Suicidal Zinc Phosphide Poisoning Unmasking Brugada Syndrome and Triggering Near Fatal Ventricular Arrhythmia

Brugada syndrome (BrS) is an inherited channelopathy associated with increased incidence of ventricular arrhythmias and has many acquired triggers. Zinc phosphide (ZnP) is a rodenticide and is commonly implicated in suicidal poison ingestion. ZnP poisoning can cause myocardial toxicity and death. We report a case of ZnP poisoning that triggered a type I Brugada pattern and ventricular fibrillation in a 67‐year‐old male. He had no other features of toxicity and recovered later. As metal phosphide is the commonest toxin involved in suicidal poisoning in India and BrS being endemic here, this case highlights an important clinical problem.     

Supraventricular tachycardia with a baseline ECG pattern of Brugada syndrome

The typical arrhythmias found in patients with the Brugada syndrome is either ventricular fibrillation or polymorphic ventricular tachycardia. We report the case of a patient who presented with supraventricular tachycardia accompanied by ECG features of the Brugada syndrome (BrS) during both tachyarrhythmia and sinus rhythm. This case lends support to the recently reported association between supraventricular tachyarrhythmia and BrS and the hypothesis that the arrhythmogenic substrate in BrS is not limited to the ventricular level.     

Brugada syndrome unmasked by accidental inhalation of gasoline vapors

Loss-of-function mutations in the gene SCN5A can cause Brugada syndrome (BrS), which is an inherited form of idiopathic ventricular fibrillation. We report the case of a 46-year-old patient, with no previous medical history, who had ventricular fibrillation after accidental inhalation of gasoline vapors. His electrocardiogram (ECG) showed a typical type-1 BrS pattern that persisted after the acute event. Genetic investigations allowed the identification of a novel SCN5A mutation leading to a frame-shift and early termination of the channel protein. Biochemical and cellular electrophysiology experiments confirmed the loss-of-function of the mutant allele. The patient was implanted with a cardioverter/defibrillator.     

Brugada syndrome associated with out-of-hospital cardiac arrest: A case report

BACKGROUNDBrugada syndrome (BrS) is an inherited disease characterized by an electrocardiogram (ECG) with a coved-type ST-segment elevation in the right precordial leads (V1-V3), which predisposes to sudden cardiac death (SCD) due to polymorphic ventricular tachycardia or ventricular fibrillation in the absence of structural heart disease. We report the case of a 29-year-old man with out-of-hospital cardiac arrest. BrS is associated with a high incidence of SCD in adults, and increasing the awareness of BrS and prompt recognition of the Brugada ECG pattern can be lifesaving.CASE SUMMARYA 29-year-old man suffered from out-of-hospital cardiac arrest, and after defibrillation, his ECG demonstrated a coved-type elevated ST segment in V1 and V2. These findings were compatible with type 1 Brugada pattern, and ECG of his brother showed a type 2 Brugada pattern. The diagnosis was BrS, NYHF IV, multiple organ dysfunction syndrome, sepsis, and hypoxic ischemic encephalopathy. The patient had no arrhythmia episodes after discharge throughout a follow-up period of 36 mo. CONCLUSIONIncreasing awareness of BrS and prompt recognition of the Brugada ECG pattern can be lifesaving.     

Pericarditis mimicking Brugada syndrome

Introduction

Brugada syndrome (BrS) is a genetic heart disorder due to alteration of the ion channels function that causes an impaired in the cardiac conduction system. It is characterized by an abnormal electrocardiogram pattern and may be complicated by malignant ventricular arrhythmias.Pericarditis is an inflammation of the pericardium and 90% of isolated cases of acute pericarditis are idiopathic or viral. Acute pericarditis may appears with chest pain, fever, pericardial friction rub, and cardiac tamponade. Moreover, widespread ST segment changes occur due to involvement of the underlying epicardium.

Brugada Pattern in Toxic Myocarditis due to Severe Aluminum Phosphide Poisoning

Brugada pattern electrocardiogram (ECG) unmasking can occur due to various drugs. There are old reports of the acute infarction pattern in aluminum phosphide (rodenticide)-related toxic myocarditis. The given case illustrates the Brugada pattern and various other ECG abnormalities in a patient with this poisoning. The old reported cases of the acute infarction pattern are also likely the Brugada pattern.     

Comparisons of clinical impacts on individuals with Brugada electrocardiographic patterns defined by ISHNE criteria or EHRA/HRS/APHRS criteria: a nationwide community-based study

Introduction: Identifying Brugada electrocardiographic pattern (BrP) early is crucial to prevent sudden cardiac death. Two different diagnostic criteria proposed by International Society for Holter and Noninvasive Electrocardiography (ISHNE) and Heart Rhythm Society/European Heart Rhythm Association/Asia-Pacific Heart Rhythm Society (HRS/EHRA/APHRS) were widely used in clinical practice. The difference in prevalence and prognosis of BrP by applying the two different criteria was never studied before.

Methods: This study was prospectively conducted in a nationwide large-scale stratified random sampling community-based cohort (HALST) from Han Chinese population in Taiwan from December 2008 to December 2012. We compared the prevalence and prognosis of BrP defined by the two diagnostic criteria.

Results: A total of 5214 adults were enrolled (2530 men) with mean age of 69.3 years. Four had spontaneous type 1 BrP (0.077%). By the HRS/EHRA/APHRS criteria, 68 individuals have type 2 BrP (1.30%) and 101 have type 3 BrP (1.94%) whereas by the ISHNE criteria, 46 individuals exhibited type 2 BrP (0.88%). When applying the ISHNE criteria, the number of individuals with BrP decreased by 71%. However, all-cause mortality and cardiovascular mortality were not different between individuals with or without BrP, irrespective of the criteria used.

Conclusions: The two different criteria may impact the diagnostic yield of individuals with BrP, but do not affect the prognosis of the individuals with BrP.

• Key messages

• Comparing with the use of HRS/EHRA/APHRS criteria, the number of individuals with Brugada ECG patterns was decreased by 71% when applying the ISHNE criteria.

• The prognosis of individuals with Brugada ECG patterns defined by 2012 ISHNE or 2013?HRS/EHRA/APHRS criteria were not different.

     

Brugada Syndrome: A Primer for Nurse Practitioners

Brugada syndrome (BrS) is a less known cardiac condition which falls into the category of a channelopathies. BrS has been diagnosed for more than 2 decades. Currently BrS remains a major cause of sudden cardiac death in young adults who have no known abnormal heart structure. Nurse practitioners’ awareness of the clinical presentation, diagnosis, treatment, and ongoing care is essential for maximizing patient outcomes.     

Drug‐Induced Brugada Syndrome by Noncardiac Agents

Drug‐induced Brugada syndrome (BrS) represents a great challenge for the prescribing clinicians as well as for those involved in the development of novel pharmaceuticals and in the regulatory bodies responsible with monitoring drug safety. Apart from well‐known cardiac agents (mainly Class I antiarrhythmics), an increasing number of noncardiac agents, including psychotropic and anesthetic drugs, have been shown to induce the characteristic Brugada electrocardiogram pattern predisposing to fatal ventricular arrhythmias. Up to now, both repolarization and depolarization abnormalities are thought to be related to the development of ventricular fibrillation in BrS patients. This review highlights the mechanisms and the noncardiac medical agents that unmask a genetic predisposition to BrS.     

Prognosis, risk stratification,and management of asymptomatic individuals with Brugada syndrome: A systematic review

Brugada syndrome (BrS) is a primary electrical disease associated with increased risk of sudden cardiac death due to polymorphic ventricular arrhythmias. The prognosis, risk stratification, and management of asymptomatic individuals remain the most controversial issues in BrS. Furthermore, the decision to manage asymptomatic patients with an implantable cardioverter‐defibrillator should be made after weighing the potential individual risk of future arrhythmic events against the risk of complications associated with the implant and follow‐up of patients living with such devices, and the accompanying impairment of the quality of life. Several clinical, electrocardiographic, and electrophysiological markers have been proposed for risk stratification of subjects with BrS phenotype, but the majority have not yet been tested in a prospective manner in asymptomatic individuals. Recent data suggest that current risk factors are insufficient and cannot accurately predict sudden cardiac death events in this setting. This systematic review aims to discuss contemporary data regarding prognosis, risk stratification, and management of asymptomatic individuals with diagnosis of Brugada electrocardiogram pattern and to delineate the therapeutic approach in such cases.     

Intensive care and anesthetic management of patients with Brugada syndrome and COVID-19 infection

Coronavirus disease 2019 (COVID-19) spreads across the world, and the intensive care unit (ICU) community must prepare for the challenges associated with this pandemic viral infection. Rapid diagnosis, isolation, and intensive clinical management are very important for all patients with COVID-19, especially for those with cardiac diseases as Brugada syndrome (BrS). BrS is an arrhythmogenic disease reported to be one among the leading causes of sudden cardiac death. In these patients, episodes of lethal arrhythmias may be induced by several factors or situations, and for this reason management during ICU permanence or anesthesia must provide some precautions, avoiding factors that are known to have the potential to worsen the probability to induce arrhythmias. For ICU practitioners, management of acute respiratory failure, hemodynamics, and cardiovascular complications certainly are the key for the best treatment of these patients but to date specific data on supportive ICU care for these patients are lacking, and current recommendations are based on existing evidence from other viral infections and general intensive care management. We want to focus on some general rules, resulted from cases series and clinical practice, to be followed during the ICU management of patients with BrS and concomitant COVID-19 infection.     

Brugada syndrome in the presence of coronary artery disease and parasympathomimetic drug therapy

Brugada pattern ECG changes have been described in various disease states and drug therapies, including electrolyte abnormalities, myocardial pathology, medications, and mechanical abnormalities. Therefore, the diagnosis of Brugada syndrome cannot be made in the presence of confounding variables according to prevailing guidelines. We present a case report which illustrates two important principles regarding Brugada syndrome, the dynamic ECG manifestations and the elimination of confounding variables (in this case significant coronary artery disease and cholinergic pharmacotherapy) prior to definitive diagnosis.     

Arrhythmic storm responsive to quinidine in a patient with Brugada syndrome and vasovagal syncope

A 37-year-old man with Brugada syndrome (BrS) and arrhythmic storm is described. One month after implantation of a cardioverter-defibrillator he presented with recurrent appropriate shocks for spontaneous ventricular fibrillation (VF). Because of this arrhythmic storm, quinidine therapy was initiated with total suppression of all spontaneous arrhythmias. He had remained free of arrhythmias for 22 months since quinidine initiation. Two episodes of VF occurred after the patient stopped taking the medication. The patient resumed quinidine and has been free of VF for the last 3 months. This response to quinidine in a patient with symptomatic BrS supports its role in the prophylaxis of arrhythmic events in BrS.     

Autonomic dysfunction in patients with Brugada syndrome: further biochemical evidence of altered signaling pathways

Background: In patients with Brugada syndrome (BrS), life‐threatening ventricular tachyarrhythmias predominantly occur during vagal stimulation at rest or during sleep. Previous imaging studies displayed an impaired autonomic function in BrS patients. However, it remains unclear whether these alterations primarily stem from a reduction of synaptic release of norepinephrine (NE) or an enhanced presynaptic reuptake. Both conditions could lead to reduced NE concentrations in the synaptic cleft. Therefore, we analyzed key components of the sympathoadrenergic signaling pathways in patients with BrS. Methods and Results: Endomyocardial biopsies were obtained from eight BrS patients (seven male; age 49 ± 15 years) and five controls (three male; age 43 ± 13 years; P = ns). The concentrations of NE, epinephrine (Epi), NE transport (NET) carrier protein, cyclic adenosine 5′monophosphate (cyclic adenosine monophosphate [cAMP]), inhibitory G‐proteins (G_i1,2α), troponin‐I (TNI), and phosphorylated TNI were analyzed. Levels of NET, G_i1,2α, TNI, Epi, and phosphorylated TNI were comparable between the groups. Compared to controls, patients with BrS showed reduced cAMP and NE concentrations. Conclusions: The current findings expand the concept of adrenergic dysfunction in BrS: the reduction of NE in BrS could lead to an impaired stimulation of β‐adrenoceptors resulting in a reduction of cAMP and alterations of the subsequent signaling pathway with potential implication for arrhythmogenesis. (PACE 2011; 34:1147–1153)     

Propafenone-induced Brugada-like ECG changes mistaken as acute myocardial infarction

Brugada syndrome is one of the important causes of sudden cardiac death in young adults. The condition is associated with typical ECG changes in anteroseptal leads V1 and V2 that can be unmasked by various medications, electrolyte disturbances, and even by the febrile state in susceptible individuals. The case history is reported of a patient with atrial flutter and atrial fibrillation who developed Brugada-like ECG changes when treated with propafenone. He was mistakenly diagnosed as having acute myocardial infarction when he presented to the emergency room with acute precordial chest pain. Cardiac catheterisation revealed normal coronary arteries and normal left ventricular systolic function. A review of previous ECGs showed the temporal relationship of ECG changes to initiation of propafenone a few years earlier. The ECG changes resolved with discontinuation of propafenone and re-emerged when he was rechallenged with oral propafenone. This case highlights the importance of recognising the characteristic ECG changes of Brugada syndrome and being able to differentiate them from those of acute myocardial infarction and other conditions manifesting with similar changes.     

J wave syndromes as a cause of malignant cardiac arrhythmias

The J wave syndromes, including the Brugada (BrS) and early repolarization (ERS) syndromes, are characterized by the manifestation of prominent J waves in the electrocardiogram appearing as an ST segment elevation and the development of life‐threatening cardiac arrhythmias. BrS and ERS differ with respect to the magnitude and lead location of abnormal J waves and are thought to represent a continuous spectrum of phenotypic expression termed J wave syndromes. Despite over 25 years of intensive research, risk stratification and the approach to therapy of these two inherited cardiac arrhythmia syndromes are still rapidly evolving. Our objective in this review is to provide an integrated synopsis of the clinical characteristics, risk stratifiers, as well as the molecular, ionic, cellular, and genetic mechanisms underlying these two syndromes that have captured the interest and attention of the cardiology community over the past two decades.     

Transcranial Magnetic Stimulation as an Antidepressant Alternative in a Patient With Brugada Syndrome and Recurrent Syncope

Brugada syndrome (BrS) is a common occult cause of sudden cardiac arrest in otherwise healthy-appearing adults. The pathognomonic electrocardiographic pattern may be unmasked only by certain medications, many of which are unknown. We report a case of a depressed but otherwise healthy man with an asymptomatic right bundle branch block on electrocardiography who experienced antidepressant-induced BrS and ultimately recovered with transcranial magnetic stimulation (TMS). After an initial trial of nortriptyline, the patient’s depressive symptoms improved; however, he experienced a syncopal event and was subsequently diagnosed as having BrS. Cross titration to bupropion, which had not previously been known to exacerbate BrS, was followed by another cardiac event. As a result, the patient was referred for TMS as a substitute for pharmacotherapy. After 31 TMS sessions over 8 weeks, the patient demonstrated significant improvement by subjective report and objective reduction in his Patient Health Questionnaire-9 scores from 10 (moderate) to 1 (minimal). Transcranial magnetic stimulation is a Food and Drug Administration–approved nonpharmacologic treatment for depression. Given the potential lethality of BrS with known and unknown psychopharmacologic agents, providers should consider TMS as first-line therapy in this patient population. Bupropion should be added to the list of agents known to exacerbate this disease.     

Hypothyroid patient with Brugada electrocardiographic waveforms: case report

We report a 46-year-old man who presented with hypothyroidism. An electrocardiogram obtained at the time of the first examination revealed Brugada electrocardiographic (Brugada-ECG) waveforms in leads V1 to V3. The patient and his family had no history of arrhythmia and syncopal attack. The Brugada-ECG waveforms disappeared with the normalization of thyroid function. The case suggested that hypothyroidism could lead to secondary Brugada-ECG waveforms because of its effect on myocardial ion channels.     

Pneumopericardium mimicking acute myocardial ischemia after laparoscopic cholecystectomy.

Pneumopericardium occurred after laparoscopic cholecystectomy in a 57-year-old woman. The patient had chest pain accompanied by T-wave inversion on electrocardiogram, with signs and symptoms suggestive of acute myocardial ischemia. Evaluation for myocardial infarction, however, was negative and clinical findings resolved spontaneously. Although pneumopericardium after laparoscopic procedures has been previously reported, this case illustrates how associated findings may mimic those of acute myocardial ischemia or infarction.     

Unmasking effect of propafenone on the concealed form of the Brugada phenomenon

A case report of a patient with frequent ventricular premature beats but with an otherwise normal ECG and no structural heart disease. Propafenone in therapeutical doses unmasked the ECG picture of the Brugada phenomenon.