Fever Associated with Gastrointestinal Shigellosis Unmasks Probable Brugada Syndrome

Since it was first described approximately 15 years ago, the Brugada Syndrome has spurred a significant quantity of interest in its underlying mechanism and physiology. The Brugada electrocardiographic pattern is characterized by right bundle branch block morphology and ST segment elevations in the right precordial leads with an absence of identifiable underlying structural heart disease. The syndrome is clinically significant since these patients are at a higher risk of developing malignant ventricular arrhythmias. One of the mechanisms behind the disorder involves mutations in specific myocardial sodium channels. Furthermore, these electrocardiographic changes appear to be temperature dependent. We present the case of a 35-year-old male who presented with intestinal Shigellosis and was also found to have Brugada-type electrocardiographic changes on ECG. The electrocardiographic changes that were present when the patient was admitted and febrile resolved following antibiotic therapy and defervescence.

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Electrocardiographic Effects of Propofol versus Etomidate in Patients with Brugada Syndrome

Anesthesiology ◽

10.1097/aln.0000000000003030 ◽

2020 ◽

Vol 132 (3) ◽

pp. 440-451 ◽

Cited By ~ 4

Author(s):

Panagiotis Flamée ◽

Varnavas Varnavas ◽

Wendy Dewals ◽

Hugo Carvalho ◽

Wilfried Cools ◽

...

Keyword(s):

Brugada Syndrome ◽

St Segment Elevation ◽

St Depression ◽

St Segment ◽

Qrs Prolongation ◽

Significant Difference ◽

Electrocardiographic Changes ◽

St Elevation ◽

The Right ◽

Double Blinded

Abstract Background Brugada Syndrome is an inherited arrhythmogenic disease, characterized by the typical coved type ST-segment elevation in the right precordial leads from V1 through V3. The BrugadaDrugs.org Advisory Board recommends avoiding administration of propofol in patients with Brugada Syndrome. Since prospective studies are lacking, it was the purpose of this study to assess the electrocardiographic effects of propofol and etomidate on the ST- and QRS-segments. In this trial, it was hypothesized that administration of propofol or etomidate in bolus for induction of anesthesia, in patients with Brugada Syndrome, do not clinically affect the ST- and QRS-segments and do not induce arrhythmias. Methods In this prospective, double-blinded trial, 98 patients with established Brugada syndrome were randomized to receive propofol (2 to 3 mg/kg-1) or etomidate (0.2 to 0.3 mg/kg-1) for induction of anesthesia. The primary endpoints were the changes of the ST- and QRS-segment, and the occurrence of new arrhythmias upon induction of anesthesia. Results The analysis included 80 patients: 43 were administered propofol and 37 etomidate. None of the patients had a ST elevation greater than or equal to 0.2 mV, one in each group had a ST elevation of 0.15 mV. An ST depression up to −0.15mV was observed eleven times with propofol and five with etomidate. A QRS-prolongation of 25% upon induction was seen in one patient with propofol and three with etomidate. This trial failed to establish any evidence to suggest that changes in either group differed, with most percentiles being zero (median [25th, 75th], 0 [0, 0] vs. 0 [0, 0]). Finally, no new arrhythmias occurred perioperatively in both groups. Conclusions In this trial, there does not appear to be a significant difference in electrocardiographic changes in patients with Brugada syndrome when propofol versus etomidate were administered for induction of anesthesia. This study did not investigate electrocardiographic changes related to propofol used as an infusion for maintenance of anesthesia, so future studies would be warranted before conclusions about safety of propofol infusions in patients with Brugada syndrome can be determined. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

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Clinical aspects and physiopathology of Brugada syndrome: review of current concepts

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y06-038 ◽

2006 ◽

Vol 84 (8-9) ◽

pp. 795-802 ◽

Cited By ~ 8

Author(s):

E. Herbert ◽

M. Chahine

Keyword(s):

Brugada Syndrome ◽

Structural Heart Disease ◽

Polymorphic Ventricular Tachycardia ◽

Clinical Aspects ◽

Gene Encoding ◽

Bundle Branch Block ◽

St Segment Elevation ◽

Disease Mutations ◽

St Segment ◽

Cardiac Sodium Channel

Brugada syndrome (BS) is an inherited cardiac disorder characterized by typical electrocardiographic patterns of ST segment elevation in the precordial leads, right bundle branch block, fast polymorphic ventricular tachycardia in patients without any structural heart disease, and a high risk of sudden cardiac death. The incidence of BS is high in male vs. female (i.e., 8–10/1: male/female). The disorder is caused by mutations in the SCN5A gene encoding Nav1.5, the cardiac sodium channel, which is the only gene in which mutations were found to cause the disease. Mutations in SCN5A associated with the BS phenotype usually result in a loss of channel function by a reduction in Na+ currents. We review the clinical aspects, risk stratification, and therapeutic management of this important syndrome.

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Role of Catheter Ablation for Ventricular Arrhythmias in Brugada Syndrome

Current Cardiology Reports ◽

10.1007/s11886-021-01479-2 ◽

2021 ◽

Vol 23 (5) ◽

Author(s):

Ronpichai Chokesuwattanaskul ◽

Koonlawee Nademanee

Keyword(s):

Catheter Ablation ◽

Brugada Syndrome ◽

Ventricular Arrhythmias ◽

Structural Heart Disease ◽

Therapeutic Modalities ◽

Good Target ◽

Arrhythmogenic Substrate ◽

Life Threatening ◽

The Right

Abstract Purpose of Review To discuss the role of catheter ablation in treating life-threatening ventricular arrhythmias associated with Brugada syndrome (BrS), by presenting recent findings of BrS arrhythmogenic substrate, mechanisms underlying ventricular arrhythmias, and how they can be treated with catheter ablation. Recent Findings Almost three decades ago when the clinical entity of Brugada syndrome (BrS) was described in patients who had abnormal coved-type ST elevation in the right precordial EKG leads in patients who had no apparent structural heart disease but died suddenly from ventricular fibrillation. Since its description, the syndrome has galvanized explosive research in this field over the past decades, driving major progress toward better understanding of BrS, gaining knowledge of the genetic pathophysiology and risk stratification of BrS, and creating significant advances in therapeutic modalities. One of such advances is the ability for electrophysiologists to map and identify the arrhythmogenic substrate sites of BrS, which serve as good target sites for catheter ablation. Subsequently, several studies have shown that catheter ablation of these substrates normalizes the Brugada ECG pattern and is very effective in eliminating these substrates and preventing recurrent VF episodes. Summary Catheter ablation has become an important addition for treatment of symptomatic BrS patients with recurrent VT/VF episodes.

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Brugada-Like Electrocardiographic Patterns Induced by Hyperkalemia

Medicina ◽

10.3390/medicina49030024 ◽

2013 ◽

Vol 49 (3) ◽

pp. 24 ◽

Cited By ~ 1

Author(s):

Dagmara Reingardienė ◽

Jolita Vilčinskaitė ◽

Diana Bilskienė

Keyword(s):

Brugada Syndrome ◽

Structural Heart Disease ◽

Electrolyte Disorders ◽

St Segment Elevation ◽

Wave Inversion ◽

St Segment ◽

Acute Renal Insufficiency ◽

Channel Mutation ◽

The Right ◽

Ecg Abnormalities

Brugada syndrome was described in 1992 as a new clinical and electrocardiographic syndrome involving susceptibility to ventricular arrhythmias and sudden cardiac death in patients with no obvious structural heart disease. Brugada syndrome is characterized by a hereditary anomaly in the sodium ion channel (mutation of the SCN5A gene) identified by a wide QRS associated with the ST-segment elevation and the T‑wave inversion in the right precordial leads. The Brugada-like electrocardiographic pattern can be caused by sodium channel-blocking drugs and electrolyte disorders. Hyperkalemia may produce multiple ECG abnormalities, including the ST-segment elevation and pseudomyocardial infarction with a resolution of these abnormalities after the correction of hyperkalemia. This article describes 8 cases of pseudoanteroseptal myocardial infarction in acute renal insufficiency with hyperkalemia. The ST-segment elevation related to hyperkalemia is resolved by the reduced serum potassium level. Clinicians should recognize that hyperkalemia is one of the etiologies of the Brugada-like electrocardiographic pattern.

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Intermittent Brugada Syndrome Presenting with Syncope in an Adult Female

Case Reports in Emergency Medicine ◽

10.1155/2014/742076 ◽

2014 ◽

Vol 2014 ◽

pp. 1-3

Author(s):

Patricia Chavez ◽

Daniel Bamira ◽

Abel Casso Dominguez ◽

Akshai Bhandary ◽

Eyal Herzog

Keyword(s):

Brugada Syndrome ◽

Fatal Outcome ◽

Structural Heart Disease ◽

Bundle Branch Block ◽

St Segment Elevation ◽

T Wave ◽

Shockable Rhythm ◽

St Segment ◽

History Of

Background.Brugada syndrome accounts for 4–12% of all sudden deaths worldwide and at least 20% of sudden deaths in patients with structurally normal hearts.Case Report.A 48-year-old female presented to the emergency department after two witnessed syncopal episodes. While awaiting discharge had a third collapse followed by cardiac arrest with shockable rhythm. Initial electrocardiogram showed wide QRS complex with left axis deviation, ST-segment elevation of <1 mm in V1 and V2, and flattening of T waves in V1. The angiogram did not demonstrate obstructive coronary disease. The electrocardiogram obtained two days after these events showed a right bundle branch block with ST-segment elevation of >2 mm followed by a negative T wave with no isoelectric separation, suggestive of spontaneous intermittent Brugada type 1 pattern. Cardiac magnetic resonance imaging demonstrated neither structural heart disease nor abnormal myocardium. After placement of an implantable cardioverter defibrillator the patient was discharged. Why should an emergency physician be aware of this? Brugada syndrome is an infrequently encountered clinical entity which may have a fatal outcome. This syndrome primarily presents with syncope. It should be considered as a component of differential diagnosis in patients with family history of syncope and sudden cardiac death.

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Rhabdomyoma of the interventricular septum presenting as a Brugada phenocopy

Cardiology in the Young ◽

10.1017/s1047951111000424 ◽

2011 ◽

Vol 21 (5) ◽

pp. 591-594 ◽

Cited By ~ 7

Author(s):

Timothy Nguyen ◽

John Smythe ◽

Adrian Baranchuk

Keyword(s):

Sudden Death ◽

Brugada Syndrome ◽

Ventricular Arrhythmias ◽

Interventricular Septum ◽

St Segment Elevation ◽

St Segment ◽

The Right

AbstractBrugada 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.

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Fever Unmasked Brugada Syndrome in Pediatric Patient: A Case Report

Clinical Practice and Cases in Emergency Medicine ◽

10.5811/cpcem.2020.2.44418 ◽

2020 ◽

Vol 4 (2) ◽

pp. 244-246

Author(s):

Orhay Mirzapolos ◽

Perry Marshall ◽

April Brill

Keyword(s):

Emergency Medicine ◽

Case Report ◽

Brugada Syndrome ◽

Ventricular Arrhythmias ◽

Cardiac Monitoring ◽

St Segment Elevation ◽

Cardioverter Defibrillator ◽

St Segment ◽

Viral Illness ◽

Automatic Implantable Cardioverter Defibrillator

Introduction: Brugada syndrome is an arrhythmogenic disorder that is a known cause of sudden cardiac death. It is characterized by a pattern of ST segment elevation in the precordial leads on an electrocardiogram (EKG) due to a sodium channelopathy. Case Report: This case report highlights the case of a five-year-old female who presented to the emergency department with a febrile viral illness and had an EKG consistent with Brugada syndrome. Discussion: Fever is known to accentuate or unmask EKG changes associated with Brugada due to temperature sensitivity of the sodium channels. Conclusion: Febrile patients with Brugada are at particular risk for fatal ventricular arrhythmias and fevers should be treated aggressively by the emergency medicine provider. Emergency medicine providers should also consider admitting febrile patients with Brugada syndrome who do not have an automatic implantable cardioverter-defibrillator for cardiac monitoring.

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Sudden Cause of Cardiac Death—Be Aware of Me: A Case Report and Short Review on Brugada Syndrome

Case Reports in Medicine ◽

10.1155/2010/823490 ◽

2010 ◽

Vol 2010 ◽

pp. 1-3 ◽

Cited By ~ 3

Author(s):

Jagadeesh K. Kalavakunta ◽

Vishwaroop Bantu ◽

Hemasri Tokala ◽

Mihas Kodenchery

Keyword(s):

Brugada Syndrome ◽

Past History ◽

Short Review ◽

Case Presentation ◽

St Segment Elevation ◽

First Case ◽

St Segment ◽

The Right ◽

Malignant Arrhythmias

Introduction. Brugada syndrome accounts for about 4% of sudden cardiac deaths (SCD). It is characterized by an ST-segment elevation in the right precordial electrocardiogram (EKG) leads.Case Presentation. We describe a 39-year-old healthy Caucasian man who was admitted to the intensive care unit after being cardioverted from ventricular fibrillation (VF) arrest. His past history was significant for an episode of syncope one month prior to this presentation for which he was admitted to an outlying hospital. EKG during that admission showed ST elevations in V1 and V2 leads, a pattern similar to Type 1 Brugada. A diagnosis of Brugada syndrome was missed and the patient had a cardiac arrest a month later. We discuss a short review of Brugada syndrome and emphasize the need to look for it in patients presenting with SCD and malignant arrhythmias.Conclusion. Physicians should always consider Brugada syndrome in the differential diagnosis of ST-segment elevation in anterior precordial leads of EKG and associated VT/VF. Although more than 17 years have passed since the first case was reported, increased awareness of this syndrome is needed to identify patients with EKG changes and treat them accordingly to prevent incidence of (SCD) and its deleterious complications.

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Experimental Models of Brugada syndrome

International Journal of Molecular Sciences ◽

10.3390/ijms20092123 ◽

2019 ◽

Vol 20 (9) ◽

pp. 2123 ◽

Cited By ~ 6

Author(s):

Sendfeld ◽

Selga ◽

Scornik ◽

Pérez ◽

Mills ◽

...

Keyword(s):

Brugada Syndrome ◽

Experimental Models ◽

Model Systems ◽

Patient Specific ◽

Canine Heart ◽

Stem Cell Technology ◽

St Segment Elevation ◽

St Segment ◽

Cardiac Sodium Channel ◽

The Right

Brugada syndrome is an inherited, rare cardiac arrhythmogenic disease, associated with sudden cardiac death. It accounts for up to 20% of sudden deaths in patients without structural cardiac abnormalities. The majority of mutations involve the cardiac sodium channel gene SCN5A and give rise to classical abnormal electrocardiogram with ST segment elevation in the right precordial leads V1 to V3 and a predisposition to ventricular fibrillation. The pathophysiological mechanisms of Brugada syndrome have been investigated using model systems including transgenic mice, canine heart preparations, and expression systems to study different SCN5A mutations. These models have a number of limitations. The recent development of pluripotent stem cell technology creates an opportunity to study cardiomyocytes derived from patients and healthy individuals. To date, only a few studies have been done using Brugada syndrome patient-specific iPS-CM, which have provided novel insights into the mechanisms and pathophysiology of Brugada syndrome. This review provides an evaluation of the strengths and limitations of each of these model systems and summarizes the key mechanisms that have been identified to date.

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