Dietary and emotional triggers of ventricular fibrillation in Brugada syndrome: insights from a long-term subcutaneous implantable cardioverter-defibrillator case report

Introduction

Brugada syndrome (BrS) is an inherited cardiac channelopathy characterized by an increased risk of malignant arrhythmias and sudden cardiac death (SCD). It is more prevalent in Asian populations and displays marked phenotypic heterogeneity (1); although many patients remain asymptomatic, others may experience sudden cardiac arrest as their first manifestation. Early identification, risk stratification, and long-term follow-up are therefore critical. We describe the clinical course of a patient with BrS, from diagnosis through management, including seven-year follow-up data supporting the long-term efficacy of a subcutaneous implantable cardioverter-defibrillator (S-ICD) therapy. Additionally, this case highlights the role of high-calorie intake and emotional stress as potential triggers for ventricular fibrillation (VF), offering important insights for comprehensive risk management in BrS. We present this case in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-275/rc).

Case presentation

A 42-year-old Chinese male, with a weight of 65 kg and a height of 173 cm, was transferred to the Emergency Department of Affiliated Kunshan Hospital of Jiangsu University from a peripheral medical facility after experiencing multiple recurrent episodes of VF. During sleep, he abruptly developed convulsive movements of the extremities and lost consciousness, causing a fall from bed. He regained consciousness minutes later. The patient was transported by his wife to a local hospital, where initial imaging and laboratory results were within normal limits. Further history taking revealed that the patient reported no chest pain or dyspnea on the evening prior to the event, had no history of nocturnal sleep apnea, denied alcohol consumption, but admitted to consuming a large amount of bubble tea during a late-night snack. During evaluation in the emergency department, he experienced another syncopal episode with convulsions. Cardiac monitoring demonstrated VF, with sinus rhythm restored following chest compressions and one 150-joule biphasic defibrillation (Figure 1). Approximately 30 minutes later, VF recurred and was again successfully terminated by electrical defibrillation. The patient remained hemodynamically stable with a blood pressure of 133/91 mmHg, a regular heart rate of 72 beats/min, and oxygen saturation of 99%. The patient was admitted to Affiliated Kunshan Hospital of Jiangsu University for further evaluation and management.

Figure 1 Brugada syndrome devolving into VF and was converted to sinus rhythm by electrical defibrillation. VF, ventricular fibrillation.

The patient had no history of any previous cardiovascular disease or family history of SCD.

The patient is diagnosed with BrS. The differential diagnosis included coronary spastic angina, J-wave syndrome and pulmonary embolism.

Initial laboratory studies at our institution demonstrated a negative troponin result, elevated myoglobin (246 ng/mL), hypokalemia (serum potassium 3.3 mmol/L), a venous glucose level of 8.7 mmol/L, and an N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) level of 182.0 pg/mL (reference range <125 pg/mL). Standard 12-lead electrocardiography (ECG) and high intercostal space ECG leads revealed a type 1 Brugada pattern (Figure 2). His echocardiogram revealed a preserved left ventricular ejection fraction without any valvular or other structural abnormalities. Coronary computed tomography angiography and 24-hour Holter monitoring showed no significant abnormalities. Carotid artery ultrasonography identified a 7.7 mm × 2.7 mm plaque at the bulb of the left common carotid artery. During the same period, standard 12-lead ECGs obtained from the patient’s son, father, and younger sister revealed no abnormalities and were within normal limits (Figure 3).

Figure 2 The patient’s ECG on admission was consistent with type 1 Brugada pattern: (A) standard 12-lead; (B) high intercostal space precordial leads. ECG, electrocardiography.

Figure 3 ECGs of the patient’s immediate family members are within normal ranges: (A) the patient’s son; (B) the patient’s father; (C) the patient’s sister. ECG, electrocardiography.

During the hospitalization, the patient underwent implantation of a S-ICD and was subsequently discharged in stable condition.

Two years later, on the evening of September 4, 2020, following emotional distress due to his father’s traffic accident, the patient experienced two episodes of transient loss of consciousness, each lasting approximately 10 seconds. Upon regaining consciousness, he reported a burning pain over the precordial skin. His family brought him to our emergency department. Interrogation of his S-ICD revealed two episodes of VF, both successfully terminated by appropriate S-ICD shocks (Figure 4). He was admitted for continuous telemetry monitoring. Repeat laboratory tests, including serum potassium, were within normal limits. ECG during this admission confirmed a type 1 Brugada pattern. Over the subsequent 5-year follow-up, no further syncope occurred, and no inappropriate shocks were delivered by the S-ICD. ECGs obtained during the acute events in 2018 and 2020 showed type 1 Brugada pattern, while his baseline ECG exhibited type 2 Brugada pattern. At the most recent follow-up in 2025, the patient’s ECG continued to show a type 2 Brugada pattern (Figure 5).

Figure 4 Two episodes of VF (A,B), initiated by emotional stress, were detected and successfully terminated by the S-ICD. (A) S-ICD recognition and successful defibrillation of first VF episode. (B) S-ICD recognition and successful defibrillation of second VF episode, 2 hours later. S-ICD, subcutaneous implantable cardioverter defibrillator; VF, ventricular fibrillation.

Figure 5 The follow-up ECG revealed a type 2 Brugada pattern: saddle-back pattern with >2 mm ST segment elevation in lead V2. ECG, electrocardiography.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

This case report describes the clinical course of a 42-year-old Asian male with a classic presentation of BrS, who presented with recurrent VF and aborted SCD. The patient was successfully managed with a S-ICD. During the 7-year follow-up, the S-ICD effectively terminated a recurrent VF episode triggered by acute emotional stress. Notably, the patient remained free of further arrhythmic events or inappropriate shocks over the subsequent 5 years, supporting the long-term efficacy and safety of S-ICD for secondary prevention in BrS.

BrS is an autosomal dominant inherited channelopathy with strong male predominance and higher prevalence among Southeast and East Asian populations, particularly those of Japanese, Thai, and Filipino descent (1,2). The clinical presentation of BrS in Asian populations exhibits distinct characteristics: a majority of asymptomatic patients may display the typical type 1 electrocardiographic pattern, while arrhythmic events frequently occur at rest or during sleep, associated with increased vagal tone or an imbalance in sympathovagal activity (2). In this case, the initial VF episode occurred during early morning sleep, consistent with this profile. Additionally, the patient had consumed approximately 3 liters of bubble tea the night before the event, which contains high-calorie ingredients such as high-fructose corn syrup or white sugar, along with substantial amounts of components like tea polyphenols and caffeine. Previous reports have linked high-calorie meals, energy drink, strong tea and specific dietary components to arrhythmogenesis in BrS (3-6). It was demonstrated that caffeine is able to stimulate calcium release from the sarcoplasmic reticulum (7), and calcium imbalances, particularly sarcoplasmic reticulum calcium stores, may be altered in BrS (8). Thus, although dietary modification alone is insufficient to prevent events entirely, prudent nutritional guidance may help mitigate risk. Emotional stress also emerged as a clear trigger for VF in this patient, underscoring the importance of psychological support and avoidance of intense emotional exposures.

Current guidelines strongly recommend ICD implantation for secondary prevention in BrS patients with a history of SCD or life-threatening arrhythmias (9,10). For this young patient with an inherited channelopathy, who required only defibrillation therapy without the need for pacing or cardiac resynchronization, implanting a S-ICD rather than a transvenous system was a superior choice, as it eliminates the long-term risks associated with transvenous leads, such as infection, lead fracture, or tricuspid regurgitation. The efficacy of the device was unequivocally demonstrated 2 years post-implantation, when the S-ICD successfully terminated two subsequent episodes of VF, both triggered by intense emotional distress—a well-documented and potent arrhythmic stimulus in BrS, potentially mediated by autonomic nervous system activation and catecholamine surges (11).

Long-term follow-up is essential in BrS. This case, through its 7-year follow-up, not only confirms the effectiveness of the S-ICD but also suggests that BrS may exhibit a relatively stable disease course following an “electrical storm”. The recurrence of VF in 2020 followed by 5 years without events highlights the need for sustained vigilance and lifelong monitoring, as the risk does not dissipate but rather lurks intermittently. Concurrently, this case also documented that the patient’s baseline electrocardiogram showed a type 2 BrS pattern, which converted to type 1 prior to the event, highlighting the significant value of identifying event triggers and employing dynamic ECG monitoring for risk stratification (10). Consequently, meticulous patient guidance by specialists is required, encompassing safe pharmacotherapy (BrugadaDrugs.org), adaptations in neuromodulation, lifestyle interventions, and regular ICD programming optimization. Given the excellent efficacy of the S-ICD as a safety net and the absence of recurrent electrical storms, this case also illustrates the lack of necessity for adjunctive pharmacotherapy, such as quinidine, in this specific patient.

We acknowledge the limitations of this case report. Although electrocardiogram screening was performed on the immediate family members of the patient, genetic testing was not conducted. This precludes the identification of potential pathogenic mutations and limits cascade screening among asymptomatic relatives. Furthermore, as a single-case observation, this report cannot alter population-based risk stratification models; however, it contributes to the growing collective experience regarding the management of BrS in Asian patients.

Conclusions

This case illustrates a classic presentation of BrS in a 42-year-old Asian male, characterized by recurrent VF and aborted SCD. The patient was successfully managed with S-ICD, which effectively terminated two further VF episodes triggered by emotional stress during 7 years of follow-up. Notably, the patient remained event-free for the subsequent 5 years, underscoring the long-term efficacy and safety of S-ICD in secondary prevention for BrS. The case also highlights the role of high-calorie food and emotional stress as potential triggers for VF in susceptible individuals, reinforcing the importance of lifestyle modifications and psychological support in comprehensive BrS management.

Electrocardiographic dynamic changes—from type 2 BrS pattern at baseline to type 1 prior to events—emphasize the value of continuous risk stratification through repeated monitoring. Future efforts should focus on systematic genetic screening and familial cascade testing to improve early identification and risk prediction. Larger prospective studies in Asian populations are needed to validate these observations and refine management strategies.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-275/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2025-275/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2025-275/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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