Coexistence of Wolff–Parkinson–White and Brugada Syndrome: Mere Curiosity?

The association between Brugada syndrome (BS) and ventricular preexcitation is a rare condition, with sporadic cases already reported. We report the case of a 29‐year‐old man, with palpitation unrelated to physical or emotional stress. The electrocardiogram of the first visit revealed a ventricular preexcitation pattern and an end‐conduction delay, with negative T wave in V₁ and intraventricular conduction disturbance in V₂ (atypical for BS). The typical aspect of BS occurred after introduction of propafenone for the prevention of atrioventricular tachycardia. We discuss the recognition of this rare association, the proarrhythmic effects of some drugs, treatment options, and prognosis.     

Wolff-Parkinson-White VCG patterns that mimic other cardiac pathologies: a correlative study with the preexcitation pathway localization

Vectorcardiograms (VCGs) of 44 patients with a Wolff-Parkinson-White (WPW) syndrome have been analyzed with the aim to correlate the QRS loop patterns with specific preexcitation sites. The VCG QRS loops were analyzed to determine whether conduction abnormalities and myocardial infarction (MI)-like patterns observed in the WPW syndrome could be related to specific preexcitation sites identified by surgery as well as by body surface potential mapping (BSPM). Left bundle branch block pattern was observed with anteroseptal (AS) preexcitation, anterior MI pattern was seen with lateral right ventricle (LRV) preexcitation, left anterior fascicular block was observed with posterior right ventricle (PRV) preexcitation, inferoposterior and strictly posterior MI pattern was found with posteroseptal (PS) and posterior left ventricle (PLV) preexcitation, right bundle branch block was seen in lateral left ventricle (LLV) preexcitation, and right bundle branch block was observed with left posterior fascicular block in anterior left ventricle (ALV) preexcitation. These VCG criteria seem to identify accurately the preexcitation sites as observed by delta wave BSPM and at surgery investigations. Consequently, they could be useful in localizing the preexcitation site in cases of ambiguous delta vector orientation.     

Adenosine and Preexcitation Variants: Reappraisal of Electrocardiographic Changes

Intravenous adenosine is a short‐acting blocker of the atrioventricular node that has been used to unmask subtle or latent preexcitation, and also to enable catheter ablation in selected patients with absent or intermittent preexcitation. Depending on the accessory pathway characteristics, intravenous adenosine may produce specific electrocardiographic changes highly suggestive of the preexcitation variant. Herein, we view different ECG responses to this pharmacological test in various preexcitation patterns that were confirmed by electrophysiological studies. Careful analysis of electrocardiographic changes during adenosine test, with emphasis on P‐delta interval, preexcitation degree, and atrioventricular block, can be helpful to diagnose the preexcitation variant/pattern.     

Brugada syndrome,Brugada phenocopy or none?

Brugada syndrome is a form of inherited arrhythmia syndrome characterized by a distinct ST‐segment elevation in the right precordial leads. Brugada phenocopies are clinical entities that present with an electrocardiographic pattern identical to Brugada syndrome and may obey to various clinical conditions. We present a case of a suicidal attempt using a high dose of propafenone causing a Brugada‐type electrocardiographic pattern. Is this a Brugada syndrome case, a Brugada phenocopy or something else?     

Brugada Phenocopy in Concomitant Ethanol and Heroin Overdose

Brugada phenocopy describes conditions with Brugada‐like ECG pattern but without true congenital Brugada syndrome. We report a case of 44‐year‐old man with no known medical history who presented with loss of consciousness. Toxicology screening was positive for opiates and high serum alcohol level. His initial ECG showed Brugada type 1 pattern which resolved after several hours of observation and treatment with continuous naloxone infusion. Patient regained his consciousness and disclosed heroin abuse and drinking alcohol. This case highlights the heroin overdose as a possible cause of Brugada phenocopy.     

Brugada phenocopy secondary to extensive inferior wall ischemia induced by coronary steal effect

The diagnosis of Brugada syndrome is usually made with a typical ECG pattern. However, different disorders can emulate this pattern (Brugada phenocopies). Pathophysiologic mechanisms underlying this phenomenon remain controversial. We describe the development of type‐1 Brugada ECG pattern associated with extensive coronary steal effect during myocardial perfusion scintigraphy. Proximal occlusion of the right coronary artery and severe proximal stenosis in distally occluded left circumflex artery were confirmed by coronary angiogram. Brugada ECG pattern can be a reversible sign associated with inferior left ventricular and right ventricular ischemia. Its presence during acute ischemia deserves appropriate risk stratification.     

Brugada electrocardiographic pattern due to tricyclic antidepressant overdose

The Brugada syndrome is an arrhythmogenic disease with characteristic coved ST-segment elevation 2 mm or greater in the right precordial leads (type 1 Brugada electrocardiogram [ECG] pattern or “Brugada sign”] and is estimated to be responsible for at least 20% of sudden deaths in patients with structurally normal hearts [Circulation 2005;111(5):659-70]. The Brugada sign has been described in asymptomatic patients after exposure to various drugs. As published reports of the drug-induced Brugada sign have become increasingly prevalent, there is growing interest in the mechanisms responsible for this acquired ECG pattern and its clinical significance.We report a case of a patient who developed the type 1 Brugada ECG pattern after intentional overdose of a tricyclic antidepressant agent, review the literature concerning tricyclic antidepressant agent-induced Brugada sign, discuss potential mechanisms, and evaluate the clinical significance of this ECG abnormality.     

Brugada phenocopy in a patient with unstable angina and three-vessel coronary artery disease

A 52-year-old male was admitted with unstable angina and three-vessel coronary artery disease. Electrocardiography (ECG) changes consistent with type-1 Brugada ECG pattern were noted during admission. The patient was asymptomatic for syncope and had no family history of sudden cardiac death, ICD implantation, and Brugada syndrome. After coronary by-pass graft the Brugada ECG pattern resolved, and ajmaline test did not elicit type-1 ECG pattern, confirming the suspicion of Brugada phenocopy.     

Padrão de Brugada em doente medicada com lamotrigina

The authors report the case of a 52-year-old woman with depressive syndrome, treated with lamotrigine for about five months, who went to the emergency department for atypical precordial pain. The electrocardiogram (ECG) revealed a 2-mm downsloping ST-segment elevation and negative T waves in V1 and V2. Due to suspicion of ST-elevation acute coronary syndrome, cardiac catheterization was performed, which revealed normal coronary arteries. The initial ECG was suggestive of type 1 Brugada pattern, but subsequent serial ECGs were less typical. A flecainide test showed the same pattern.After discontinuation of lamotrigine reversal of the typical Brugada ECG pattern was observed.Although not currently contraindicated in Brugada syndrome, the antidepressant lamotrigine blocks sodium channels, which are usually inactivated in heart cell membranes in Brugada syndrome, and may be responsible for the expression of type 1 Brugada pattern.     

Current electrocardiographic criteria for diagnosis of Brugada pattern: a consensus report

Brugada syndrome is an inherited heart disease without structural abnormalities that is thought to arise as a result of accelerated inactivation of Na channels and predominance of transient outward K current (I(to)) to generate a voltage gradient in the right ventricular layers. This gradient triggers ventricular tachycardia/ventricular fibrillation possibly through a phase 2 reentrant mechanism. The Brugada electrocardiographic (ECG) pattern, which can be dynamic and is sometimes concealed, being only recorded in upper precordial leads, is the hallmark of Brugada syndrome. Because of limitations of previous consensus documents describing the Brugada ECG pattern, especially in relation to the differences between types 2 and 3, a new consensus report to establish a set of new ECG criteria with higher accuracy has been considered necessary. In the new ECG criteria, only 2 ECG patterns are considered: pattern 1 identical to classic type 1 of other consensus (coved pattern) and pattern 2 that joins patterns 2 and 3 of previous consensus (saddle-back pattern). This consensus document describes the most important characteristics of 2 patterns and also the key points of differential diagnosis with different conditions that lead to Brugada-like pattern in the right precordial leads, especially right bundle-branch block, athletes, pectus excavatum, and arrhythmogenic right ventricular dysplasia/cardiomyopathy. Also discussed is the concept of Brugada phenocopies that are ECG patterns characteristic of Brugada pattern that may appear and disappear in relation with multiple causes but are not related with Brugada syndrome.     

Cibenzoline induced Brugada ECG pattern.

We report a case of a 61-year-old female patient who presented with palpitations. The baseline electrocardiogram showed incomplete right bundle branch block with saddle back pattern of the ST segment in one precordial lead, but without any significant ST elevation. She was treated with oral cibenzoline. The subsequent ECG showed a coved Brugada ECG (type I) pattern, which resolved following the discontinuation of cibenzoline. An ajmaline test reproduced the coved type Brugada ECG pattern. Our case is the first report of oral cibenzoline therapy unmasking the diagnostic coved Brugada ECG pattern in a patient with a baseline normal ECG. Cibenzoline, a class I sodium channel blocker antiarrhythmic drug, should probably be avoided in the treatment of patients with Brugada syndrome.     

隐匿性预激综合征和早期复极综合征相关性的研究

目的了解隐匿性预激综合征和早期复极综合征的相关性。方法将经心内电生理检查证实为隐匿性预激综合征且心电图上存在早期复极征象的23例患者设为观察组,分析其临床资料及射频导管消融术前和术后的心电图差异;将我院体检中心检查发现心电图上存在早期复极征象但无心动过速病史的30例患者设为对照组,比较观察组和对照组心电图,了解隐匿性预激综合征与早期复极综合征之间的相关性。结果观察组射频导管消融术前和术后心电图无明显差异,观察组和对照组心电图无明显差异。结论隐匿性预激综合征和早期复极综合征的发生无相关性。     

Alternating Wolff-Parkinson-White (preexcitation) pattern

An electrocardiogram is presented which shows sinus rhythm with alternating Wolff-Parkinson-White (preexcitation) pattern. The frequency of intermittent preexcitation and mechanisms for its production are discussed.     

Síncope em contexto febril – caso clínico de síndrome de Brugada

In 1992, Brugada and Brugada first described a new entity, which became known as Brugada syndrome, that is associated with a high risk of ventricular arrhythmias and sudden cardiac death in patients without structural heart disease. This syndrome is characterized by a distinct electrocardiographic phenotype, type 1 Brugada pattern, consisting of a coved ST‐segment elevation (≥0.2 mV) followed by a negative T wave in more than one right precordial lead. This pattern is dynamic, and can be spontaneous or concealed, but is unmasked under certain circumstances, like febrile states.The authors report a case in which the diagnosis of Brugada syndrome was made in the course of etiologic investigation of recurrent syncope in a febrile state.     

Das Oberflächen-EKG in der Diagnostik von Arrhythmien

The surface electrocardiogram (ECG) is a simple noninvasive method to assess the electrical activity of the heart and provides important information to identify patients with cardiac arrhythmias and increased arrhythmic risk. This brief review highlights cardiac conditions in which the right precordial leads recorded on the surface ECG during sinus rhythm or tachycardia are of important diagnostic and prognostic value. Epsilon waves seen in the right precordial ST segments are the electrocardiographic hallmark of arrhythmogenic right ventricular cardiomyopathy. The diagnosis of Brugada syndrome and risk stratification of affected patients are based on a coved-type >or=2 mm ST-segment elevation in the right precordial leads. This typical ECG pattern may be present persistently, intermittently or only after administration of sodium-channel blockers. The early repolarization syndrome, most commonly seen in healthy young individuals, is characterized by a ST-segment elevation of 1 to 4 mm in the mid-precordial leads with a notched and elevated J point in lead V4. The precordial ECG T-wave repolarization pattern may be helpful in identifying the genotype in patients with suspected long QT syndrome. In patients with overt preexcitation, the surface leads V1 and V2 play a key role in localizing the site of bypass-tract insertion. Finally, the right precordial lead V1 is often crucial in the diagnosis of narrow and broad QRS-complex tachycardias.     

Rhabdomyoma of the interventricular septum presenting as a Brugada phenocopy

Brugada syndrome is a channelopathy characterised electrocardiographically by distinctive coved ST-segment elevation in the right precordial leads and is associated with a predisposition for sudden death secondary to ventricular arrhythmias in otherwise healthy patients. Previously known as Brugada-like patterns, Brugada phenocopies include agents and conditions that mimic true Brugada syndrome, presenting with an acquired Brugada Type-1 ECG pattern. We describe the first reported case of a 17-month-old female with an asymptomatic rhabdomyoma of the interventricular septum that presented as a Brugada phenocopy.     

Propranolol intoxication revealing a Brugada syndrome

This is the first report of Brugada syndrome revealed by beta-blocker intoxication. A 24-year-old healthy man ingested propranolol (2.28 g) to commit suicide. After early gastric lavage, electrolytes, cardiac enzymes, chest X-ray, and echocardiography were normal. Dosages of psychotropic drugs were negative. ECG showed a typical coved-type pattern of Brugada syndrome. Follow-up showed partial ECG normalization of the discrete saddleback-type pattern. The ajmaline- test confirmed Brugada syndrome. These ECG modifications may be explained by the stabilizing membrane effect of high concentration of propranolol and/or inhibition of ICaL. This case illustrates the possible deleterious effects of beta-blockers in patients with Brugada syndrome.     

The Brugada ECG pattern in a neonate

We report a neonate resuscitated from sudden death with a Brugada ECG pattern several days after the initial event. The baby was subsequently diagnosed with a fatty acid oxidation disorder (medium chain Acyl-CoA dehydrogenase deficiency or MCAD). We speculate that free fatty acid accumulation can give rise to the Brugada ECG pattern.     

Brugada Phenocopy as a Dynamic Electrocardiographic Pattern during Acute Anterior Myocardial Infarction

Brugada phenocopies represent some unusual clinical cases with identical characteristics to Brugada syndrome (BrS) elicited by various clinical circumstances. We report the case of a woman exhibiting “Brugada Phenocopy” during an acute anterior myocardial infarction, highlighting differential diagnosis with true BrS and discussing possible mechanisms underlying its dynamic ECG pattern.