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Brugada syndrome: Case report  [PDF]
Biseni? Vesna,Hini? Sa?a,Krotin Mirjana,Milovanovi? Branislav
Srpski Arhiv za Celokupno Lekarstvo , 2012, DOI: 10.2298/sarh1202084b
Abstract: Introduction. Brugada syndrome is an arrhythmogenic disease characterized by coved ST segment elevation and J point elevation of at least 2 mm in at least two of the right precordial ECG leads (V1-3) and ventricular arrhythmias, syncope, and sudden death. Risk stratifications of patients with Brugada electrocardiogram are being strongly debated. Case Outline. A 23-year-old man was admitted to the Coronary Care Unit of the Clinical Centre “Be anijska kosa” due to weakness, fatigue and chest discomfort. The patient suffered from fainting and palpitations. There was a family history of paternal sudden death at 36 years. Electrocardiogram showed a coved ST segment elevation of 4 mm in leads V1 and V2, recognised as spontaneous type 1 Brugada pattern. Laboratory investigations revealed normal serum cardiac troponin T and serum potassium, and absence of inflammation signs. Echocardiographic finding was normal, except for a mild enlargement of the right atrium and ventricle. The diagnosis of Brugada syndrome was made by Brugada-type 1 electrocardiogram and the family history of sudden death <45 years. The patient was considered as a high risk, because of pre-syncope and palpitations. He underwent ICD implantation (Medtronic MaximoVR7232Cx) using the standard procedure. After implantation, noninvasive electrophysiology study was done and demonstrated inducible VF that was interrupted with the second 35 J DC shock. The patient was discharged in stable condition with beta-blocker therapy. After a year of pacemaker check-ups, there were no either VT/ VF events or ICD therapy. Conclusion. Clinical presentation is the most important parameter in risk stratification of patients with Brugada electrocardiogram and Brugada syndrome.
Recurrent cardiac events in patients with idiopathic ventricular fibrillation, excluding patients with the Brugada syndrome
Jean Champagne, Peter Geelen, Fran?ois Philippon, Pedro Brugada
BMC Medicine , 2005, DOI: 10.1186/1741-7015-3-1
Abstract: Since 1992, 18 patients (72% male) with idiopathic VF out of 455 ICD implants were treated with an implantable cardioverter defibrillator (ICD). The mean age at first ICD implantation was 42 ± 14 years. Brugada syndrome, as well as other primary electrical diseases (e.g. long QT), were systematically excluded in all patients by the absence of the typical electrocardiogram (ST elevation in the right precordial leads) at rest and/or after pharmacological tests (ajmaline, flecainide, or procainamide). Recurrence of cardiac events was prospectively assessed.During a mean follow-up period of 41 ± 27 months, VF recurrence with appropriate shock occurred in 7 patients (39%) covering a total of 27 shocks. The median time to first appropriate shock was 12 ± 9 months. There were no deaths. In the electrophysiological study, 39% of patients were inducible, but inducibility failed to predict subsequent arrhythmic events. Forty-four percent of patients suffered 21 inappropriate shocks, which were caused by sinus tachycardia, atrial arrhythmias or lead malfunction.Idiopathic ventricular fibrillation patients have a high recurrence rate of potentially fatal ventricular arrhythmias, excluding patients with the Brugada syndrome or other known causes. ICD prevents sudden cardiac death but inappropriate shocks remained a major issue in this young and active population.Idiopathic ventricular fibrillation (VF) is defined as spontaneous ventricular fibrillation in the absence of any structural heart disease, including coronary artery disease, valvular heart disease, myocarditis, cardiomyopathy or electrophysiological diseases, with a well-defined cause, such as the long QT syndrome, the Brugada syndrome, ventricular pre-excitation (WPW), and drug intoxication [1]. The consensus statement of the joint steering committees of the UCARE registry of Europe and of the idiopathic VF registry of US reported in 1997 that patients with the Brugada syndrome should be considered a variant of idiopat
Brugada syndrome  [cached]
Rachel Bastiaenen,Elijah R. Behr
Cardiogenetics , 2011, DOI: 10.4081/cardiogenetics.2011.s1.e3
Abstract: The Brugada syndrome demonstrates characteristic electrocardiogram features and is a significant cause of sudden death in young adults with overtly normal cardiac structure and function. The genetic basis has not yet been fully elucidated but our understanding of the causative mutations and modifiers of arrhythmic events is advancing rapidly alongside sequencing technologies. We expect that the future will include risk stratification according to genotype and management tailored to the genetic diagnosis.
Brugada syndrome
Carlo Napolitano, Silvia G Priori
Orphanet Journal of Rare Diseases , 2006, DOI: 10.1186/1750-1172-1-35
Abstract: Brugada syndrome (BrS; OMIM 601144), or "Idiopathic ventricular fibrillation" as defined by some authors [1], is an autosomal dominant form of cardiac arrhythmia, presenting with a typical electrocardiographic (ECG) pattern of ST segment elevation in leads V1 to V3, and incomplete or complete right bundle branch block [2]. Syncope, typically occurring at rest or during sleep, is a common presentation of BrS [3], and it is caused by fast polymorphic ventricular tachycardia. In some cases, tachycardia does not terminate spontaneously. It may degenerate into ventricular fibrillation and lead to sudden death.The incomplete information concerning the genetic bases of BrS prevents a prevalence assessment among the general population. The current estimate is based upon ECG surveys among healthy subjects. These studies have been mostly done in the Asian population and only one has been carried out among Caucasians. The suggested prevalence ranges from 5/1,000 (Caucasians) to 14/1,000 (Japanese) [4-6]. The higher prevalence of the BrS ECG pattern in far eastern countries has been recently confirmed in a large clinical study [7] (see paragraph Genetic bases and pathophysiology). In this region the disease is thought to represent a frequent cause of sudden death among young individuals and is named as: lai-tai, pokkuri, sudden unexplained death syndrome, sudden unexplained nocturnal death syndrome.BrS manifests with syncope and cardiac arrest, typically occurring in the third and fourth decade of life, and usually at rest or during sleep. In 1998 Brugada et al. presented data on 63 patients in whom, after a mean follow up of 34 ± 32 months, 34% of previously symptomatic (syncope and/or cardiac arrest) patients had recurrence, while a first cardiac event occurred in 27% of the asymptomatic individuals. These results called for an aggressive therapeutic strategy in all patients with BrS and, since no pharmacological treatment of proven efficacy was (and still is) available, it l
Approach to the asymptomatic patients with Brugada syndrome
Masahiko Takagi,Hiroaki Tatsumi,Minoru Yoshiyama
Indian Pacing and Electrophysiology Journal , 2007,
Abstract: Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of coved-type ST segment elevation in the right precordial leads and an increased risk of sudden cardiac death (SCD) as a result of polymorphic ventricular tachyarrhythmia or ventricular fibrillation (VF). Data from large patient studies and a meta-analysis of previous reports have shown that patients with a history of syncope or SCD and a spontaneous type 1 Brugada ECG are at high risk for SCD. However, risk stratification of asymptomatic patients with Brugada type ECG is still a challenge. In particular, the use of electrophysiological study (EPS) for risk stratification remains controversial. Although some investigators have reported the possibility of use of EPS for distinguishing between high- and low-risk patients with Brugada type ECG, no precise predictor of risk for SCD in asymptomatic patients has yet been determined. The approach to treatment of these patients is thus still unclear. Large clinical prospective studies with uniform diagnostic criteria and protocols for EPS as well as extended follow-up periods of over ten years are required for prediction of SCD.
The metabolic syndrome and progression of carotid atherosclerosis over 13?years. The Troms? study
Marit Herder, Kjell Arntzen, Stein Johnsen, Ellisiv B Mathiesen
Cardiovascular Diabetology , 2012, DOI: 10.1186/1475-2840-11-77
Abstract: Participants were 1442 men and 1532 women in the population-based Troms? Study who underwent carotid ultrasound examinations at baseline in the 4th (1994–5) and at follow-up in the 6th survey (2007–8). Of these, 278 men and 273 women fulfilled the criteria for the MetS, defined according to a modified version of the National Cholesterol Education Program Adult Treatment Panel III (NCEP, ATPIII). Carotid atherosclerosis was assessed as total plaque area (TPA) and mean intima-media thickness (IMT) at follow-up and as change in IMT and TPA from baseline to follow-up. Associations between MetS and its components and carotid atherosclerosis were assessed in linear regression models adjusted for age, total cholesterol and daily smoking, stratified by sex.IMT and TPA levels at follow-up (p?<?0.0001) and progression of TPA (p?=?0.02) were higher in the MetS group compared to the non-MetS group. In stepwise multivariable models, MetS was associated with TPA (β?=?0.372?mm2, p?=?0.009) and IMT (β?=?0.051?mm, p?<?0.0001) in men, and with IMT (β?=?0.045?mm, p?=?0.001) in women after 13?years of follow-up, but not with progression of IMT or TPA. In analyses stratified by age, MetS predicted progression of IMT (β?=?0.043?mm, p?=?0.046) and TPA (β?=?1.02?mm2, p?=?0.002) in men below 50?years of age. Hypertension was predictive of follow-up TPA and IMT in both genders and of progression of TPA in women. Impaired glucose tolerance was associated with follow up levels of IMT and TPA as well as progression in IMT in men. None of the other components of MetS were associated with progression of atherosclerosis.Subjects with MetS had higher levels of IMT and TPA at follow up than those without MetS. Mets predicted progression of IMT and TPA in those below 50?years of age, but not in other age groups, indicating that MetS may be involved in the initiation of the atherosclerotic process.Metabolic syndrome (MetS) is a cluster of metabolic and non-metabolic cardiovascular risk factors, includ
Brugada Syndrome: A Review  [PDF]
Laxmi Narayan Goit, Shaning Yang
Yangtze Medicine (YM) , 2019, DOI: 10.4236/ym.2019.34023
Abstract: The Brugada syndrome is a form of cardiac arrhythmia, characterized by electrocardiographic ST-Segment elevation in right precordial leads that affect young male patient, predisposing to malignant ventricular arrhythmia and sudden cardiac deaths. The majority of the patients with Brugada syndrome remain asymptomatic, however, patient can present with symptom like syncope, palpitation and aborted sudden cardiac death. Several pathogenic genes have been identified as associated with the disease but SCN5A is most prevalent one. The Brugada syndrome is diagnosed by typically cove shaped ST-segment elevation of >2 mm in greater than one precordial lead V1 and V2, occurring spontaneously or after provocative drugs test with IV administration of class 1 antiarrhythmic drug such flecainide or Ajmaline. Risk stratification and the need for treatment depend on the patient symptom, electrocardiography, family history and electrophysiological study. The treatment by implantable cardioverter defibrillators, the only effective treatment to date is appropriate. Other treatment options included pharmacological therapy (Quinidine) and Radiofrequency ablation of ventricular ectopies. This brief review focuses on epidemiology of Brugada syndrome, Genetic basis, mechanism, clinical presentation, ECG changes, risk stratification, Diagnostic criteria and management.
Ageing and Brugada syndrome: considerations and recommendations
Pieter G Postem,Hanno L Tan,Arthur AM Wilde,
Pieter G. Postem
,Hanno L Tan,Arthur AM Wilde

老年心脏病学杂志(英文版) , 2013,
Abstract: Brugada syndrome is an inherited disease associated with an increased risk of lethal ventricular arrhythmias. Such arrhythmias stem from innate disruptions in cardiac electrophysiology. Typically, such arrhythmias occur in the third or fourth decade of life. However, Brugada syndrome may also affect geriatric patients. In this paper, we focus on the ageing patient with Brugada syndrome, and specifically, on the interaction between Brugada syndrome and the more usually acquired clinical problems that may occur with increasing age, such as the use of cardiovascular and non-cardiovascular drugs, or the need for surgery. Such common conditions may also disrupt cardiac electrophysiology, thereby conferring added risk for Brugada syndrome patients. We present some considerations and recommendations that may serve as guidance to address these complexities.
Brugada Syndrome: Case Report and Overview  [cached]
Murat Yüce,Fethi Yavuz,Musa ?ak?c?,?brahim Sar?
Journal of Academic Emergency Medicine , 2012,
Abstract: Brugada syndrome is an autosomal dominant geneticl disease which is characterised by abnormal ECG and risk of sudden cardiac death. A typical finding of this syndrome is the presence of ST segment elevation in precordial V1, V2 and V3 leads with concomitant right bundle branch block on ECG. We observed that misdiagnosis or difficulty in diagnosis are generally encountered in routine clinical practice for Brugada syndrome. Herein we would like to share a typical case and overview of Brugada syndrome in the context of the latest published literature.
Brugada syndrome: A brand new case  [PDF]
Jur?evi? Ru?ica,Angelkov Lazar,Vukajlovi? Dejan,Risti? Velibor
Vojnosanitetski Pregled , 2009, DOI: 10.2298/vsp0908667j
Abstract: Background: Brugada syndrome (BS) is a disorder characterized by syncope or sudden death associated with one of several electrocardiographic (ECG) patterns characterized by incomplete right bundle branch block and ST elevation in the anterior precordial leads. Patients with BS are prone to develop ventricular tachyarrhythmias that may lead to syncope, cardiac arrest, or sudden cardiac death. Case report. A 58-year-old woman is the first described case of Brugada syndrome in Serbia with intermittent typical changes in basic electrocardiography (ECG): ST segment elevation in the precordial chest leads like dome or coved - major form or type I. For the last 27 years the patient had suffered of palpitations and dizziness, without syncopal events. Her sister had died suddenly during the night in sleep. During 24-hour Holter monitoring the patient had ventricular premature beats during the night with R/T phenomenon and during the recovery phase of exercise testing had rare premature ventricular beats as the consequence of parasympatethic stimulation. Late potentials were positive. Echocardiography revealed left ventricular ejection fraction of 60%. We performed coronary angiography and epicardial coronary arteries were without significant stenosis and structural heart disease was excluded. In the bigining of the electrophysiological study ECG was normal, and after administration of Propaphenon i.v. Brugada syndrome unmasked with appearance of type I ECG pattern. A programed ventricular stimulation induced non sustained ventricular tachycardia. One-chamber implantable cardioverter defibrillator was implanted and the patient was treated with a combination od amiodarone and metoprolol per os. After one-year follow-up, there were no episodes of ventricular tachycardia and ventricular fibrillation. Conclusion. Brugada syndrome is a myocardial disorder which prognosis and therapy are related to presence of ventricular fibrillation or ventricular tachycardia. Electrophysiologicaly induced malignant ventricular disorders class I are indication for implantation of cardioverter defibrilator, as also occurred in presented patient.
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