Database : MEDLINE
Search on : Brugada and Syndrome [Words]
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[PMID]: 29242054
[Au] Autor:Barcos JC; Tello Santacruz IA; Monié CC; Fernández Recalde ML; Humphreys JD
[Ad] Address:Department of Cardiology, Hospital Británico de Buenos Aires, Ciudad Autónoma de Buenos Aires, Argentina. Electronic address: jbarcos@hbritanico.com.ar.
[Ti] Title:Brugada phenocopy induced by severe pneumothorax.
[So] Source:J Electrocardiol;51(2):343-345, 2018 Mar - Apr.
[Is] ISSN:1532-8430
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A Brugada phenocopy has been defined as a clinical situation that presents with an abnormal electrocardiogram identical to any of the electrocardiographic patterns found in Brugada syndrome in the absence of the characteristic congenital genetic abnormalities. The first confirmed case of type 1 Brugada phenocopy associated with severe left pneumothorax is presented. A provocative test with ajmaline, which proved to be negative, was performed to confirm the diagnosis. The presence of ST-segment elevation in the context of pneumothorax is most infrequent.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

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[PMID]: 29174707
[Au] Autor:Alanzalon RE; Burris JR; Vinocur JM
[Ad] Address:Division of Pediatric Cardiology, University of Rochester School of Medicine and Dentistry, 601 Elmwood Ave, Box 631, Rochester, NY, USA.
[Ti] Title:Brugada phenocopy associated with diabetic ketoacidosis in two pediatric patients.
[So] Source:J Electrocardiol;51(2):323-326, 2018 Mar - Apr.
[Is] ISSN:1532-8430
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Two patients without cardiac history demonstrated type 1 Brugada pattern during hospitalization for diabetic ketoacidosis (DKA). Both patients had normalization of their ECGs after treatment of marked electrolyte abnormalities and metabolic acidosis. In this report, we describe two cases of Brugada phenocopy associated with DKA in children.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Data-Review

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[PMID]: 29372449
[Au] Autor:de Almeida Fernandes D; António N; Madeira M; Sousa P; Ventura M; Cristóvão J; Nascimento J; Elvas L; Gonçalves L; Pego GM
[Ad] Address:Institute of Pharmacology and Therapeutics, Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
[Ti] Title:Unsafe Drug Use and Arrhythmic Events in Brugada Patients with ICD: Results of a Long-Term Follow-Up.
[So] Source:Cardiovasc Drugs Ther;32(1):23-28, 2018 Feb.
[Is] ISSN:1573-7241
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:PURPOSE: Brugada syndrome is a hereditary disease linked with an increased risk of sudden death that may require an implantable cardioverter-defibrillator (ICD) in order to halt the arrhythmic events. The aim of this study was to identify possible triggers for appropriate ICD therapies in patients with Brugada syndrome, focusing on their past and current therapeutic profiles. METHODS: Thirty patients with high-risk Brugada syndrome, with ICD implanted at the Coimbra Hospital and University Center, were enrolled. Patients were questioned about their Brugada syndrome history, previous cardiac events, comorbidities, present and past medications, and physical activity. Patients were followed up during 5.8 ± 5.3 years. The ICD was interrogated, and arrhythmic events and device therapies were recorded. The cohort who received appropriate ICD therapies was compared with the remaining patients to determine the potential link between clinical variables and potentially fatal arrhythmic events. RESULTS: More than half of the patients (53.3%) took at least one non-recommended drug, and 16.7% received appropriate ICD therapies, with a long-term rate of 4.0%/year. There was a tendency for more appropriate ICD therapies in patients who took unsafe drugs (85.7 versus 45.5%, p = 0.062), and the mean time between unsafe drug intake and appropriate ICD therapies was 3.8 ± 7.5 days. CONCLUSIONS: This study revealed that the medical community is still unaware of the pharmacological restrictions imposed by Brugada syndrome. Patients who took non-recommended drugs seem to have a higher risk of ventricular arrhythmic events.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1007/s10557-018-6770-5

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[PMID]: 29332241
[Au] Autor:Rattanawong P; Upala S; Riangwiwat T; Jaruvongvanich V; Sanguankeo A; Vutthikraivit W; Chung EH
[Ad] Address:University of Hawaii Internal Medicine Residency Program, Honolulu, HI, USA.
[Ti] Title:Atrial fibrillation is associated with sudden cardiac death: a systematic review and meta-analysis.
[So] Source:J Interv Card Electrophysiol;51(2):91-104, 2018 Mar.
[Is] ISSN:1572-8595
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:PURPOSE: Recent studies suggest that atrial fibrillation (AF) is associated with increased cardiovascular risk and mortality including sudden cardiac death (SCD). According to the Cardiovascular Heath Study cohort, the incident rate of SCD was higher in the AF population (2.9 per 1000 per year) compared with non-AF controls (1.3 per 1000 per year). In this study, we performed a systematic review and meta-analysis to explore the association between AF and SCD. METHODS: We comprehensively searched the databases of MEDLINE and EMBASE from inception to January 2017. Included studies were published prospective or retrospective cohort studies that compared the risk of developing SCD, defined by World Health Organization's criteria, in AF patients versus non-AF patients. Data from each study were combined using the random-effects, generic inverse variance method of DerSimonian and Laird to calculate the risk ratios and 95% confidence intervals. RESULTS: Twenty-seven studies from January 1991 to February 2017 involving 8401 AF patients and 67,608 non-AF controls were included in this meta-analysis. Compared with controls, AF patients had a significantly higher risk of SCD in overall analysis (pooled risk ratio = 2.04, 95% confidence interval: 1.77-2.35, p < 0.01, I = 42.66) as well as subgroups of general population studies, previous myocardial infarction or coronary artery disease, heart failure, hypertrophic cardiomyopathy (HCM), Brugada syndrome, and patients with either a pacemaker or implantable cardioverter defibrillator (ICD). In subgroup analysis of multivariate-adjusted studies, AF also had a significantly higher risk of SCD (pooled risk ratio = 2.22, 95% confidence interval = 1.59-3.09, p < 0.01, I = 73.95). Incident rate of SCD in AF was 2-fold higher than controls but not statistically significant (pooled rate ratio = 2.06, 95% confidence interval = 0.66-7.53, p = 0.292, I = 88.58). CONCLUSIONS: Our meta-analysis demonstrates a statistically significant increased risk of SCD with AF in the general population and in those with previous myocardial infarction, coronary artery disease, heart failure, HCM, Brugada syndrome, and an implanted rhythm device.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.1007/s10840-017-0308-9

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[PMID]: 29215340
[Au] Autor:Yakut K; Erdogan I; Varan B; Atar I
[Ad] Address:Department of Pediatric Cardiology, Baskent University Ankara Hospital, Ankara, Turkey.
[Ti] Title:A Report of Brugada Syndrome Presenting with Cardiac Arrest Triggered by Verapamil Intoxication.
[So] Source:Balkan Med J;34(6):576-579, 2017 12 01.
[Is] ISSN:2146-3131
[Cp] Country of publication:Turkey
[La] Language:eng
[Ab] Abstract:BACKGROUND: Brugada syndrome is a disease characterized by a specific electrocardiographic pattern and an increased risk of sudden cardiac death. We present this case with the updated literature to emphasise the need to consider the diagnosis of Brugada syndrome in patients admitted to the emergency ward with sudden cardiac arrest. CASE REPORT: A 16-year-old female patient was admitted to the emergency ward with complaints of weakness and abdominal pain, and she had four cardiac arrests during her evaluation period. She was referred to our clinic for permanent pacemaker implantation. She was on a temporary pace maker after having had C-reactive protein. Her physical exam was normal except for bilaterally decreased lung sounds. Lung x-ray and computed tomography, which were performed by another institution, revealed minimal pleural effusion and nothing else of significance. Blood and peritoneal fluid samples were sterile. Echocardiographic exam and cardiac enzymes were also in the normal ranges. Electrocardiographic showed incomplete right branch block in leads V1 and V2. An ajmaline test revealed specific electrocardiographic findings of the type I Brugada pattern. We proposed implanting an implantable cardioverter defibrillator to the patient as there were positive findings on the ajmaline test as well as a history of sudden cardiac arrest. After this treatment proposal, the patient's family admitted that she had taken a high dose of verapamil and thus, the encountered bradycardia was associated with verapamil overuse. The ajmaline test was repeated as it was contemplated that the previous positive ajmaline test had been associated with verapamil overuse. Implantable cardioverter defibrillator implantation was proposed again as there was a history of sudden cardiac arrest; however, the family did not consent to implantable cardioverter defibrillator, and the patient was discharged and followed up. CONCLUSION: Brugada syndrome should be considered for patients who are admitted to the emergency ward with sudden cardiac arrest though surface electrocardiographic is normal. If there is a suspicion of Brugada syndrome, repeated electrocardiographic should be performed on different occasions. Diagnosis can be clarified by upper costal electrocardiographic or by administering Na channel blockers during electrocardiographic performance.
[Mh] MeSH terms primary: Anti-Arrhythmia Agents/poisoning
Brugada Syndrome/chemically induced
Heart Arrest/chemically induced
Verapamil/poisoning
[Mh] MeSH terms secundary: Adolescent
Ajmaline/pharmacology
Brugada Syndrome/diagnosis
Brugada Syndrome/physiopathology
Diagnosis, Differential
Electrocardiography
Female
Genetic Testing
Heart Arrest/physiopathology
Humans
Precipitating Factors
Sodium Channel Blockers/administration & dosage
Suicide, Attempted
Treatment Outcome
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:0 (Anti-Arrhythmia Agents); 0 (Sodium Channel Blockers); 1PON08459R (Ajmaline); CJ0O37KU29 (Verapamil)
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[Js] Journal subset:IM
[Da] Date of entry for processing:171208
[St] Status:MEDLINE
[do] DOI:10.4274/balkanmedj.2016.1301

  6 / 3485 MEDLINE  
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[PMID]: 29489690
[Au] Autor:Yang L; Ma G; Yu T; Gao H; Wang Y; Wu Y
[Ad] Address:Department of Cardiology, Beijing Friendship Hospital.
[Ti] Title:A case report of Brugada-like ST-segment elevation probably due to coronary vasospasm.
[So] Source:Medicine (Baltimore);97(9):e9900, 2018 Mar.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Vasospastic angina is caused by sudden occlusive vasoconstriction of a segment of an epicardial artery, with transient ST-segment elevation on electrocardiography. Brugada Syndrome is an inherited arrhythmogenic cardiac disorder with a diagnostic electrocardiography characterized by coved-type ST-segment elevation in right precordial leads (V1-V3). Those two diseases usually have no correlation. In this report, we discuss an interesting case of a patient who was diagnosed as vasospastic angina according to his coronary angiography, but his electrocardiography showed a Brugada-like ST-segment elevation. PATIENT CONCERNS: Our patient had a 9-month history of temporary but progressive substernal burning sensation with acid bilges of shoulders and arms, as well as profuse sweating at night. DIAGNOSES: Although he had no abnormal laboratory test result, no dysfunctional recorded echocardiogram or documented arrhythmia after being admitted to the hospital, his electrocardiography showed a Brugada-like ST-segment elevation. The coronary angiography result confirmed a diagnosis of vasospastic angina. INTERVENTIONS: The patient was prescribed diltiazem, aspirin, isosorbide mononitrate and rosuvastatin and was strongly advised to quit cigarettes and alcohol. OUTCOMES: Follow-up at half a year turned out well. LESSONS: This case links Brugada syndrome to coronary vasospasm. They may share similar mechanisms. Provocation test and gene test needs to be ran to distinguish both. Long-term follow-up is essential for it may bring a warning sign for life threatening ventricular arrhythmias.
[Mh] MeSH terms primary: Angina Pectoris/complications
Brugada Syndrome/etiology
Coronary Vasospasm/complications
[Mh] MeSH terms secundary: Aged
Angina Pectoris/diagnostic imaging
Brugada Syndrome/diagnostic imaging
Coronary Angiography
Coronary Vasospasm/diagnostic imaging
Electrocardiography
Humans
Male
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180301
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009900

  7 / 3485 MEDLINE  
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[PMID]: 29309564
[Au] Autor:Pablo Flórez J; García D; Valverde I; Rubín J; Pérez D; González-Vasserot M; Reguero J; María de la Hera J; Avanzas P; Gómez J; Coto E; Morís C; Calvo D
[Ad] Address:Department of Cadiology, Hospital Universitario Central de Asturias, C/Avd de Roma, s/n, 33006 Oviedo, Spain.
[Ti] Title:Role of syncope in predicting adverse outcomes in patients with suspected Brugada syndrome undergoing standardized flecainide testing.
[So] Source:Europace;, 2017 Dec 22.
[Is] ISSN:1532-2092
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Aims: Sensitivity to flecainide testing results in suboptimal findings in patients with Brugada syndrome (BrS), leading to safety concerns. Because cardiac syncope effectively predicts outcomes in BrS, we aimed to explore its predictive value in a large cohort of negative and positive responders (NR and PR) to standard flecainide testing. Methods and results : We analysed the data of 251 consecutive patients, 177 NR vs. 74 PR, to flecainide testing, performed according to standard recommendations. Cardiac syncope was defined as syncope presenting without prodromal symptoms and in the absence of any specific situation. Comparing PR with NR, there were no differences regarding age (39 ± 15 vs. 44 ± 13 years; P = 0.052), male gender (70.1% vs. 66.2%; P = 0.553), and family history of sudden cardiac death in relatives younger than 45 years (27% vs. 27%; P = 1). Cardiac syncope was more frequent in PR (12.2% vs. 4%; P = 0.022), and previous sudden cardiac arrest (SCA) was documented only in PR (5.4% vs. 0%; P = 0.007). During the follow-up period (6.2 ± 3.3 years), one NR, who had previously experienced cardiac syncope, developed SCA 3 months after flecainide testing. Following resuscitation, a type I electrocardiogram was spontaneously recorded. The follow-up event rate was higher in patients with cardiac syncope, both in PR and in NR (P < 0.001 both). In a multivariate analysis, cardiac syncope was the unique variable that predicted adverse outcomes (hazard ratio 14.9, 95% confidence interval 1.84-121.25; P = 0.011). Conclusions: In patients with false-negative responses to the provocative testing with flecainide, cardiac syncope predicts SCA, allowing a more extensive and individualized evaluation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/europace/eux315

  8 / 3485 MEDLINE  
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[PMID]: 29267949
[Au] Autor:Kelly A; Salerno S; Connolly A; Bishop M; Charpentier F; Stølen T; Smith GL
[Ad] Address:Department of Circulation & Medical Imaging, St Olav's Hospital, Norwegian University of Science & Technology (NTNU), Trondheim, Norway.
[Ti] Title:Normal interventricular differences in tissue architecture underlie right ventricular susceptibility to conduction abnormalities in a mouse model of Brugada syndrome.
[So] Source:Cardiovasc Res;, 2017 Dec 18.
[Is] ISSN:1755-3245
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:AIMS: Loss-of-function of the cardiac sodium channel NaV1.5 is a common feature of Brugada syndrome. Arrhythmias arise preferentially from the right ventricle (RV) despite equivalent NaV1.5 downregulation in the left ventricle (LV). The reasons for increased RV sensitivity to NaV1.5 loss-of-function mutations remains unclear. Because ventricular electrical activation occurs predominantly in the transmural axis, we compare RV and LV transmural electrophysiology to determine the underlying cause of the asymmetrical conduction abnormalities in Scn5a haploinsufficient mice (Scn5a+/-). METHODS AND RESULTS: Optical mapping and two-photon microscopy in isolated-perfused mouse hearts demonstrated equivalent depression of transmural conduction velocity in the LV and RV of Scn5a+/- vs wild type littermates. Only RV transmural conduction was further impaired when challenged with increased pacing frequencies. Epicardial dispersion of activation and beat-to-beat variation in activation time were increased only in the RV of Scn5a+/- hearts. Analysis of confocal and histological images revealed larger intramural clefts between cardiomyocyte layers in the RV vs LV, independent of genotype. Acute sodium current inhibition in wild type hearts using TTX reproduced beat-to-beat activation variability and frequency-dependent conduction velocity slowing in the RV only, with the LV unaffected. The influence of clefts on conduction was examined using a two-dimensional monodomain computational model. When peak sodium channel conductance was reduced to 50% of normal the presence of clefts between cardiomyocyte layers reproduced the activation variability and conduction phenotype observed experimentally. CONCLUSION: Normal structural heterogeneities present in the RV are responsible for increased vulnerability to conduction slowing in the presence of reduced sodium channel function. Heterogeneous conduction slowing seen in the RV will predispose to functional block and the initiation of re-entrant ventricular arrhythmias.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/cvr/cvx244

  9 / 3485 MEDLINE  
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[PMID]: 29513181
[Au] Autor:Hamoir C; Dano H; Komuta M; Druez P; Dastis SN
[Ti] Title:Cholestatic hepatitis after diagnostic ajmaline challenge.
[So] Source:Acta Gastroenterol Belg;80(3):425-426, 2017 Jul-Sep.
[Is] ISSN:1784-3227
[Cp] Country of publication:Belgium
[La] Language:eng
[Ab] Abstract:We report a cholestatic hepatitis in an elderly woman after ajmaline challenge during electrophysiological testing for Brugada syndrome. No other medication was reported in the previous 6 months of the onset of jaundice. Liver biopsy showed a cholestatic hepatitis with mild biliary damage. Liver enzymes normalized within 2 weeks as well as jaundice. To the best of our knowledge this is the second case of histologically proved cholestatic hepatitis induced by intravenous ajmaline testing.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review

  10 / 3485 MEDLINE  
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[PMID]: 29512803
[Au] Autor:Ben Kilani M; Naccache S; Tlili R; Mbarek D; Longo S; Ben Ameur Y; Boujnah MR
[Ti] Title:Attempted suicide by Flécainide overdose: A case report.
[So] Source:Tunis Med;95(6):451-453, 2017 Jun.
[Is] ISSN:0041-4131
[Cp] Country of publication:Tunisia
[La] Language:eng
[Ab] Abstract:Class Ic antiarrythmic overdose is associated with a relatively high mortality. We presenta case report regarding a suicidal intoxication of an 18-year old female with a medical history of Wolff-Parkinson-White syndrome. The preliminary examination highlighted a profound cardiovascular collapse. The electrocardiogram showed a PR interval extended to 360 ms. The QRS complexes were enlarged to 360 ms with a right bundle brunch block appearance associated with left posterior hemibloc. There were repolarization abnormalities such as elevation of the J-point, convex ST segment and biphasic T wave in the right precordial leads ("Brugada-Like ECG pattern"). Sodium bicarbonate was administered. A rapid decrease in the duration of the QRS complexes was noted as well as a slowing of the heart rate. The electrocardiogram aspect on the 4th day showed the reappearance of the ventricular pre-excitation. The severity and lethal potential of Flecainide poisoning are linked to the cardiotoxic effects of these molecules. The prognosis remains poor despite progress in intensive care procedures.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review


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