Brugada syndrome is a rare hereditary ion channelopathy associated with ventricular arrhythmias and sudden cardiac death, most commonly linked to mutations in the SCN5A gene. We report the case of a 47-year-old Hispanic male who experienced out-of-hospital cardiac arrest due to ventricular fibrillation. Post-resuscitation electrocardiogram revealed a Type I Brugada pattern with coved ST-segment elevations in leads V1–V3. Echocardiography showed mildly reduced left ventricular systolic function, and coronary angiography demonstrated no obstructive disease. The patient underwent successful implantable cardioverter-defibrillator placement and was referred for genetic evaluation. Sepsis was identified as the precipitating factor for his malignant arrhythmia. Although Brugada syndrome has been described more frequently in Asian populations, its occurrence in Hispanic patients is rare and underrecognized. This case highlights the importance of considering Brugada syndrome in patients presenting with unexplained ventricular arrhythmias and anterior ST-segment elevation, even in demographics where the condition is less commonly reported.
Case Presentation:
A 47-year-old Hispanic male with a history of obesity, cervical disc disease andprimary hypertension was admitted following a witnessed out-of-hospital cardiac arrest. He had recently traveled from Mexico to Georgia and collapsed suddenly while playing with his daughter, exhibiting eye-rolling, abnormal jerky movements, and labored breathing. Emergency medical services arrived within 5–10 minutes and found him in ventricular tachycardia/fibrillation, requiring five shocks, CPR, and intubation. Return of spontaneous circulation was achieved, and he was transported to the emergency department. On arrival, he was tachycardic and hypertensive, with arterial blood gas demonstrating metabolic acidosis. Laboratory findings were notable for leukocytosis, elevated lactate, electrolyte disturbances, elevated liver enzymes, and mildly elevated troponin. Urine toxicology and chest X-ray was unremarkable. He was initiated on IV fluids, broad-spectrum antibiotics, sedation, and therapeutic hypothermia.
Post-resuscitation electrocardiogram revealed a type 1 Brugada pattern, with coved ST-segment elevation in leads V1–V3 (Figure 1). The diagnosis was further confirmed by repeating the ECG with leads V1–V2 placed one intercostal space higher, which again demonstrated the characteristic Type 1 Brugada pattern.His wife denied prior cardiac symptoms, syncope, or family history of sudden cardiac death. Echocardiography revealed mildly reduced left ventricular systolic function with an ejection fraction of 46–50% and mild concentric left ventricular hypertrophy. Coronary angiography demonstrated patent coronary arteries with normal hemodynamics. The patient was managed with strict fever control, avoidance of sodium channel–blocking agents, and aggressive correction of electrolytes. He stabilized with supportive care, and repeat echocardiography showed improvement of ejection fraction to 60%.Interestingly, his ECG normalized once the sepsis resolved after 7 days, as demonstrated in Figure 2.
Given the diagnosis of Brugada syndrome complicated by cardiac arrest, a dual-chamber ICD was implanted for secondary prevention (Figure 3). The patient tolerated the procedure well, and post-implant chest X-ray confirmed appropriate device positioning. At discharge, he was advised to follow up closely for Genetic Counseling and a Cardiologist. This case underscores the importance of considering Brugada syndrome as a cause of unexplained sudden cardiac arrest, particularly in underrepresented populations such as Hispanics, where reports remain scarce.
Figure 1: Type 1 Brugada pattern with coved ST-segment elevations inlead V1-V2and Right axis deviation
Figure 2: Electrocardiogram obtained on hospital day 7 demonstrating normalization of the tracing with resolution of the Brugada pattern following treatment of sepsis.
Figure 3: Chest X-ray showing Dual camber
Brugada syndrome is an autosomal dominant condition linked to mutations in the SCN5A gene, which accounts for about 30% of identified cases. It is characterized by a pseudo–right bundle branch block and persistent ST-segment elevation in right precordial leads, predisposing patients to malignant ventricular arrhythmias and sudden cardiac death. The type 1 ECG pattern shows a coved ST elevation (≥2 mm) followed by an inverted T wave, whereas the type 2 pattern displays a saddleback configuration with the ST segment descending toward baseline and then rising to an upright or biphasic T wave.Patients with Brugada pattern show characteristic ECG changes but lack clinical criteria. A diagnosis of Brugada syndrome requires a type 1 ECG plus at least one clinical feature, such as ventricular arrhythmia, syncope, nocturnal agonal respiration, or a family history of sudden cardiac death.[1] In our patient, the diagnosis was confirmed by cardiac arrest due to VT/VF in the presence of a type 1 Brugada ECG pattern.
Ventricular fibrillation–induced sudden cardiac arrest is a defining manifestation of Brugada syndrome and represents a major cause of sudden death in these patients.[2]In children and adolescents, Brugada syndrome is most often detected on surveillance ECG when there is a known family history. Without such a history, diagnosis can be difficult since the Brugada pattern may remain concealed unless triggered by factors like fever.[3] In our patient, the Brugada type 1 ECG became evident after a febrile illness, ultimately leading to cardiac arrest and confirming the diagnosis.
Brugada syndrome is exceptionally rare in Hispanic populations; it is estimated to be approximately 36 times more prevalent in Asians compared to Hispanics. Consistently, a U.S.-based screening study found only one Hispanic patient (out of 20.8% of the study population) with a Brugada-type ECG, reinforcing its rarity in this ethnic group.[4,5]
Brugada syndrome carries a lifelong risk of sudden cardiac death, and no pharmacologic therapy has been shown to reliably reduce this risk. Implantable cardioverter-defibrillators (ICDs) remain the most effective strategy for prevention and are generally the treatment of choice. Medications are reserved for acute arrhythmic storms, patients with frequent ICD shocks, or when an ICD is contraindicated or refused.[6] In our patient, ICD implantation was successfully performed as the definitive preventive measure.
Management in our patient included aggressive hydration, electrolyte replacement, and antipyretic therapy. Antiarrhythmic use remains controversial in Brugada syndrome, with amiodarone and lidocaine having uncertain benefit and procainamide generally contraindicated.[7] Brugada syndrome cannot be anticipated in any specific demographic or age group. While its occurrence in geriatric and Hispanic populations is exceptionally rare and poorly studied, it remains a life-threatening condition that demands careful recognition, clear management strategies, and an understanding of the associated mortality risks in these patients.[8]
This case highlights the unusual presentation of Brugada syndrome in a Hispanic patient, an ethnic group in which the condition is rarely reported. It underscores the importance of maintaining a high index of suspicion when evaluating patients who present with sudden cardiac arrest due to ventricular fibrillation. Recognition of a Type I Brugada pattern on ECG, combined with thorough clinical assessment, is essential for timely diagnosis. Early identification and appropriate management, including ICD implantation where indicated, remain key strategies in preventing sudden cardiac death in these patients.
This case underscores the importance of considering Brugada syndrome in diverse populations, including Hispanics, and highlights the need for heightened clinical suspicion when evaluating unexplained ventricular arrhythmias and anterior ST-segment elevation. Early diagnosis and prompt ICD placement remain critical in preventing sudden cardiac death.
Key Points:
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