Complex mechanism of brugada phenocopy: moderate hyponatremia and right ventricular compression by liver metastatic tumor - case report.

Brugada phenocopy (BrP) occurs in various clinical conditions and manifests as a Brugada-like ECG pattern with coved (type 1) or saddle-back (type 2) ST-segment elevation in the right precordial leads. Unlike Brugada syndrome (BrS), which is an inherited channelopathy, BrP is not associated with an increased risk of malignant arrhythmia. BrP has been reported in severe metabolic disturbances (significant hyponatremia, hypokalemia or hyperkalemia), mechanical heart compression, coronary artery disease, pulmonary embolism and myocarditis/pericarditis. The authors described a case of a 69-year-old female whose Brugada-like ECG was atypically associated with only moderate hyponatremia (127 mmol/l). She was admitted due to a skin and subcutaneous tissue infection of the left shank and coexistent urinary tract infection (without a fever). She had the history of advanced melanoma with multiple liver metastases. Her cardiac history was negative, especially the patient has never suffered from ventricular arrhythmias. ECG on admission showed saddle-back ST-segment elevation in the right precordial leads; however, the patient did not report any chest pain. Troponin I level and left ventricular function in echocardiography were normal while regional longitudinal strain in RV apex was decreased and showed post-systolic shortening. The substernal view revealed compression of the right ventricle (RV) by liver metastatic tumor. ECG changes disappeared quickly during natrium chloride supplementation and did not recur during hospitalization. This case illustrates that even moderate hyponatremia may be a reversible cause of BrP when other predisposing conditions (e.g. heart compression by tumor) coexist.

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.

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.

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.

Diagnostic and therapeutic dilemmas in a patient with myocarditis, Brugada syndrome and arrhythmic syncope.

We present a case of a previously healthy 23-year-old male who presented with chest pain, palpitations and spontaneous type 1 Brugada electrocardiographic (ECG) pattern. Positive family history for sudden cardiac death (SCD) was remarkable. Initially, clinical symptoms in combination with myocardial enzymes elevation, regional myocardial oedema with late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) and inflammatory lymphocytoid-cell infiltrates in the endomyocardial biopsy (EMB) suggested the diagnosis of a myocarditis-induced Brugada phenocopy (BrP). Under immunosuppressive therapy with methylprednisolone and azathioprine, a complete remission of both symptoms and biomarkers was accomplished. However, the Brugada pattern did not resolve. The eventually spontaneous Brugada pattern type 1 established the diagnosis of Brugada syndrome (BrS). Due to his previous history of syncope, the patient was offered an ICD that he declined. After his discharge he experienced a new episode of arrhythmic syncope. He was readmitted and received an ICD.

Brugada pattern as part of the electrocardiographic abnormalities in hyperkalemia.

A 78-year-old man presented to the emergency department with a 10-day history of diarrhea and presyncope. His electrocardiogram showed a type-1 Brugada pattern but also a first-degree atrioventricular block, right bundle branch block, and peaked and symmetrical hyperacute T waves. A blood test revealed a potassium level of 9.3 mEq/L. After hemodialysis with normalization of serum potassium, the electrocardiographic abnormalities disappeared. An ajmaline challenge excluded the possibility of Brugada syndrome.

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.

A dynamic Brugada sign due to left anterior descending coronary artery occlusion.

Brugada phenocopies (BrP) include several conditions with a common electrocardiographic (ECG) pattern that are indistinguishable from classical Brugada syndrome (BrS). In this report, we describe two cases of acute myocardial infarction (AMI) presenting as BrP. The majority of cases of BrP in AMI have been reported due to right coronary artery (RCA) occlusion. Rarely, the left anterior descending artery (LAD) is incriminated as the cause. In both our cases of BrP, LAD was the culprit vessel.

A case of cardiac sarcoidosis mimicking Brugada syndrome.

A 17-year-old boy was admitted for management of ventricular fibrillation (VF) with intermittent Brugada pattern on ECG. On evaluation, cardiac MRI revealed myocardial scar and mediastinal lymphadenopathy. 18-Fluorodeoxyglucose positron emission tomography scan showed inflammation in the heart, lungs, and lymph nodes. He was diagnosed as a case of cardiac sarcoidosis (CS) and treated with steroids. However, there was a reactivation of cardiac inflammation and the development of a second VF storm. Following catheter ablation, the patient's arrhythmia improved. This report highlights the inflammation due to CS mimicking channelopathic features.

Brugada phenocopy in pulmonary embolism - clinicopathological case study and literature review.

Brugada syndrome (BrS) is an inherited channelopathy characterized on ECG by coved (type 1) or saddle-back (type 2) ST-segment elevation (STE) of 2 or more mm in the right precordial leads and is associated with an increased risk of malignant ventricular arrhythmias. The term Brugada phenocopy (BrPh) indicates conditions that may reversibly induce Brugada-like ECG pattern in patients without true BrS; e.g.: metabolic abnormalities, mechanical heart compression, ischemia, myocarditis/pericarditis, and pulmonary embolism (PE). Only 9 cases of BPh associated with PE have been described so far. The authors present another case of a 41-year-old-male and analyze the clinical data of all 10 subjects (7 males and 3 females). Type 1 of ECG Brugada pattern was present in 7 patients (including ours), type 2 was found in 2 persons; in 1 case ECG pattern was not defined. In 7 patients STE was prominent (5 mm or more in at least 1 lead). STE was limited to V1-V2 leads in 4 persons, extended to V3 in 3 patients and even to V4 in 3 other patients, which correlated with the significant right ventricular (RV) dilatation. Concomitant left ventricular (LV) systolic dysfunction was reported only in 1 patient, which suggested that paradoxical embolization of coronary artery was not the mechanism of BrS-like STE. Clinical course of PE was usually severe (5 individuals were treated with thrombolysis) and in 3 cases it ended with death. The autopsy was only performed on our patient. It showed diffuse (ischemic) injury of RV and LV secondary to RV overload, decreased cardiac output and severe oxygen deficiency in myocardium, which could have led to BrS pattern in ECG.

Brugada phenocopy in a patient with unstable angina and three-vessel coronary artery disease.

A 52-year-old male was admitted with unstable angina and three-vessel coronary artery disease. Electrocardiography (ECG) changes consistent with type-1 Brugada ECG pattern were noted during admission. The patient was asymptomatic for syncope and had no family history of sudden cardiac death, ICD implantation, and Brugada syndrome. After coronary by-pass graft the Brugada ECG pattern resolved, and ajmaline test did not elicit type-1 ECG pattern, confirming the suspicion of Brugada phenocopy.

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.

An unusual ECG change after a car crash.

A 34-year-old male patient was preparing for splenic artery embolization because of a car crash. Personal or family histories of cardiovascular diseases, sudden cardiac death, or Brugada syndrome were denied. Type 1 Brugada pattern was observed in the preoperative electrocardiogram and gradually resolved within a week. Chest blunt trauma may contribute to the transient ECG changes, and some particular considerations should be taken in this patient.

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.

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.

Brugada phenocopy secondary to extensive inferior wall ischemia induced by coronary steal effect.

The diagnosis of Brugada syndrome is usually made with a typical ECG pattern. However, different disorders can emulate this pattern (Brugada phenocopies). Pathophysiologic mechanisms underlying this phenomenon remain controversial. We describe the development of type-1 Brugada ECG pattern associated with extensive coronary steal effect during myocardial perfusion scintigraphy. Proximal occlusion of the right coronary artery and severe proximal stenosis in distally occluded left circumflex artery were confirmed by coronary angiogram. Brugada ECG pattern can be a reversible sign associated with inferior left ventricular and right ventricular ischemia. Its presence during acute ischemia deserves appropriate risk stratification.

Brugada phenocopy induced by consumption of yellow oleander seeds - A case report.

Brugada phenocopy is a brugada-like pattern in ECG seen in some diseases without an inherited channelopathy. The causes of brugada phenocopy are usually reversible. Once the reversible condition resolves, the ECG pattern disappears. There are many conditions that cause brugada phenocopy like myocardial infarction, hyperkalemia etc. Here we report a case of brugada phenocopy induced by consumption of yellow oleander seeds (T. Peruviana).

Link between Brugada phenocopy and myocardial ischemia: Results from the International Registry on Brugada Phenocopy.

BACKGROUND: Brugada phenocopies clinical entities that have indistinguishable electrocardiographic (ECG) patterns from true congenital Brugada syndrome. However, they are induced by other clinical circumstances such as myocardial ischemia. The purpose of our study was to examine the clinical features and pathogenesis of ischemia-induced Brugada phenocopy (BrP). METHODS: Data from 17 cases of ischemia-induced BrP were collected from the International Registry (www.brugadaphenocopy.com). Data were extracted from these publications and authors were contacted to provide further insight into each case. RESULTS: Of the patients included in this study, 71% were male. Mean age was 59 ± 11 years (range: 38-76). Type-1 Brugada ECG pattern occurred in 15/17 (88%) of the cases, while a type-2 Brugada ECG pattern was observed in the other 2/17 (12%). In all cases, the Brugada ECG pattern resolved upon correction of the ischemia, indicating ischemia as the inducing circumstance. No arrhythmic events have been detected acutely or during the follow-up. Reported time to resolution ranged from 2 minutes to 5 hours. Provocative challenges using sodium channel blocking agents were performed in 7/17 cases (41%), and all failed to induce a Brugada ECG pattern (BrP Class A). The remaining 10/17 cases (59%) did not undergo provocative testing due to various clinical reasons. CONCLUSIONS: Myocardial ischemia is a commonly reported etiology of BrP. Importantly, this study found no association between BrP induced by myocardial ischemia and sudden cardiac death or malignant ventricular arrhythmias.

Brugada phenocopy: Mechanisms, diagnosis, and implications.

Brugada phenocopies are Brugada-like ECG patterns induced by reversible clinical conditions. Baranchuk and colleagues characterized this condition in 2012, and since then the phenomenon has been increasingly reported. It has the same pattern classification of Brugada syndrome (i.e., types 1 and 2), but differs substantially regarding etiology and prognosis. Awareness of Brugada phenocopies must be sought to help understanding the mechanisms of ion channel dysfunction and to avoid misdiagnosis and mistreatment of Brugada syndrome.

Brugada phenocopy caused by a compressive mediastinal tumor.

Recently, it has been shown that even experts in electrocardiography cannot differentiate the electrocardiographic pattern of genuine Brugada syndrome (BrS) from Brugada phenocopy (BrP). For this reason, this differentiation depends on the presence of established criteria both for BrS and BrP. In this manuscript, we present a patient with type 1 Brugada electrocardiographic pattern caused by expansive anterior mediastinal non-Hodgkin's lymphoma (NHL) with mechanical compression on the right ventricular outflow tract. The electrocardiographic pattern disappeared rapidly after antineoplastic measures.