than 2 mm; and saddleback-shaped patterns with a high initial increase followed by an ST elevation less than 2 mm (Figure 1). The second Brugada Consensus Report proposed that only type I is diagnostic for BrS 7 and, in 2013, it was proposed that a definitive diagnosis of BrS considers both spontaneous type I pattern and a provoked type I pattern (with a baseline type II or III pattern) in at least one right precordial lead (V1 or V2). 8 The diagnosis of BrS is currently accepted in those patients ...

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Section: Diagnostic Toolsmentioning

confidence: 99%

Brugada syndrome: clinical and genetic findings

Sarquella-Brugada

Campuzano

Arbelo

et al. 2016

Genetics in Medicine

125

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“…In this sense, it is important to remark how this constitutive part along the QRS may present a dynamic behavior with time and also change under different clinical situations even within the same patient. At different states of the pathology the morphology of the ECG may change, which might make diagnosis of those patients difficult [ 18 ]. In addition, those changes on the ECG morphology may also change the distribution of the frequency content along the QRS, depending on the severity of the disease or the administration of various drugs.…”

Section: Discussionmentioning

confidence: 99%

“…As will be stated below, the Wavelet continuous transform might also have the advantage to efficiently locate the high-frequency content along the QRS complexes. The latter will be particularly interesting in characterizing dynamic process in which the electrical conduction delay in the myocardium varies according to physiological or interventional procedures [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Analysis of the High-Frequency Content in Human QRS Complexes by the Continuous Wavelet Transform: An Automatized Analysis for the Prediction of Sudden Cardiac Death

Iglesias

Gutiérrez

Cos

et al. 2018

Sensors

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Background: Fragmentation and delayed potentials in the QRS signal of patients have been postulated as risk markers for Sudden Cardiac Death (SCD). The analysis of the high-frequency spectral content may be useful for quantification. Methods: Forty-two consecutive patients with prior history of SCD or malignant arrhythmias (patients) where compared with 120 healthy individuals (controls). The QRS complexes were extracted with a modified Pan-Tompkins algorithm and processed with the Continuous Wavelet Transform to analyze the high-frequency content (85–130 Hz). Results: Overall, the power of the high-frequency content was higher in patients compared with controls (170.9 vs. 47.3 103nV2Hz−1; p = 0.007), with a prolonged time to reach the maximal power (68.9 vs. 64.8 ms; p = 0.002). An analysis of the signal intensity (instantaneous average of cumulative power), revealed a distinct function between patients and controls. The total intensity was higher in patients compared with controls (137.1 vs. 39 103nV2Hz−1s−1; p = 0.001) and the time to reach the maximal intensity was also prolonged (88.7 vs. 82.1 ms; p < 0.001). Discussion: The high-frequency content of the QRS complexes was distinct between patients at risk of SCD and healthy controls. The wavelet transform is an efficient tool for spectral analysis of the QRS complexes that may contribute to stratification of risk.

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“…History of frequent supraventricular arrhythmias and palpitations has been described in the follow-up of patients who underwent PFO closure [9]. One of the most common antiarrhythmic drug, flecainide, is currently used for the diagnosis of Brugada syndrome, administered intravenously, under ECG monitoring [10,11]. In our case, flecainide administration was crucial to unmask a latent Brugada pattern on the ECG, leading, also based on the clinical history, to ICD implantation for prevention of malignant ventricular arrhythmias [12][13][14].…”

Section: Discussionmentioning

confidence: 99%

How often is patent foramen ovale an innocent bystander?

Versaci

Vizzari

Sergi

et al. 2017

Clinical Case Reports

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Key Clinical MessagePatent foramen ovale (PFO) is a risk factor for cryptogenetic stroke; its closure should be considered in selected patients. It is not always clear whether symptoms (presyncope, paresthesia) apparently due to paradoxical embolism are related with other cardiovascular disorders such as arrhythmias. Flecainide administration for post‐PFO‐closure supraventricular arrhythmias can unmask a latent undiagnosed Brugada syndrome.

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Time-dependent responses to provocative testing with flecainide in the diagnosis of Brugada syndrome

Cited by 17 publications

References 15 publications

Brugada syndrome: clinical and genetic findings

Brugada syndrome: clinical and genetic findings

Analysis of the High-Frequency Content in Human QRS Complexes by the Continuous Wavelet Transform: An Automatized Analysis for the Prediction of Sudden Cardiac Death

How often is patent foramen ovale an innocent bystander?

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