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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.

Mechanical heart compression, including that from mediastinal tumor, may cause Brugada-like ECG pattern. Such ECG pattern might also be observed in intracardiac tumor obstructing the right ventricular out"ow tract (RVOT). Eight cases with Brugada-like ECG and tumors involving RVOT have been described so far; 4 growing in the mediastinum (with one example of in"ammatory mass), 3 with intracardiac location, and 1 being an organized pericardial hematoma. The authors present other 3 cases of intracardiac metastatic tumors in RVOT and Brugada-like ECG pattern with coved ST-segment elevation in the right precordial leads. All patients had negative history of cardiovascular disease or familiar malignant arrhythmia occurrence. ECG were done routinely; none of the patients had chest pain or an increased level of cardiac troponins. In all patients, neoplastic disease was at advanced stage. A 76-year-old male, had a history of four neoplasms: bladder cancer was being treated with chemotherapy, while prostate, tongue, and lung cancers had been resected years ago and no signs of local relapse were found. A 78-year-old female, was diagnosed with colon cancer 1 month after an episode of venous thromboembolism. Six months after the resection of cancer, second focus of adenocarcinoma was found in the rectum. Third patient, a 65-year-old-male had undergone nephrectomy for renal cancer a year before cardiac metastasis diagnosis.

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., (© 2022 MEDPRESS.)