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brugada phenocopies

Mehmet Emre Arı, Filiz Ekici
BACKGROUND: Brugada syndrome is an inherited arrhythmogenic disease that may cause sudden cardiac death due to ventricular fibrillation in young adults. Brugada syndrome caused by propafenone intoxication has been noted rarely in the literature. We reported a rare case, Brugada-phenocopy due to propafenone intoxication and its treatment. CASE REPORT: A fifteen-year-old girl having a seizure was brought to the emergency room. She took 1.5 g propafenone (Rythmol, Abbott, Chicago, IL, USA) for suicidal intention...
April 6, 2017: Balkan Medical Journal
Muhammad Ameen, Ghulam Akbar, Naeem Abbas, Ghazi Mirrani
Brugada syndrome (BrS) is an inherited disorder of cardiac ion channels characterized by peculiar ECG findings predisposing individuals to ventricular arrhythmias, syncope, and sudden cardiac death (SCD). Various electrolyte disturbances and ion channels blocking drugs could also provoke BrS ECG findings without genetic BrS. Clinical differentiation and recognition are essential for guiding the legitimate action. Hyperkalemia is well known to cause a wide variety of ECG manifestations. Severe hyperkalemia can even cause life threatening ventricular arrhythmias and cardiac conduction abnormalities...
2017: Case Reports in Cardiology
Prabhakar A, Bansal B L, Patel R K, Dwivedi R, Padia G
No abstract text is available yet for this article.
January 2016: Journal of the Association of Physicians of India
Yashwant Agrawal, Sourabh Aggarwal, Jagadeesh K Kalavakunta, Vishal Gupta
Brugada syndrome (BS), a life-threatening channelopathy associated with reduced inward sodium current due to dysfunctional sodium channels, is characterized by ST-segment elevation with downsloping "coved type" (type 1) or "saddle back" (type 2) pattern in V1-V3 precordial chest leads (1, 2). Brugada phenocopy, a term describing conditions inducing Brugada-like pattern of electrocardiogram (EKG) manifestations in patients without true BS, is an emerging condition (3). We describe a case series of Brugada phenocopy with hyponatremia...
October 2016: Journal of the Saudi Heart Association
Byron H Gottschalk, Daniel D Anselm, Adrian Baranchuk
No abstract text is available yet for this article.
April 2016: Journal of Arrhythmia
Ozgur Kirbas, Ozcan Ozeke, Ozlem Karabulut, Sefa Unal, Fatih Sen, Kumral Cagli, Zehra Golbasi, Serkan Topaloglu, Dursun Aras, Sinan Aydogdu
No abstract text is available yet for this article.
October 2016: American Journal of Emergency Medicine
János Tomcsányi
Brugada phenocopies are clinical entities that are different from the true Brugada syndrome which is a channelopathy. Brugada phenocopy has reversible underlying conditions and, if underlying conditions resolve, the ECG pattern disappears. In this paper the author reviews and illustrates the known Brugada phenocopies. The most important etiologic categories of Brugada phenocopy include metabolic abnormalities (most commonly hyperkalemia), myocardial infarction, pulmonary embolism (massive), right ventricular mechanical compression, and others...
March 27, 2016: Orvosi Hetilap
Gregory Dendramis
To date Brugada syndrome (BrS) is considered a primary electrical heart disease and the diagnosis is based on precise clinical and electrocardiographic features. Many other diseases and conditions can lead to a Brugada-like ECG pattern but the vast majority of patients with BrS possess a structurally normal heart, which is consistent with the notion that this is a primary electrical heart disease. Presently, the terminology used in the literature to describe Brugada type 1 ECG pattern induced in patients without BrS is diverse and variable...
May 1, 2016: International Journal of Cardiology
Aysel Hunuk, Burak Hunuk, Ozlem Kusken, Ozge Ecmel Onur
Brugada syndrome (BrS) is an important cause of sudden cardiac death (SCD) with well-defined ST-segment elevation patterns on V1 -V3 . Observation of BrS-Type-electrocardiogram (ECG) patterns in medical conditions without true BrS is called "Brugada Phenocopy" (BrP). We present a case of 61-year-old male patient with hyperkalemia, hyponatremia, and BrS-Type-1 ECG pattern in the setting of acute postrenal failure. He was denying any syncope or family history of SCD. With normalization of electrolyte levels, BrS-Type-1-ECG resolved...
July 2016: Annals of Noninvasive Electrocardiology
Federico Ferrando-Castagnetto, A Garibaldi-Remuñan, G Vignolo, R Ricca-Mallada, A Baranchuk
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.
July 2016: Annals of Noninvasive Electrocardiology
Byron H Gottschalk, Javier Garcia-Niebla, Daniel D Anselm, Atul Jaidka, Antoni Bayés De Luna, Adrian Baranchuk
BACKGROUND: Brugada phenocopies (BrP) are clinical entities characterized by ECG patterns that are identical to true Brugada syndrome (BrS), but are elicited by various clinical circumstances. A recent study demonstrated that the patterns of BrP and BrS are indistinguishable under the naked eye, thereby validating the concept that the patterns are identical. OBJECTIVE: The aim of our study was to determine whether recently developed ECG criteria would allow for discrimination between type-2 BrS ECG pattern and type-2 BrP ECG pattern...
March 2016: Journal of Electrocardiology
Jennifer Meloche, Byron H Gottschalk, Usama Boles, Stephen LaHaye, Adrian Baranchuk
No abstract text is available yet for this article.
April 1, 2016: International Journal of Cardiology
Colin H Peters, Mena Abdelsayed, Peter C Ruben
Cardiac arrhythmias are a prevalent cause of morbidity and mortality. In many cases, inheritable mutations in the genes encoding cardiac ion channels are the underlying cause of arrhythmias. Relative to other arrhythmogenic disorders, Brugada syndrome (BrS) is recently identified and not well-understood. Although most often referred to as a disease of cardiac sodium channels, familial BrS is now associated with 9 different genes. Of these genes, 4 alter sodium currents, and the most common known genetic cause remains loss-of-function mutants in the cardiac sodium channel gene SCN5A...
January 2016: Progress in Biophysics and Molecular Biology
Stefan Peters
No abstract text is available yet for this article.
January 15, 2016: International Journal of Cardiology
Andres Enriquez, Josep Brugada, Adrian Baranchuk
No abstract text is available yet for this article.
March 2016: Journal of Cardiovascular Electrophysiology
Nauman Khalid, Lovely Chhabra, Jeffrey Kluger
Brugada syndrome (BS) is characterized by a typical electrocardiographic (ECG) pattern in the right precordial leads and a predisposition to develop ventricular arrhythmias. Mutations in a subunit of cardiac sodium channel (SCN5A) have been linked to BS. Experimental studies in the literature suggest that this dysfunction of the mutated channel can be temperature sensitive. Several antiarrhythmics have been used in the management of BS but Implantable Cardioverter Defibrillators (ICD) remains the only effective treatment...
January 2015: Journal of Ayub Medical College, Abbottabad: JAMC
Abdulrahman Naseef, Elijah R Behr, Velislav N Batchvarov
The Brugada syndrome (BrS) is a malignant, genetically-determined, arrhythmic syndrome manifesting as syncope or sudden cardiac death (SCD) in individuals with structurally normal hearts. The diagnosis of the BrS is mainly based on the presence of a spontaneous or Na + channel blocker induced characteristic, electrocardiographic (ECG) pattern (type 1 or coved Brugada ECG pattern) typically seen in leads V1 and V2 recorded from the 4th to 2nd intercostal (i.c.) spaces. This pattern needs to be distinguished from similar ECG changes due to other causes (Brugada ECG phenocopies)...
April 2015: Journal of the Saudi Heart Association
David S Park, Marina Cerrone, Gregory Morley, Carolina Vasquez, Steven Fowler, Nian Liu, Scott A Bernstein, Fang-Yu Liu, Jie Zhang, Christopher S Rogers, Silvia G Priori, Larry A Chinitz, Glenn I Fishman
SCN5A encodes the α subunit of the major cardiac sodium channel Na(V)1.5. Mutations in SCN5A are associated with conduction disease and ventricular fibrillation (VF); however, the mechanisms that link loss of sodium channel function to arrhythmic instability remain unresolved. Here, we generated a large-animal model of a human cardiac sodium channelopathy in pigs, which have cardiac structure and function similar to humans, to better define the arrhythmic substrate. We introduced a nonsense mutation originally identified in a child with Brugada syndrome into the orthologous position (E558X) in the pig SCN5A gene...
January 2015: Journal of Clinical Investigation
Daniel D Anselm, Byron H Gottschalk, Adrian Baranchuk
No abstract text is available yet for this article.
December 2014: Canadian Journal of Cardiology
C Asteriou, N Barbetakis
No abstract text is available yet for this article.
April 2014: Hippokratia
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