Brugada Phenocopy Research Articles

Transient Brugada Like after Scorpion Sting: An Unexpected Connection

Introduction: Brugada syndrome was described in 1992 as a new clinical and electrocardiographic syndrome involving susceptibility to ventricular arrhythmias and sudden cardiac death in patients without obvious structural heart disease. Brugada phenocopy (BrP) is an evolving term for Brugada-like ECG patterns due to reversible causes. In this article, we will illustrate the case of a patient presenting with a transient Brugada pattern following a scorpion sting. Case Report: A 65-year-old woman with age and menopause as cardiovascular risk factors, but no notable medical history, presented to the emergency department with atypical chest pain five hours after a scorpion sting. She had no associated symptoms such as dyspnoea, syncope, or palpitations, nor a personal or family history of sudden death. On admission, she was conscious, hemodynamically stable, normotensive, and tachycardic, with no signs of heart failure. Her ECG showed a 2 mm elevation at the J point and an inverted T wave in V1 and V2, indicating a Brugada pattern. She was admitted to the ICU for close monitoring. An echocardiogram revealed normal left and right ventricular function. Lab tests showed negative troponins, a normal blood ionogram, and normal renal and hepatic function. The Brugada pattern resolved within a few hours, and the patient remained stable. Discussion and Conclusion: Our case highlights the importance of conducting a thorough medical history to rule out the presence of arrhythmia, syncope, or a family history of sudden cardiac death in similar situations. If the history raises concerns, cardiological follow-up is essential to investigate the possibility of Brugada syndrome. Performing a follow-up ECG at discharge is beneficial to confirm the reversibility of the findings. This distinction is crucial as it helps differentiate between Brugada syndrome and the Brugada pattern, the latter being a condition that may occur in patients with scorpion stings or other triggers.

Toxic Myocarditis with Brugada Phenocopy in a Case of Aluminum Phosphide Poisoning

Brugada phenocopy is considered when a Brugada-type ECG pattern is present but with a low likelihood of true Brugada syndrome, as indicated by negative family history, genetic testing, or provocative testing with drugs, or ECG normalization after the removal of precipitants. Brugada phenocopy has been reported due to various causes such as fever and electrolyte imbalance. We describe a 22-year-old man who presented with aluminum phosphide poisoning, resulting in severe metabolic acidosis, myocarditis, and profound myocardial depression. He developed transient Brugada-like ECG changes and multiorgan dysfunction, requiring intensive management, including mechanical ventilation and inotropes. Brugada phenocopy is a rare manifestation of aluminum phosphide-associated toxic myocarditis. After a week of treatment, there was a significant improvement in cardiac function and overall clinical status.

Brugada Phenocopy Induced by Electrocution: About a Case

Brugada Syndrome (BrS) is an inherited channelopathy secondary to a sodium channel defect (SCN5A), predisposing to ventricular arrhythmia and sudden death. The BrS electrocardiogram is often dynamic and can change from a type 1 to a type 2 pattern, passing through periods of normalisation. The term Brugada phenocopy was proposed by Pérez-Riera et al to describe the electrocardiographic aspect of Brugada observed in other situations, such as acute myocarditis, muscular dystrophy, or secondary to other agents such as electrocution, the taking of drugs such as psychotropic drugs, prolonged exposure to cold or carbon monoxide intoxication. Electrocution can cause serious cardiovascular damage, in particular malignant ventricular arrhythmias. We report the case of a 59-year-old patient who consulted the emergency ward for a cardiac work-up following electrocution. An ECG was performed, which revealed a transient Brugada type 1. In this case, we discuss the diagnostic procedures for this channelopathy, which carries a risk of ventricular rhythm disorders and sudden death, and the therapeutic management.

A case of Brugada phenocopy unmasked following giant Asian honey bee stings

This case report details a rare occurrence of Brugada phenocopy (type 1 Brugada electrocardiographic pattern) precipitated following giant Asian honey bee (Apis dorsata) stings in a previously healthy Sri Lankan male. The patient had an uneventful course. While similar ECG patterns can arise from non-genetic factors, Giant Asian honey bee sting as a causal factor is exceedingly unusual and unreported previously. This case adds to the spectrum of cardiac manifestations of Hymenopteran venom highlighting the requirement for close cardiac monitoring and clinical vigilance in these patients.

A case of Brugada phenocopy alteration induced by immune checkpoint inhibitors

Immunotherapy has shown remarkable efficacy in various cancer treatments. However, enhanced T-cell immune surveillance can lead to aberrant immune responses, resulting in severe immune checkpoint inhibitor-related adverse events. This is a case report of a patient previously treated with immune checkpoint inhibitors who presented with ST-segment elevation without abnormal troponin and cardiac enzyme spectrum test results. Cardiac toxicity of immune checkpoint inhibitors mainly manifests as acute immune-mediated myocarditis. While Brugada phenocopy is commonly caused by fever, electrolyte abnormalities, tricyclic/tetracyclic antidepressants, and marijuana use, we suspect that it was induced by immune checkpoint inhibitors in the current case.

Brugada phenocopy associated with multiple psychotic drugs

Brugada phenocopy (BrP) is a clinical condition characterized by transient ECG changes of Brugada syndrome (BrS), which can be due to various clinical conditions. We describe a case report of BrP due to psychotic drugs.

Captagon-induced Brugada phenocopy: A report of two cases.

Brugada phenocopies (BrP) represent electrocardiogram changes identical to those of true congenital Brugada syndrome but are induced by reversible clinical conditions. Previous cases have been reported in patients following recreational drug use. This report presents two cases of type 1B BrP associated with Fenethylline abuse, a recreational drug known by its trade name, Captagon.

313 BRUGADA SYNDROME MIMICRY: THE IMPORTANCE OF AN EXTENDED FOLLOW-UP

Abstract Introduction Brugada Syndrome (BrS) is a genetically inherited condition associated with the risk of fatal arrhythmias and sudden cardiac death (SCD) occurring in a structurally normal heart. This disorder was historically related to mutations in the SCN5A gene, but recent observations suggest a more complex genetic inter-play, highlighting the possible overlap with structural cardiomyopathies, including hypertrophic cardiomyopathy (HCM). Case Presentation In May 2005, an asymptomatic 56-year-old man with a family history of unexplained SCD was referred to our outpatient clinic. A 12-lead ECG showed a type 2 Brugada pattern whilst transthoracic echocardiogram (TTE) was normal. Ventricular fibrillation (VF) was induced during an elective electrophysiological study and a transvenous implantable cardioverter-defibrillator (ICD) was implanted for primary prevention. More than 10 years later, in March 2022, our patient was admitted to the hospital because of palpitations. The ECG revealed a typical atrial flutter with a high ventricular rate, successfully treated with catheter ablation. Post-procedural ECG showed the persistence of type 2 Brugada pattern in association with new-onset T wave inversion in inferolateral leads and signs of ventricular hypertrophy. TTE revealed asymmetric left ventricular hypertrophy, with left ventricular outflow tract (LVOT) obstruction determined by mitral systolic anterior motion and preserved LV systolic function. The patient was treated with optimal medical therapy with symptom improvement and reduction of LVOT obstruction at a 3-month follow-up TTE. Discussion The distinction between Brugada phenocopy and BrS electrocardiogram patterns is not obvious, and according to our experience a Brugada type 2 pattern could be an early ECG marker of a concealed HCM which became manifest over an extended follow-up. Brugada ECG phenocopies are clinical entities characterized by type 1 or type 2 Brugada patterns elicited by an underlying condition, the disappearance of the pattern with the resolution of the condition and the absence of classical symptoms. Several pathogenic variants involving other and different genes have been recently reported suggesting a possible overlap with structural cardiomyopathies. Recently, two other cases of incidental findings of a Brugada ECG pattern in the context of HCM were described. Both patients had a common pathogenetic splicing mutation in the MYBPC3 sarcomeric gene (encoding for the cardiac myosin-binding protein C) responsible for HCM with no genetic mutations associated with Brugada syndrome. This fact suggests that patients are not simultaneously affected by BrS and HCM but a clinically manifest HCM with a specific genetic background can lead to an early BrS electrical manifestation. Conclusion Our experience confirms that a Brugada type 2 ECG pattern could be a very early sign of a concealed HCM manifested over 10 years later. The importance of proper risk stratification and regular follow-up has thus crucial implications in patient clinical management. However, whether Brugada pattern associated with structural heart disease is linked to an increased risk of sudden cardiac death is still unknown and needs further investigations.

Brugada Phenocopy That Lurks After Hemodialysis: A Case Report

Brugada phenocopies (BrP) are clinical commodities that are etiologically distinguishable from genuine congenital Brugada syndrome. BrP is marked by type-1 or type-2 Brugada electrocardiogram (ECG) patterns in precordial V1 to V3, which is provoked by various underlying clinical disorders. Hemodialysis may improve the BrP ECG image. This case report describes the occurrence of a transient Brugada pattern that was seen on the ECG of an asymptomatic 64-years-old woman after administering hemodialysis due to renal failure. Diagnosis of Brugada phenocopy and BrS is necessary to achieve appropriate further treatment. Hemodialysis may improve the BrP ECG image.

A Case of Brugada Phenocopy in Adrenal Insufficiency-Related Pericarditis

This is a report of a 27-year-old man with known history of Addison’s disease, noncompliant with medications, and hypothyroidism who presented with shortness of breath, nausea, vomiting, fever, and chest pain as well as Brugada sign seen on electrocardiogram. Echocardiogram revealed a moderate pericardial effusion and laboratory findings were suggestive of adrenal insufficiency. Patient was determined to have Type I Brugada phenocopy, which is a Brugada sign seen on EKG with a reversible cause. In this instance, the Brugada phenocopy was caused by adrenal insufficiency with associated pericarditis. Treatment with high-dose steroids led to resolution of both the pericardial effusion and Brugada sign, providing further evidence of Brugada phenocopy.

AN UNCOMMON STEMI MASQUERADER: A CASE OF IMIPRAMINE INDUCED BRUGADA PHENOCOPY (BRP)

Brugada syndrome(BrS) is an arrhythmogenic disorder characterized by a bulging ST-segment elevation and a J-point elevation of at least 2 mm in at least two of the right precordial electrocardiogram (ECG) leads (V1-3). It has an incidence of 4 to 12% in sudden cardiac death (SCD) patients due to ventricular tachycardia (VT) or ventricular fibrillation (VF). The Brugada type 1 ECG pattern may occur in various conditions independent of the actual syndrome, and this clinical phenomenon is often referred to as Brugada phenocopy (BrP). A wide variety of other drugs have been reported to unmask or induce Brugada phenotype which may otherwise be concealed, including antianginals, antidepressants, antipsychotics, and antihistamines. In this article, we present a case of Drug-induced BrP due to Imipramine. A 60-year-old hypertensive female patientwith 3 days of chest pain, who was referred to us as possible Acute Coronary Syndrome (ACS) by a general practitioner. She had a history of psychiatric illness and her ECG showed type 1 Brugada pattern with elevation of the J point with an elevation of the curved ST segment in leads V1 to V3. We found that the patient had been taking imipramine for 8 years due to her psychiatric disorder. Psychiatric opinion was sought and drug induced Brugada was suspected following which Imipramine was discontinued. After 2 weeks of follow-up there was resolution of the ST-T changes on the ECG, supporting the diagnosis of drug-induced BrP.

True Brugada syndrome ECG or Brugada phenocopy ECG? Can the ECG itself tell us the diagnosis?

We described a type 1 Brugada electrocardiogram and discussed about the potential diagnostic electrocardiographic indicators to differentiate true Brugada syndrome and Brugada phenocopy.

Brugada syndrome: should we be screening patients before prescribing psychotropic medication?

Brugada syndrome (BrS) presents with a characteristic electrocardiogram (ECG) and is associated with sudden cardiac death. Until now, prolongation of QTc interval and its association with Torsade de Pointe and possible fatal arrhythmia have been the focus of routine baseline ECGs before prescribing psychotropic medication. A semi-systematic literature review was conducted using PubMed. The terms ‘Brugada’, ‘Brugada Syndrome’ AND ‘psychotropic’ ‘antipsychotic’ ‘antidepressant’ ‘mood stabilisers’ ‘clozapine’ ‘Tricyclic Antidepressants’ ‘Lithium’ were searched. From a search that delivered over 200 articles, 82 articles were included. Those that included details around causative medication, doses of medication and where clear timeline on drug cause were included. Where clarification was needed, the manufacturer of the medication was contacted directly. Psychotropic medication can be associated with BrS, Brugada phenocopy or unmasking of BrS, in overdose or in normal doses. Our results include a table summarising a number of psychotropic overdoses that led to BrS unmasking. Routine screening for BrS in patients before prescribing psychotropic medication is a natural extension of the baseline ECG currently routinely done to rule out QTc prolongation. Psychiatrists need to invest in ensuring better skills in interpreting ECGs and work closer with cardiologists in interpreting ECGs.

Hyperkalemia-induced brugada phenocopy: A rare electrocardiogram manifestation

Hyperkalemia-induced Brugada ECG pattern is rare. Although the association of hyperkalemia with Brugada pattern is a known entity, it is also very important to be aware of this presentation as the treatment of this Brugada Phenocopy is different from Brugada syndrome . This case presented with a Brugada like ECG but had hyperkalemia. On correcting the hyperkalemia, the ECG settled to normal.

Brugada syndrome unmasked by left ventricle posteromedial papillary muscle ventricular tachycardia: Coincidence or consequence

A 46-year-old man presented with left ventricle posteromedial papillary muscle ventricular tachycardia, presyncope, and a type-1 Brugada pattern on the post-electrical cardioversion electrocardiogram. There was a probability of a Brugada syndrome with the expression of its disease in the left ventricle; or a left monomorphic ventricular tachycardia as a part of Brugada phenocopy; or a Brugada syndrome with left monomorphic ventricular tachycardia as an epiphenomenon. Cardiac magnetic resonance, electrophysiological study, and ajmaline test were the key diagnostic tools employed.

Yellow Oleander seed poisoning induced expression of Brugada phenocopy in Electrocardiogram – A rare case report

Yellow Oleander seed poisoning induced expression of Brugada phenocopy in Electrocardiogram – A rare case report

Brugada phenocopy induced by tricyclic antidepressant poisoning

The Journal of the Ceylon College of Physicians (JCCP) is a peer-reviewed, open access journal published bi-annually by the Ceylon College of Physicians (CCP) in the last week of June and December.The objective of the Journal is to promote good clinical practice and influence policy making across the medical world through publication of original research and peer reviewed articles on current issues and to foster responsible and balanced debate on issues that affect medicine and health care in Sri Lanka. Contributions to the JCCP reflect its national and multidisciplinary readership and include current thinking across a range of medical specialties.

Tachycardia dependent early repolarisation pattern in subarachnoid haemorrhage related takotsubo syndrome.

We present a case of a patient who suffered subarachnoid haemorrhage (SAH), complicated by takotsubo syndrome, paroxysmal atrial fibrillation and ECG repolarisation abnormality, compatible with Brugada phenocopy. The early repolarisation morphology showed a paradox association with the cardiac cycle length; a relationship not yet documented in SAH. Our observation also sheds light on the genesis of the “spiked helmet” ECG sign.

A case of anomalous aortic origin of coronary artery associated with a coved‐type electrocardiogram

Brugada syndrome (BrS) is a sudden cardiac death syndrome characterized by a coved-type electrocardiogram (ECG). Different disorders, such as ischemia, can emulate a Brugada-pattern ECG (Brugada phenocopy). We report herein, the first case of surgical epicardial electrophysiological mapping in a successfully resuscitated patient with an anomalous aortic origin of the coronary artery (AAOCA) associated with a coved-type ECG. It was debatable whether the coved-type ECG and the abnormal arrhythmogenic substrate in the epicardial right ventricular outflow tract were derived from BrS or from repetitive ischemia due to AAOCA; however, the epicardial electrophysiological mapping helped in deciding the treatment strategy.

Electrocardiogram (ECG) changes of a patient with severe hyperkalemia

A 55-year-old gentleman with underlying type 2 diabetes mellitus, dyslipidemia, hypertension, and end stage renal disease presented with shortness of breath, vomiting and worsening fatigue for one day after missing his scheduled hemodialysis. Physical examination in revealed tachypnoea with a respiratory rate of 30 breaths per minute, and fine mid inspiratory crepitations at the lung bases. Initial blood investigations in the emergency department revealed severe metabolic acidosis and hyperkalemia with a potassium of 7.6 mmol/L. A 12 lead electrocardiogram was done and several features that suggest hyperkalemia were detected such as a narrow based and symmetrical tall, tented T wave. In V1 the QRS complex is reminiscent of Brugada type 1 which is probably Brugada phenocopy and are often seen in hyperkalemia. There is ST elevation in V2, a single precordial lead. There is no reciprocal ST depression, and a lone ST elevation does not indicate ischemia. This may be caused by hyperkalemia as well. There is a broad QRS of 136ms, widened QRS is characteristic of hyperkalemia. There is a broad P wave and the PR interval is approximately 200ms. Left ventricular hypertrophy is also present. Due to impending respiratory collapse, he was subsequently intubated. His hyperkalemia was treated with intravenous short acting human insulin, dextrose 50%, calcium gluconate, sodium bicarbonate and calcium polystyrene sulfonate. He was subsequently admitted to the intensive care unit (ICU) and had undergone emergency hemodialysis.